Database Query Results : Selenium, ,

Se, Selenium: Click to Expand ⟱
Features: micronutrient
Naturally occurring element. Selenium is incorporated into selenoproteins, such as glutathione peroxidases (GPxs) and thioredoxin reductases (TrxRs), which play critical roles in protecting cells from oxidative damage.
Involved in GPx, TrxR, ans Selenoprotien P which protect normal cells from oxidative stress.
Important in Thyroid hormone metabolism, immune system regulation, reproductive health, and Brain and heart protection.

-recommended daily allowance (RDA) for selenium is about 55 µg/day for adults. (upper tolerance 400ug/day)
-One Brazil nut may contain 50-300ug/nut

Sodium selenite (Na₂SeO₃) is a selenium compound with well-documented anticancer and chemopreventive properties
-Oxidation state: +4 (selenite form of selenium)
-Type: Inorganic selenium compound (water-soluble)

-Sodium selenite generates reactive oxygen species (ROS) selectively in tumor cells.
-Induces cytochrome c release, caspase-3 activation, and DNA fragmentation.
-Reduces VEGF expression and endothelial cell migration.
-Blocks cell division at G2/M phase
-Suppresses MMP-2 and MMP-9 activity
-Activates p53
-Inhibits NF-κB
-PI3K/Akt/mTOR Suppression
-Inactivation of Thioredoxin/Glutathione systems
-NRF2 inhibition in cancer cell might be connected with O2 level

Narrow therapeutic window:
-Low micromolar (≤5 µM) → anticancer
-High (>10 µM) → toxic to normal cells

Some Selenium Supplements use Sodium Selenite as the active ingredient.
- NOW Foods Selenium, Nature's Bounty Selenium, etc

Other common form is Selenomethionine, as it is better absorbed (found in brazil nuts), but might be less effective?

Sodium selenite might protect against toxicity of AgNPs. also here

In the chemical synthesis of selenium nanoparticles, a precursor such as sodium selenite (Na₂SeO₃) is dissolved in water to form a homogenous solution. A reducing agent, like ascorbic acid or sodium borohydride (NaBH₄), is then added to the solution. The reducing agent donates electrons to the selenium ions (SeO32−SeO32), reducing them to elemental selenium (Se0Se^0). This reduction process leads to the nucleation of selenium atoms, which subsequently grow into nanoparticles through controlled aggregation.

Se NPs might be hepatoprotective.
(chemoprotective) (radioprotective) (radiosensitizer)

Selenium nanoparticles (SeNPs) are a biocompatible, less-toxic, 
and more controllable form of selenium compared to inorganic salts (like sodium selenite).
Major SeNPs hepatoprotective mechanisms
Mechanism	              Description	                       Key markers affected
1. Antioxidant activity	      SeNPs boost antioxidant enzyme          ↓ ROS, ↓ MDA, ↑ GSH, ↑ GPx
                              systems (GPx, SOD, CAT) and scavenge 
                              ROS directly.	
2. Anti-inflammatory effect   Downregulate NF-κB, TNF-α,              ↓ TNF-α, ↓ IL-1β, ↓ IL-6
                              IL-6, and COX-2 pathways.	
3. Anti-apoptotic action      Balance between Bcl-2/Bax and reduce    ↑ Bcl-2, ↓ Bax, ↓ Caspase-3
                              caspase-3 activation in hepatocytes.	
4. Metal/toxin chelation      SeNPs can bind or transform toxic       ↓ liver metal accumulation
                              metals (Cd²⁺, Hg²⁺, As³⁺) 
                              into less harmful complexes.	
5. Mitochondrial protection   Maintain membrane potential,            Preserved ΔΨm, ↑ ATP
                              prevent mitochondrial ROS burst, 
                              and ATP loss.	
6. Regeneration support	      Stimulate hepatocyte proliferation      ↑ PCNA, improved histology
                              and repair via redox signaling 
                              and selenoproteins.

Comparison: SeNPs vs. Sodium Selenite
Property	             SeNPs	                   Sodium Selenite
Toxicity	             Low	                   Moderate–high
Bioavailability	             Controlled, often slow-       Rapid, less controllable
                             release	
ROS balance	             Adaptive, mild antioxidant	   Can flip to pro-oxidant easily
Safety margin	             Wide	                   Narrow
Hepatoprotection	     Strong, sustained	           Protective at low dose, 
                                                           toxic at high dose
Form of SeNPs matter:
1. Core composition / capping agent: SeNPs can be stabilized with polysaccharides, proteins, or small molecules. Some stabilizers may interact with cellular redox systems differently—e.g., a protein-capped SeNP may have slower release and less ROS generation, whereas a bare SeNP might induce stronger ROS in cancer cells.
2. Particle size: Smaller SeNPs (<50 nm) tend to generate more ROS and may enhance anticancer activity, but could theoretically interfere with ROS-dependent chemo if administered simultaneously. Larger SeNPs are slower-acting and may be safer alongside chemo.
3. Surface charge / coating: Positively charged or functionalized SeNPs can preferentially enter tumor cells, whereas neutral or negatively charged forms may distribute more evenly. This affects both selective cytotoxicity and interaction with normal cells.

"30 mg of Na2SeO3.5H2O was added to 90 mL of Milli-Q water. Ascorbic acid (10 mL, 56.7 mM) was added dropwise to sodium selenite solution with vigorous stirring. 10 µL of polysorbate were added after each 2 ml of ascorbic acid. Selenium nanoparticles were formed after the addition of ascorbic acid. This can be visualized by a color change of the reactant solution from clear white to clear red. All solutions were made in a sterile environment by using a sterile cabinet and double distilled water."
Scientific Papers found: Click to Expand⟱
4746- antiOx,  Chemo,  VitA,RetA,  VitC,  Se  Using Supplements During Chemo: Yes or No?
- Review, Var, NA
eff↓, Taking antioxidants in supplement form (again, remember that antioxidants in food are fine) may actually “protect” cancer cells during treatment.
ChemoSen↓, In other words, antioxidants in pill form have the potential to counteract the effects of chemotherapy or radiation therapy.
RadioS↓,
other↝, Common antioxidant supplements taken by patients include vitamins A, C, and E, carotenoids (such as beta-carotene and lycopene) as well as selenium and Coenzyme Q10.

3517- Bor,  Se,    The protective effects of selenium and boron on cyclophosphamide-induced hepatic oxidative stress, inflammation, and apoptosis in rats
- in-vivo, Nor, NA
*hepatoP↑, However, it was found that Se protects the liver slightly better against CP damage than B
*ALAT↓, statistically significant difference was observed in the serum levels of ALT, AST, ALP, TAS, TOS and OSI.
*AST↓,
*ALP↓,
*NF-kB↓, A statistically significant difference was observed in serum levels of NF-kB, TNF-α, IL -1β, IL -6 and IL -10 when the Se + CP and B + CP-treated groups were compared with the CP-treated group
*TNF-α↓, fig 9
*IL1β↓,
*IL6↓,
*IL10↑,
*SOD↑, A statistically remarkable change in serum levels of SOD, CAT, GPx, MDA and GSH was observed in the group receiving only CP compared to groups Se, B and the control.
*Catalase↑,
*MDA↓, Fig 10
*GSH↑,
*GPx↑,
*antiOx↑, suggests that B and Se increase intracellular antioxidant status.
*NRF2↑, Se and B treatment can protect rat liver tissue from CP-induced oxidative stress, inflammation, and apoptosis by regulating Bax/Bcl-2 and Nrf2-Keap-1 signaling pathways.
*Keap1↓,

4489- Chit,  Se,    Inhibiting Metastasis and Improving Chemosensitivity via Chitosan-Coated Selenium Nanoparticles for Brain Cancer Therapy
- in-vitro, GBM, U87MG
TumCG↓, Compared with SeNPs, Cs-SeNPs more strongly inhibited 3D-tumor spheroid growth.
TumCMig↓, Cs-SeNPs exhibited stronger effects in inhibiting cell migration and cell invasion than SeNPs.
TumCI↓,
ChemoSen↑, Improved 5-FU sensitivity was observed in Cs-SeNP-treated cells.
*BBB↑, capability of coumarin-6 associated Cs-SeNPs to pass through the BBB was confirmed.
eff↑, nanotechnology plays a crucial role in developing selenium nanoparticles (SeNPs) to overcome this obstacle by reducing toxicity and improving biocompatibility
eff↑, result obviously indicates that Cs-SeNPs have a significantly higher positive charge than SeNPs; CS-SeNPs provided strong positive charges to the nanoparticles due to the positive charge of chitosan
eff↑, The size of SeNPs was also found to be greater than that of Cs-SeNPs
selectivity↑, 0.2% CS-SeNPs provided a large difference in toxicity between normal and cancer cells
MMP2↓, Cs-SeNPs Inhibited Cell Migration and Cell Invasion of Glioma Cells by Inhibiting MMP-2/9 Activities
MMP9↓,
EPR↑, Chitosan Coating Enhanced Cellular Uptake of Cs-SeNPs in U87 Cells

4493- Chit,  Selenate,  Se,    A novel synthetic chitosan selenate (CS) induces apoptosis in A549 lung cancer cells via the Fas/FasL pathway
- in-vitro, Lung, A549
tumCV↓, CS could significantly inhibit A549 cells viability in a dose-dependent manner.
Apoptosis↑, CS induced cell death via apoptosis and not necrosis.
TumCCA↑, CS triggered S and G2/M phase arrest in a dose-dependent manner
Fas↑, CS up-regulated the expression levels of Fas, FasL, and Fadd
FasL↑,
FADD↑,
Casp↑, activated the caspase cascade in A549 cells

2806- CHr,  Se,    Selenium-containing chrysin and quercetin derivatives: attractive scaffolds for cancer therapy
- in-vitro, Var, NA
eff↑, SeChry elicited a noteworthy cytotoxic activity with mean IC50 values 18- and 3-fold lower than those observed for chrysin and cisplatin, respectively
selectivity↑, differential behavior toward malignant and nonmalignant cells was observed for SeChry and SePQue, exhibiting higher selectivity indexes
Dose↝, 5 min. of microwave irradiation at 175 W (150 ºC) of an acetonitrile WR and flavonoid solution on a sealed pyrex microwave vial,
TrxR↓, Both compounds were able to decrease cellular TrxR
GSH↓, The results clearly showed that after treatment with both seleno-flavonoids total glutathione concentration (GSH + GSSG) decreased
MMP↓, MMP reduced by up to four times compared to control cells
ROS↑, Both seleno-derivatives were able to increase the oxidant basal production
H2O2↑, ore dramatic decrease of the MMP and a higher ability to increase the hydrogen peroxide basal production,

3994- CoQ10,  Se,    Coenzyme Q10 Supplementation in Aging and Disease
- Review, AD, NA - Review, Park, NA
*AntiAge↑, supplementation positively affects mitochondrial deficiency syndrome and the symptoms of aging based mainly on improvements in bioenergetics.
*cardioP↑, Cardiovascular disease and inflammation are alleviated by the antioxidant effect of CoQ10
*Inflam↓, Administration of CoQ10 in doses ranging from 60 to 500 mg/day for a 1-week to 4-month intervention period significantly decreased production of inflammatory cytokines
*antiOx↑,
*lipid-P↓, The concentrations of CoQ10 in the plasma of elderly people are positively correlated with levels of physical activity and cholesterol concentrations (Del Pozo-Cruz et al., 2014a,b), as well as with lower lipid oxidative damage.
*QoL↑, Older individuals given a combination of selenium and CoQ10 over a 4-year period reported an improvement in vitality, physical performance, and quality of life
*neuroP↑, health benefits in elderly people by preventing chronic oxidative stress associated with cardiovascular and neurodegenerative diseases
*Dose↝, the highest dose for CoQ10 supplementation is 1200 mg daily according to well-designed randomized, controlled human trials, although doses as high as 3000 mg/day have been used in shorter clinical trials
*BP↓, These authors interpreted the results to indicate a significant reduction in systolic blood pressure without improvements in other CVD risk factors, such as diastolic blood pressure, total cholesterol, LDL- and high-density lipoprotein (HDL)-choleste
*IGF-1↑, elderly healthy participants who received selenium and CoQ10 supplementation for over 4 years, an increase in insulin-like growth factor 1 (IGF-1) and postprandial insulin-like growth factor-binding protein 1 (IGFBP-1) levels
*IGFBP1↑,
*eff↑, A combination of CoQ10 with red yeast rice, berberina, policosanol, astaxanthin, and folic acid significantly decreased total cholesterol, LDL-cholesterol, triglycerides, and glucose in the blood while increasing HDL-cholesterol levels
*LDL↓,
*HDL↑,
*eff↑, 60 patients suffering from statin-associated myopathy were enrolled in a 3-month study to test for efficacy of CoQ10 and selenium treatment. A consistent reduction in their symptoms, including muscle pain, weakness, cramps, and fatigue was observed
*other↑, Because of its capacity to reduce the side-effects of statins, CoQ10 has been proposed to prevent and/or slow the progression of frailty and sarcopenia in the elderly chronically treated with statins.
*RenoP↑, experiments performed on rats showed a promising protective effect of ubiquinol in the kidneys
*ROS↓, 65 patients undergoing hemodialysis, supplementation with high amounts of CoQ10 (1200 mg/day) lowered F2-isoprostane plasma levels indicative of a reduction in oxidative stress
*TNF-α↓, low grade inflammation, respond well to CoQ10 supplementation with significant decrease in TNF-α plasma levels without having an effect on C-reactive protein and IL-6 production
*IL6↓, Another study reported that CoQ10 therapy in doses ranging from 60 to 300 mg/day caused no significant decrease in C-reactive protein while eliciting a significant reduction in IL-6 levels
*other↝, Preclinical studies demonstrated that CoQ can preserve mitochondrial function and reduce the loss of dopaminergic neurons in the case of Parkinson's disease
*other∅, There was no improvement observed in oxidative stress or neurodegeneration markers in a randomized clinical trial in Alzheimer's Disease patients with CoQ10 supplementation at a dose of 400 mg/day for 16 weeks

641- EGCG,  Se,    Antioxidant effects of green tea
ROS↑, Concentration is a factor that could determine whether green tea polyphenols act as antioxidants or pro-oxidants. EGC and EGCG, both generate hydrogen peroxide at concentrations greater than 10 μM
H2O2↑, Adding milk to green tea decreases formation of hydrogen peroxide,
ROS⇅, Selenium could enhance anticancer activity of green tea [29], possibly by enhancing antioxidant activity [30, 31], or even its pro-oxidant activity [32].

4611- Se,  Rad,    Radioprotective Effect of Selenium Nanoparticles: A Mini Review
- Review, Var, NA
*antiOx↑, The reviewed studies showed that selenium nanoparticles had anti-inflammatory and antioxidant properties.
*Inflam↓,
*radioP↑, Furthermore, there was evidence of efficient radioprotection for the organs examined without significant side effects.
*ROCK1↓, Selenium nanoparticles can scavenge reactive oxygen species (ROS) produced by ionizing radiation, protect normal cells from DNA damage and apoptosis, and increase the radiosensitivity of tumor cells.
*DNAdam↓,
*Apoptosis↓,
*RadioS↑,
*Dose↝, The studies that mainly used a dose of 0.5 mg/kg body weight of SeNPs to assess its radioprotective effects were included for analysis. This dose of SeNPs was effective in preventing kidney and liver damage caused by IR.

4612- Se,  Rad,    Histopathological Evaluation of Radioprotective Effects: Selenium Nanoparticles Protect Lung Tissue from Radiation Damage
- in-vivo, Nor, NA
*radioP↑, This study highlights the significant potential of SeNPs as radioprotective agents, showing they mitigate radiation-induced lung damage by preserving tissue integrity and reducing inflammation, consistent with their known antioxidant and anti-inflamm
*Inflam↓,
*antiOx↑,
*Dose↝, SeNPs were administered via intraperitoneal (IP) injection starting 10 days before irradiation, continuing until the day of irradiation. On the tenth day, final doses were given 30 minutes prior to irradiation
*DNAdam↓, SeNPs have attracted considerable interest as radioprotective agents due to their capacity to reduce radiation-induced oxidative stress and DNA damage.[
*ROS↓, By scavenging ROS and enhancing the activity of endogenous antioxidant enzymes such as superoxide dismutase SOD and glutathione peroxidase GPx,
*SOD↑,
*GPx↑,
*Dose↝, predominant dosage of 0.5 mg/kg body weight used in our experiments is consistent with previous studies that have documented its efficacy
*eff↑, combination of SeNPs with other agents, such as fish oil, has been shown to enhance protective effects against liver toxicity induced by radiation and chemotherapy

4610- Se,  Rad,    Protection during radiotherapy: selenium
- Review, Var, NA
*radioP↑, Ebselen, and sodium selenite, emerges as a promising radioprotective agent with demonstrated efficacy across diverse radiation-injured organs, highlighting its significance as an effective and potent antioxidant that affordable for most patients.
*antiOx↑,
*Inflam↓, In short, the antioxidation, anti-inflammatory effect and DNA stabilizing formed the protective effects of selenium against DNA damage induced by radiation
*DNAdam↓,
*lipid-P↓, Se-Met could efficiently inhibit the formation of lipid peroxy radicals, preventing lipid peroxidation
*selenoP↑, primarily enhance the expression of selenoproteins, thus sodium selenite may not be inherently antioxidant until incorporated into selenoproteins with oxidoreductase functions
*GPx1↑, sodium selenite could increase GPx-1 activity in a dose- and time-dependent manner
*BUN↓, 100 µg/day of selenium in the form of sodium selenite or Se-L-Met, blood urea nitrogen (BUN) level of rats significantly decreased.

4609- Se,    Physiological Benefits of Novel Selenium Delivery via Nanoparticles
- Review, Var, NA - Review, IBD, NA - Review, Diabetic, NA
*selenoP↑, Biologically, Se is incorporated primarily into selenoproteins as the selenomethionine and selenocysteine amino acids at active sites
Risk↓, Se deficiency and high Se status is coincident with a range of pathologies, including obesity [10,11], cancer [12,13], arthropathy [14] as well as several immune- and neurological-related disorders
AntiCan↑, There is a growing body of research with a focus on the role of Se in cancer prevention which indicates a link between high Se exposure and decreased risk of breast, oesophagus, and prostate cancers
ROS↑, selenite treatment stimulated cancer cell apoptosis via a mechanism involving enhanced ROS generation and the accumulation of hydrogen peroxide which, ultimately, decreased cell viability
*Dose↝, IBD patients had lower Se levels than that of healthy individuals, potentially illustrating the importance of dietary Se as an antioxidant/micronutrient in the pathogenesis of IBD in humans
*toxicity↓, A major benefit of SeNPs is the significantly lower toxicity while retaining similar physiological impacts and efficacy in enhancing selenoprotein activities in comparison to that of other chemical seleno-forms
*BioAv↑, Selenium nanoparticles show an enhanced uptake post-ingestion as these SeNPs are smaller in size with larger surface areas and are more permeable through capillary walls, leading to superior epithelial cell uptake and enhanced bioactivity.
*GutMicro↑, research has also show that dietary Se improved the gut microbiome favourably by enhancing the abundance of beneficial bacteria and limiting the growth of undesirable pathogens
*other↓, In diabetic rats, SeNPs have shown to reduce proinflammatory markers, including IL-1β and TNF levels and renal MDA levels leading to lower oxidative stress, indicated by improved renal functions due to lower serum urea and creatinine along with reduc

4613- Se,  Rad,    Effect of Selenium and Selenoproteins on Radiation Resistance
- Review, Nor, NA
*selenoP↑, GPX1 is a selenoprotein with an active site containing selenocysteine
*GPx1↑,
*GPx4↑, GPX4 effectively inhibits lipid peroxide, it also promotes DNA repair
*lipid-P↓,
*DNAdam↓,
*ROS↓, It has been reported that selenium and selenoproteins can scavenge ROS directly.
*radioP↑, selenium and selenium protein as radiation protective agents to alleviate multiple organ damage caused by radiation or treat related diseases.

4486- Se,  Chit,    Selenium-Modified Chitosan Induces HepG2 Cell Apoptosis and Differential Protein Analysis
- in-vitro, Liver, HepG2
Apoptosis↑, selenium-modified chitosan (SMC)can induce HepG2 cell apoptosis with the cell cycle arrested in the S and G2/M phases
TumCCA↑,
MMP↓, gradual disruption of mitochondrial membrane potential
Bcl-2↓, reduce the expression of Bcl2, and improve the expression of Bax, cytochrome C, cleaved caspase 9, and cleaved caspase 3
BAX↑,
cl‑Casp9↑,
cl‑Casp3↑,
Risk↓, Relevant research suggests that an inverse relationship exists between selenium intake and cancer incidence, and selenium levels are usually lower in cancer patients.
*BioAv↑, favorable biocompatibility, good bioadhesivness, and low toxicity.
*toxicity↑,
TumCG↓, Studies have found that water-soluble chitosan can significantly inhibit the growth of liver cancer cells in a dose-dependent manner
AntiTum↑, SMC has been proved to possess stronger antitumor functions and lower toxicity in cancer patients
ROS↑, SMC induced A549 cell apoptosis via a reactive oxygen species–mediated mitochondrial apoptosis pathway, which upregulated Bax and downregulated Bcl2, promoted cytochrome C release from mitochondria to cytoplasm, and activated cleaved caspase 3
Cyt‑c↑,
Fas↑, upregulating the expression levels of Fas, FasL, and Fadd,
FasL↑,
FADD↑,

4608- Se,    Selenium Nanoparticles for Biomedical Applications: From Development and Characterization to Therapeutics
- Review, Var, NA - NA, AD, NA
*toxicity↝, Although Se shows several beneficial properties in human health, it has also a narrow therapeutic window, and therefore the excessive intake of inorganic and organic Se-based compounds often leads to toxicity
*toxicity↓, Nanoparticles based on Se (SeNPs) are less toxic than inorganic and organic Se.
*other↝, The twenty-first amino acid, selenocysteine (Sec),[4] is used to produce selenoproteins, whose function often depends on the presence of Se in their active site,[5] such as reactive oxygen species (ROS) protection.
ROS↑, SeNPs led to the production of higher levels of ROS than those obtained following the treatment of cancer cells with selenite, therefore presenting better antitumor properties than the Se salts
*Dose↝, recommended daily allowance (RDA) is 60 µg/day for women, 70 µg d−1 for men,[3] 75 µg d−1 for lactating women, and 65 µg d−1 for pregnant women according to the European Food Safety Authority
*selenoP↑, Se is mostly used for the production of selenoproteins, which are essential to human health due to their antioxidant effect, and role in controlling thyroid hormone metabolism, protein folding, redox signaling, among other functions.
AntiCan↑, Se has demonstrated antitumor, antiviral, antibacterial, and antifungal properties,[3] decreasing the risk of tuberculosis in HIV infected patients,[7, 47] and is well correlated to cancer prevention.
AntiTum↑,
*Bacteria↓,
*radioP↑, Se has shown to protect against heavy metals and radiation toxicity
*BioAv↑, food processing can also influence Se bioavailability, since increased temperatures improve protein digestibility, and enhance Se release and bioavailability
*Inflam↓, Se has anti-inflammatory and immunomodulatory actions
*Imm↑,
ChemoSen↑, Se has also been studied for cancer treatment as a radiotherapy and chemotherapeutic adjuvant since malignant cells are more susceptible to Se pro-oxidant effects than healthy cells.
*AntiAg↑, potential role of Se and selenoproteins in protecting the cardiovascular system against oxidative damage and excessive platelet aggregation
selectivity↑, SeNPs have shown potential to target specific cancer cells, by passive targeting based on the fact that the tumor environment is more acidic than the environment existing in healthy tissues
eff↑, chitosan(h)–SeNPs presented higher cellular uptake by cancer cells lines than normal cell lines, probably due to the higher amount of -NH3+ groups, which permits an enhanced electrostatic attraction between the positively charged chitosan(h)–SeNPs
other↝, In general, the charge of SeNPs is negative,[37, 138, 121] however surface modification with positive charged compounds such as chitosan can also flip the charge of SeNPs to positive
*eff↑, SeNPs have also shown to have a synergistic effect when combined with metformin
*Aβ↓, SeNPs have been shown to reduce Aβ aggregation and induce their disaggregation, in addition to acting as an antioxidant in the brain, either directly or by being part of GPx
*eff↑, SeNPs have also been studied together with other compounds that also shown properties against Alzheimer's disease, such as resveratrol (Res),[188] curcumin (Cur),[184] chiral D-penicillamine (DPen),[167] and chlorogenic acid (CGA)

4614- Se,  Rad,    Updates on clinical studies of selenium supplementation in radiotherapy
- Review, Nor, NA
*toxicity∅, At the dose of selenium used in these studies (200–500 μg/day), selenium supplementation did not reduce the effectiveness of radiotherapy, and no toxicities were reported.
Risk↓, moderate deficiency of selenium has been linked to many conditions, such as an increased risk of cancer, infections and male infertility;
*selenoP↑, Selenium in selenoproteins can reduce oxidative damage and can limit DNA damage
*ROS↓,
*DNAdam↓,
*QoL↑, Most of the studies revealed positive effects of selenium supplementation on the general condition of the patients and their quality of life.
*radioP↑, prevented or reduced the side effects of radiotherapy and did not reduce the effectiveness of radiotherapy or cause any toxicity.
*Dose↝, sodium selenite at doses ranging from 200–500 μg daily by oral administration may offer benefits for head and neck cancer; head and neck cancer with lymphedema; and oral, cervical and uterine cancer patients who undergo radiotherapy and have low sele

4607- Se,  SNP,    A Review on synthesis and their antibacterial activity of Silver and Selenium nanoparticles against biofilm forming Staphylococcus aureus
- Review, NA, NA
*Bacteria↓, antibacterial activity of Silver and Selenium nanoparticles against biofilm forming Staphylococcus aureus
*eff↑, Ag-based antiseptics that may be linked to broad-spectrum activity and far lower propensity to induce microbial resistance than antibiotics
ROS↑, In general, certain selenium compounds are catalytic and produce ROS by their interactionwith thiols, such as reduced glutathione, forming the glutathione selenide anion, GSSe. ̄ ... produced ROS which kills tumor cells
*Dose↝, According to the World Health Organization (WHO), a recommendeddaily dietary selenium intake is 40 μg Se/day
*eff↑, Silver coating of medical devices is believed to preserve infection resistance
toxicity↝, Exact mechanism of selenium toxicity remains unclear but there are many data about its prooxidant effect particularly in the form of selenite,while selenomethionine and selenocysteine are less toxic.
*Sepsis↓, We postulated that high-conc. supplementation of sodium-selenite would recover the outcome of patients with severe sepsis.(14 daily constant infusions of 1000 μg intravenously)
*other↝, Selenium is an essential dietary nutrient for most animals and humans, which is incorporated into twelve or more known proteins or enzymes as an amino acid, selenocysteine.
eff↑, Selenodiglutathione is the most potent selenium compound against cancer cells and readily arrests their growth as compared to selenite and any other selenium compound.

4606- Se,  VitC,    Antibacterial and anti-biofilm efficacy of selenium nanoparticles against Pseudomonas aeruginosa: Characterization and in vitro analysis
- in-vitro, NA, NA
*Dose↝, SeNPs were synthesized using ascorbic acid as a reducing agent and characterized.
*Dose↝, SeNPs demonstrated a round shape with a diameter of 15–18 nm.
*Bacteria↓, SeNPs could be a promising alternative or adjunctive treatment option for combating antibiotic-resistant P. aeruginosa infections.

4605- Se,    Selenium nanoparticles: An insight on its Pro-oxidant andantioxidant properties
- Review, NA, NA
*antiOx↑, unique antioxidant properties
*selenoP↑, antioxidant effect is chiefly due to the selenoenzymes such as thioredoxin reductase (TR) and glutathione peroxidasefamily (GPxs) which is having ROS scavenging activity.
*Dose↝, In humans, Se has the narrowest margin levels ranges between dietary deficiency (<40mg/day) and toxic levels (>400mg/day).
*toxicity↓, selenium having a narrow therapeutic window and the toxicity margins while, the selenium nanoparticle (SeNPs) having unusually reduced toxicity.
ROS↑, Because of the acidic pH state with redox imbalance these malignant cells will enables the selenium nanoparticles to exhibits pro-oxidant effect
ER Stress↑, cause mitochondrial membrane disruption which can cause leakageof mitochondrial (Mt) proteins and also causes endoplasmic reticulum(ER) stress.

4604- Se,  SNP,  Chit,    The ameliorative effect of selenium-loaded chitosan nanoparticles against silver nanoparticles-induced ovarian toxicity in female albino rats
- in-vivo, Nor, NA
*Dose↝, Group I (control) was given 0.5 ml/kg of distilled water; Group II was given Ag-NPs orally (100 mg/kg); Group III was given Ag-NPs orally (100 mg/kg/d) plus CS-SeNPs (0.5 mg/kg/d)
*GSH↑, successfully ameliorated by CS-SeNPs, as indicated by marked increases in GSH and SOD.
*SOD↑,
*toxicity↓, These findings indicate that CS-SeNPs supplementation may offer protection against the ovarian toxicity induced by Ag-NPs.

4603- Se,    Therapeutic applications of selenium nanoparticles
- Review, Var, NA
AntiCan↑, SeNPs have attractive anticancer and immunomodulatory properties.
Imm↑,
*AntiDiabetic↑, Figure 1
*antiOx↑,
*Inflam↓,
ROS↑, The anticancer activity is largely due to its prooxidant properties in these cells triggering reactive oxygen species (ROS) synthesis leading to mitochondrial and endoplasmic reticulum damage which in turn leads to DNA damage.
ER Stress↑,
DNAdam↑,
*toxicity↓, use of Se in the form of nanoparticles has substantially answered the toxicological concerns associated with Se
*eff↑, Bo Huang et al. showed that small sized (5–15 nm) SeNPs have better free radical scavenging capacity and prevented the oxidation of DNA.
*BioAv↑, SeNPs show better bioavailability, biological activity compared with inorganic and organic Se compounds.
selectivity↑, Interestingly, the NPs were found to preferentially localize inside the cancer cells and caused production of reactive oxygen species (ROS) thereby causing cytotoxicity
TumCCA↑, SeNPs effectively arrested the S phase in MDA-MB-231 cells at 10 μmol/L
Risk↓, In the case of lung cancer, pretreatment of SeNPs inhibited the incidence of lung cancer induced by ferric nitrilotriacetate.
*lipid-P↓, SeNPs decreased the lipid peroxidation, inflammation (TNF-α) and C reactive protein levels
*TNF-α↓,
*CRP↓,
TumMeta↓, SeNPs inhibit the matrix metalloprotein-2 expression which is mainly involved in tumor invasion, metastasis and angiogenesis in fibro-sarcoma cell lines (HT-1080)
angioG↓,
selectivity↑, SeNPs showed remarkable antiproliferative activity and no toxicity to normal HaCat cell lines
eff↑, SeNPs decorated with chitosan were found to induce comparatively higher apoptosis in A375 melanoma cells in a dose dependent manner, compared to liver (HepG2) and osteosarcoma (MG-63) cells and no toxicity to normal human kidney
*eff↑, Melatonin-SeNPs treatment (5, 10 and 20 mg/Kg) increased the activity of antioxidant enzymes like SOD, GPX activity, decreased serum ALT, AST, NO, MDA levels

4602- Se,  SNP,  GoldNP,    Advances in nephroprotection: the therapeutic role of selenium, silver, and gold nanoparticles in renal health
- NA, Nor, NA
*ROS↓, Selenium nanoparticles (SeNPs) minimize oxidative stress, a primary cause of nephrotoxicity through cell regeneration which protects kidneys.
*RenoP↑, Metallic nanoparticles of selenium, silver, and gold can protect the kidneys by lowering oxidative stress, reducing inflammation, and improving cell repair
*Inflam↓, Silver nanoparticles (AgNPs) have anti-inflammatory capabilities that help alleviate kidney damage and nephrotoxicity.

4601- Se,  SNP,    Antioxidant and hepatoprotective role of selenium against silver nanoparticles
- in-vivo, Nor, NA
*TAC↑, However, Se markedly attenuated AgNP-induced biochemical alterations, levels of TAC, CRP, and serum transaminases (AST, ALT) (P<0.05).
*CRP↓,
*AST↓, Pretreatment of rats with Se in AgNP-treated group caused reduction in the levels of AST and ALT
*ALAT↓,
*toxicity↓, Taken together, these findings suggest that administration of AgNPs produces hepatotoxicity in rats, whereas Se supplementation attenuates these effects.
*GSH↑, AgNPs’ treatment led to a decrease in the activity of GSH level, as shown in Figure 3A. However, pretreatment with Se (group 4) led to an increase in the levels of GSH
*SOD↑, Se pretreatment (group 4) increased the activities of SOD, CAT, and GSH-Px significantly (P<0.05) compared to the AgNP group.
*Catalase↑,
*hepatoP↑,

4504- Se,  Chit,  FA,  doxoR,    pH-responsive selenium nanoparticles stabilized by folate-chitosan delivering doxorubicin for overcoming drug-resistant cancer cells
- in-vitro, Var, NA
ChemoSen↑, enhance the activity of DOX by approximately 10-fold for a reduced IC50 value compared to free DOX
Apoptosis↑, Mechanistic studies suggested that DOX-SeNPs@TMC-FA induced cell death through the apoptosis pathway by involvement of caspase-3 and PARP proteins.
Casp3↑,
PARP↝,

4503- Se,    Prophylactic supplementation with biogenic selenium nanoparticles mitigated intestinal barrier oxidative damage through suppressing epithelial-immune crosstalk with gut-on-a-chip
- in-vitro, Nor, NA
*selenoP↑, further metabolized into selenocystine and trace amounts of selenite within cells, which are then incorporated into the synthesis of antioxidant selenoenzymes.
*ROS↓, antioxidant selenoenzyme activities, modulated AMPK/NLRP3/Nrf2 pathways, effectively alleviated oxidative stress, maintained mitochondrial homeostasis, inhibited pro-inflammatory factors expression.
*Inflam↓,
*other↝, eventually exhibit an effective protective effect against intestinal barrier oxidative damage.

4502- Se,    Modulatory effects of selenium nanoparticles on gut microbiota and metabolites of juvenile Nile tilapia (Oreochromis niloticus) by microbiome-metabolomic analysis
- in-vivo, Nor, NA
*GutMicro↑, PSP-SeNPs regulated the intestinal microbiota of tilapia.
*Dose↝, basal diet supplemented with 0.3 mg/kg of Na2SeO3, 0.3 mg/kg of PSP-SeNPs, and 4.5 mg/kg of PSP-SeNPs, respectively
*other↝, In summary, 0.3 mg/kg SeNPs supplementation can regulate the intestinal microbiota, while 4.5 mg/kg SeNPs and 0.3 mg/kg Na2SeO3 can cause amino acid metabolism disorders.
*toxicity↓, SeNPs showed higher safety than Na2SeO3.
*BioAv↑, Selenium nanoparticles (SeNPs) are a novel type of selenium supplement that offers high biological activity, high bioavailability, and low toxicity
*Bacteria↓, All concentrations of PSP-SeNPs significantly inhibited the growth of S. aureus (p < 0.05) from 4 to 20 h, with no significant difference in inhibition among concentrations

4501- Se,    Mechanisms of the Cytotoxic Effect of Selenium Nanoparticles in Different Human Cancer Cell Lines
- in-vitro, GBM, A172 - in-vitro, Colon, Caco-2 - in-vitro, Pca, DU145 - in-vitro, BC, MCF-7 - in-vitro, Nor, L929
*BioAv↑, In recent decades, studies on the functional features of Se nanoparticles (SeNP) have gained great popularity due to their high biocompatibility, stability, and pronounced selectivity
selectivity↑,
AntiCan↑, A large number of works prove the anticarcinogenic effect of SeNP
Apoptosis↑, SeNP concentration-dependently caused cancer cell apoptosis, but not necrosis
CHOP↑, significant increase in the expression of CHOP, GADD34, BIM, and PUMA
GADD34↑,
BIM↑,
PUMA↑,
Ca+2↝, SeNP Triggered Ca2+ Signals in All Investigated Cancer Cell Lines

4500- Se,    Dietary selenium affects host selenoproteome expression by influencing the gut microbiota
- in-vivo, Nor, NA
*GutMicro↑, dietary selenium affects both composition of the intestinal microflora and colonization of the gastrointestinal tract, which, in turn, influence the host selenium status and selenoproteome expression.
Risk↓, Supplemental Se has been shown to be effective in decreasing incidence and mortality from several forms of cancer, including colon cancer, in both mouse models and humans
*GPx↑, GPx1 and MsrB1 is maximized at ∼0.15 ppm Se in the diet

4499- Se,    Selenium and Selenoproteins in Gut Inflammation—A Review
- Review, IBD, NA
*Inflam↓, Previous studies have shown the ability of micronutrient selenium (Se) and selenoproteins to impact inflammatory signaling pathways implicated in the pathogenesis of the disease
*IL2↓, decreased pro-inflammatory cytokines such as IL-1β, tumor necrosis factor alpha (TNFα) and interferon gamma (IFNγ
*TNF-α↓,
*IFN-γ↓,
*PPARγ↓, Our laboratory has shown a crucial role for Se in the activation of PPARγ and its ligands, which are derived from the arachidonic acid (AA) pathway of cyclooxygenase metabolism, in macrophages.

4498- Se,    Selenium in Human Health and Gut Microflora: Bioavailability of Selenocompounds and Relationship With Diseases
- Review, Var, NA - Review, AD, NA - Review, IBD, NA
*Imm↑, Selenium is essential for the maintenance of the immune system, conversion of thyroid hormones, protection against the harmful action of heavy metals and xenobiotics as well as for the reduction of the risk of chronic diseases
*GutMicro↑, Selenium is able to balance the microbial flora avoiding health damage associated with dysbiosis.
*BioAv↑, highlighting their role in improving the bioavailability of selenocompounds
*Risk↓, Selenium deficiency may result in a phenotype of gut microbiota that is more susceptible to cancer, thyroid dysfunctions, inflammatory bowel disease, and cardiovascular disorders.
*Dose↝, highest sources of Se with concentrations that range from 1.80 to 320.80 μg Se/g
Risk↓, serum Se greater than or equal to 135 μg/L were associated with reduced cancer mortality
*CRP↓, Se supplementation decreases the serum levels of C-reactive protein and increases the levels of GPX, suggesting a positive effect on reduction of inflammation and oxidative stress in cardiovascular diseases
*GPx↓,
*Inflam↓,
*selenoP↑, SELENOP may be involved in some brain disorders, in particular in Alzheimer's disease, providing Se for brain tissue to produce selenoproteins.
*Dose↝, 100, 200, or 300 μg Se/day as Se-enriched yeast or placebo yeast. The results of this study warn that a 300-μg/day dose of Se (as Se yeast) taken for 5 years in a country with moderately low Se status can increase all-cause mortality by 10 years late
*ROS↓, Animals treated with SeCys and selenocystine showed a reduction in the concentration of ROS and malondialdehyde (MDA), as well as an increase in intestinal activity of SOD and GPX, which seems to indicate a protective effect against damage to the gut
*MDA↓,
*SOD↑,
*GPx↑,
*IL1↓, In addition, the levels of IL-1, MCP, IL-6, and TNF-α were significantly reduced in the group treated with SeCys
*MCP1↓,
*IL6↓,
*TNF-α↓,
Risk↓, higher SELENOP concentrations were inversely associated with colorectal cancer risk
*neuroP↑, Due to the antioxidant property of Se, some selenoproteins play a neuroprotective role
*memory↑, Long-term dietary supplementation (3 months) with Se-enriched yeast (Se-yeast) in triple transgenic mouse model of Alzheimer disease (AD), significantly improved spatial learning, retention of neuronal memory and activity

4497- Se,    Selenium and inflammatory bowel disease
- Review, Var, NA - Review, IBD, NA
*GutMicro↑, restoring gut homeostasis . gut microbiota is also altered by selenium deficiency.
*selenoP↑, selenoproteins that mediate gastrointestinal inflammation
*Inflam↓, crucial role for long-term (∼8 wk or more) selenium supplementation in suppressing gastrointestinal inflammation-based tissue damage,
Risk↓, SePP1 levels are inversely associated with the development of IBD and colorectal cancer
*NF-kB↓, ability of selenium to downregulate nuclear factor-κB (NF-κB)-dependent pathways
*ROS↓, reduce reactive oxygen specie

4496- Se,    Selenium status and survival from colorectal cancer in the European prospective investigation of cancer and nutrition
- Analysis, CRC, NA
Risk↝, Higher levels of Se showed non-significant inverse associations with reduction in both CRC and overall mortality
OS↑, We found no major association of Se status markers with survival after CRC diagnosis, but an association of SELENOP with overall mortality.

4495- Se,    Selenium status is associated with colorectal cancer risk in the European prospective investigation of cancer and nutrition cohort
- Study, CRC, NA
Risk↓, Higher Se concentrations were associated with a non-significant lower CRC risk
Dose↝, The findings indicate that Se status is suboptimal in many Europeans and suggest an inverse association between CRC risk and higher serum Se status, which is more evident in women.

4494- Se,    Advances in the study of selenium and human intestinal bacteria
- Review, IBD, NA - Review, Var, NA
*Risk↓, experts from Penn State University found that selenium levels in within individuals were strongly associated with the development of inflammatory bowel disease, and that lower selenium levels were associated with greater susceptibility to inflammator
OS↑, A study of more than 13,000 followers over 12 years found that serum Se levels ≥135 μg/L was associated with reduced cancer mortality
*CRP↓, selenium supplementation was found to reduce serum C-reactive protein levels and increase GPX levels, suggesting a positive effect of selenium on reducing inflammation and oxidative stress in cardiovascular disease
*GPx↑,
*Inflam↓,
*ROS↓,
*GutMicro↑, adequate or high levels of Se diet may optimize the intestinal microflora to prevent intestinal dysfunction and chronic diseases
*selenoP↑, Selenium intake in food also affects the selenium status and expression of selenoproteins in the host.
*other↓, Selenium deficiency is common in IBD patients, up to 30.9%

4492- Se,    Selenium in cancer prevention: a review of the evidence and mechanism of action
- Review, Var, NA
Risk↓, Since as early as the 1960s geographical studies have shown a consistent trend for populations with low Se intakes to have higher cancer mortality rates
AntiCan↑, Interventions with Sehave shown benefit in reducing the risk of cancer incidence and mortality in all cancers combined, and specifically in liver, prostate, colo-rectal and lung cancers.
*selenoP↑, data showing an effect of selenoprotein genotype on cancer risk implies that selenoproteins are indeed implicated
TumMeta↓, There is some evidence that Se may affect not only cancer risk but also progression and metastasis.
*DNAdam↓, Supplementation of the diet of sexually-intact elderly male dogs with Se, as selenomethionine or high-Se yeast, at 3 or 6 ug/kg body weight per d for 7 months was found to reduce DNA damage and up-regulate epithelial cell apoptosis in their prostate
OS↑, significant secondary end-point effects of 50% lower total cancer mortality and 37% lower total cancer incidence were found, with fewer prostate, colo–rectal and lung cancers(200 ug Se (as Se-enriched yeast)/d
*ROS↓, ability of Se in selenoproteins to reduce oxidative stress is relevant to its anti-cancer effects.

4491- Se,  Chit,  VitC,    Synthesis of a Bioactive Composition of Chitosan–Selenium Nanoparticles
- Study, NA, NA
*ROS↓, chitosan-selenium nanoparticles has a corrective effect on the oxidative processes of the body, reducing the activity of free-radical oxidation in the blood of animals
*selenoP↑, Selenium is included in selenoproteins, which have a wide range of biological effects, including antioxidant and anti-inflammatory effects.
*antiOx↑,
*Inflam↓,
*Risk↓, The lack of selenium in the body is a risk factor for the development of various pathologies.
*toxicity↓, Compared to organic and inorganic forms of selenium, selenium nanoparticles (NPs) exhibit lower toxicity and superior antioxidant, immunomodulatory, bactericidal, and antitumor activity
AntiTum↑,
Dose↝, NPs with sizes of 2–3 nm (33.4 wt %) and ~ 37 nm (66.6 wt %) are formed.

4488- Se,  Chit,  PEG,    Anticancer effect of selenium/chitosan/polyethylene glycol/allyl isothiocyanate nanocomposites against diethylnitrosamine-induced liver cancer in rats
- in-vivo, Liver, HepG2 - in-vivo, Nor, HL7702
tumCV↓, The SCPg-AI-NCs effectively decreased the cell viability and induced apoptosis in the HepG2 cells.
Apoptosis↑,
*GSH↑, The SCPg-AI-NCs treatment effectively decreased the TBARS and improved the GSH, vitamin-C & -E contents in the DEN-induced rats
*VitC↑,
*VitE↑,
*SOD↑, The activities of SOD, GPx, and GR were also improved by the SCPg-AI-NCs treatment in the DEN-induced rats.
*GPx↑,
*GR↑,
ALAT↓, The activities of ALT, ALP, AST, LDH, and GGT was remarkably decreased by the SCPg-AI-NCs treatment in the DEN-provoked liver cancer rats.
ALP↓,
AST↓,
LDH↓,
selectivity↑, same doses of SCPg-AI-NCs did not showed the cytotoxicity to the normal liver HL7702 cells
eff↑, The utilization of nanocomposites as drug delivery systems has a efficacy to solve the several side effects triggered by chemotherapeutic drugs to normal cells

4742- Se,    Antitumor Effects of Selenium
- Review, Var, NA - Review, Arthritis, NA - Review, Sepsis, NA
*antiOx↓, Functions of selenium are diverse as antioxidant, anti-inflammation, increased immunity, reduced cancer incidence, blocking tumor invasion and metastasis, and further clinical application as treatment with radiation and chemotherapy.
*Inflam↓,
Risk↓,
TumCI↓,
TumMeta↓,
radioP↑,
chemoP↑,
Apoptosis↑, (SeDG), which induces cytotoxicity as cell apoptosis, ROS production, DNA damage, and adenosine-methionine methylation in the cellular nucleus
ROS↑,
DNAdam↑,
Dose↑, In our study, advanced cancer patients can tolerate until 5000 μg of sodium selenite in combination with radiation and chemotherapy since the half-life of sodium selenite may be relatively short
selectivity↑, selenium may accumulates more in cancer cells than that of normal cells, which may be toxic to the cancer cells.
*other↓, Se-methylselenocysteine (MSeC) is most abundant in garlic, broccoli, walnut, and some other plant products.
*BioAv↑, Most Se compounds are readily absorbed from the diet and are mainly metabolized in the liver.
ROS↑, Methylselenol induced apoptosis by ROS production, subsequently altered mitochondrial membrane potential, and, further, induced caspases’ activity.
MMP↓,
Casp↑,
*Imm↑, Se activates immune functions via the activation of IL-2 receptor [59].
*Pain↓, Supplementation with 200 μg Se in a group of rheumatoid arthritis patients for three months significantly reduced pain and joint involvement
Sepsis↓, Se plays an important role in defense against acute illness, such as sepsis syndrome
MMP2↓, Several experiments by our group demonstrate that selenite inhibits tumor invasion by blocking MMP-2 and -9 expression
MMP9↓,
*Half-Life↓, a short half-life of sodium selenite and more accumulation of the Se in the cancer cells may be more toxic in cancer cells than that in normal cells.

4726- Se,  Oxy,    Oxygen therapy accelerates apoptosis induced by selenium compounds via regulating Nrf2/MAPK signaling pathway in hepatocellular carcinoma
- in-vivo, HCC, NA
eff↝, Selenium has good antitumor effects in vitro, but the hypoxic microenvironment in solid tumors makes its clinical efficacy unsatisfactory.
NRF2↓, We found that, in contrast to hypoxia, the hyperoxic environment facilitated the H2Se, produced by the selenium metabolism in cells, to be rapidly oxidized to generate H2O2, leading to inhibit the expression level of Nrf2
p‑p38↑, and to increase that of phosphorylation of p38 and MKK4, resulting in inhibiting autophagy and accelerating apoptosis
Apoptosis↑,
eff↑, These findings highlight oxygen can significantly enhance the anti-HCC effect of selenium compounds through regulating the Nrf2 and MAPK signaling pathways
TumVol↓, The results showed that hyperoxia could improve the efficacy of Na2SeO3 and CysSeSeCys in the treatment of HCC, enhance the death rate of HepG2 cells, and further reduce the tumor volume in mice
other↝, These results also suggest that the anticancer mechanism of selenium compounds may be different in different oxygen environments.
toxicity↓, staining results of the liver and kidney of mice showed that the selenium compound combined with oxygen therapy did not show toxicity or side effects on normal organs
Dose↝, therapeutic effect reached the level of the 5 mg/kg selenium compound treatment group
NRF2↝, The results showed that in the 1 % O2 environment, the two selenium compounds promoted the expression of Nrf2, and the Nrf2 level gradually decreased with increasing oxygen concentration.
HO-1↓, The expression of HO-1, CAT and SOD also showed a decreasing trend with increasing oxygen concentration
Catalase↓,
SOD↓,
e-pH↓, The results showed that the extracellular pH value decreased after treatment with selenium compounds for 48 h
pH∅, However, there was no significant change in extracellular pH value in the selenium compound treatment group compared with the oxygen alone group
MAPK↑, Selenium combined with oxygen therapy accelerates cell apoptosis by activating the MAPK signaling pathway
eff↑, In summary, oxygen can significantly enhance the antihepatocellular carcinoma effect of selenium compounds

4741- Se,    Selenium in Oncological Intervention
- Review, Var, NA
Risk↓, The trace element selenium has a long history as a cancer preventive agent.
*other↝, optimal selenium supply gives serum levels between about 110 µg/L and 130 µg/L [
Risk↓, The incidence of prostate cancer was also reduced in the selenium group (relative risk 0.51; 95% CI: 0.29–0.87) with the greatest effect being seen in the men who initially had the lowest selenium supplies (serum selenium levels <123 µg/L) [
AntiTum↑, findings from this study indicate that sodium selenite might work in three ways against cancer: the antitumor effect by itself, by reversing chemoresistance and by ameliorating toxic effects from chemotherapy.
chemoR↓,
chemoP↑,

4740- Se,    Optimising Selenium for Modulation of Cancer Treatments
- Review, Var, NA
*selenoP↑, Selenium is an essential trace element involved in many biological processes that are mediated through, at least, 25 selenoproteins expressed in humans.
*Dose↓, 50-200 μg/day have been used mainly for primary prevention (15), and Se supplementation at these doses for Se-deplete individuals has been associated with lower overall mortality and incidence of certain cancer types
Risk↓,
*toxicity↝, Animal laboratory studies have shown that the organic forms of Se are both more effective and safer than the commonly-used inorganic forms such as sodium selenite (SS), which are more genotoxic
Dose↑, All patients given 4,800 μg SLM twice daily achieved plasma Se levels >15 μM, the Se concentration required for reduced chemotherapy-induced toxicity and enhanced antitumor efficacy of chemotherapeutic drugs in preclinical animal models
chemoP↑, hence the optimal form and dose of Se to be used with chemotherapy or radiotherapy remains unclear.
radioP↑,

4739- Se,  Chemo,  Rad,    Therapeutic Benefits of Selenium in Hematological Malignancies
- Review, Var, NA
chemoP↑, Supplementing chemotherapy and radiotherapy with selenium has been shown to have benefits against various cancers.
radioP↑,
QoL↑, This approach has also been shown to alleviate the side effects associated with standard cancer therapies and improve the quality of life in patients.
Risk↓, selenium levels in patients have been correlated with various cancers
*selenoP↑, Selenium is present in all mammals and is utilized by selenoproteins
TumCP↓, It has been reported that Se possesses anti-proliferative, anti-inflammatory, and anti-viral activities in addition to immune altering properties and has been implicated in various cancers
Inflam↓,
ChemoSen↑, Selenium-based compounds exhibit chemopreventive or chemotherapeutic properties through regulation of various processes such as cell cycle arrest, apoptosis, angiogenesis, etc.
TumCCA↑,
Apoptosis↑,
angioG↓,
Dose⇅, The amount of the selenium agent administered can influence whether prooxidant or antioxidant activity is observed.
ROS↑, Selenium-based compounds have been shown to exhibit chemopreventive and anticancer properties through prooxidant activities and the regulation of cellular redox homeostasis by altering thiol groups in multiple metabolic pathways, stimulating the prod
eff↑, The potency of selenium in an in vitro model of lung adenocarcinoma was increased with the addition of fish oil
Risk↓, In clinical trials, it has been observed that selenium and vitamin C supplementation decrease the incidence and mortality of gastric and lung cancer
eff∅, A selenium supplementation did not negatively impact the efficacy of chemotherapy
CSCs↓, Selenium Is Potent in Leukemia Stem Cells through In Vitro and In Vivo AML/CML Models
ROS↑, higher intracellular oxidative stress (or levels of ROS) in chronic or acute myeloid leukemia stem cells

4738- Se,  doxoR,    Selenium Attenuates Doxorubicin-Induced Cardiotoxicity Through Nrf2-NLRP3 Pathway
- NA, Nor, NA
*NRF2↑, Se treatment markedly promoted the expression of Nrf2 and prevented the activation of NLRP3 inflammasome.
*NLRP3↓,
*cardioP↑, Selenium (Se), an essential nutrient for humans, has been reported to possess cardioprotective effect

4737- Se,  Rad,    Nrf2-modulation by seleno-hormetic agents and its potential for radiation protection
- in-vivo, Var, NA
radioP↑, Others and we have shown that seleno-compounds have the potential to protect ionizing radiation-induced toxicities in various tissues and cells both in in vitro and in vivo studies.
*NRF2↑,
NRF2↓, implied

4736- Se,  SFN,    Synergy between sulforaphane and selenium in protection against oxidative damage in colonic CCD841 cells
- in-vitro, Nor, CCD841
*TrxR1↑, Treatment of cells with SFN and Se significantly induced TrxR-1 expression.
*H2O2↓, Pretreatment of cells with SFN protects against H2O2-induced cell death; this protection was enhanced by cotreatment with Se.
*NRF2↑, SFN activates the Nrf2 signaling pathway and protects against H2O2-mediated oxidative damage in normal colonic cells.

4735- Se,    Selenium triggers Nrf2-AMPK crosstalk to alleviate cadmium-induced autophagy in rabbit cerebrum
- in-vivo, Nor, NA
*MDA↓, Se decreased the contents of MDA and H2O2 and increased the activities of CAT, SOD, GST, GSH and GSH-Px, alleviating the imbalance of the redox system induced by Cd.
*H2O2↓,
*Catalase↑,
*SOD↑,
*GSTs↑,
*GSH↑,
*NRF2↓, Cd caused the up-regulation of the mRNA levels of autophagy-related genes (ATG3, ATG5, ATG7, ATG12 and p62), AMPK (Prkaa1, Prkaa2, Prkab1, Prkab2, Prkag2, Prkag3) and Nrf2 (Nrf2, HO-1 and NQO
*ATG3↓, which were alleviated by Se, indicated that Se inhibited Cd-induced autophagy and Nrf2 signaling pathway activation
*AMPK↓,
*ROS↓, our study found that Se antagonized Cd-induced oxidative stress and autophagy in the brain by generating crosstalk between AMPK and Nrf2 signaling pathway.

4734- Se,  CPT-11,    Cytotoxicity and therapeutic effect of irinotecan combined with selenium nanoparticles
- in-vitro, CRC, HCT8 - in-vivo, NA, NA
chemoP↑, We investigated Nano Se as chemotherapy preventive agent to protect against toxicities of anticancer drug irinotecan and synergistically enhance the anti-tumor treatment effect in vitro and in vivo.
ChemoSen↑,
P53↑, The combination of Nano Se and irinotecan showed increased cytotoxic effect with HCT-8 tumor cells likely by p53 mediated apoptosis.
Apoptosis↑,
TumCG↓, Se inhibited growth of HCT-8 tumor cells partially through caspases mediated apoptosis.tumcg
Casp↑,
Dose↝, In vivo experiment showed Nano Se at a dose of 4 mg/kg/day significantly alleviated adverse effects induced by irinotecan (60 mg/kg) treatment.
NRF2↓, The beneficial effects of Nano Se for tumor therapy were mainly ascribed to selectively regulating Nrf2-ARE (antioxidant responsive elements) pathway in tumor tissues and normal tissues.
selectivity↑,
*NRF2↑,

4733- Se,    Selenium supplementation of lung epithelial cells enhances nuclear factor E2-related factor 2 (Nrf2) activation following thioredoxin reductase inhibition
- NA, Nor, NA
*selenoP↑, Se is required for the synthesis and function of selenoenzymes including thioredoxin (Trx) reductase-1 (TXNRD1) and glutathione peroxidases (GPx).
*Trx↑,
*GPx↑, TXNRD1 and GPX2 protein expression and enzymatic activity were significantly greater upon Se supplementation
*NRF2↑, Se levels positively influence Nrf2 activation and selenoenzyme responses following TXNRD1 inhibition.

4732- Se,    Selenium inhibits ferroptosis and ameliorates autistic-like behaviors of BTBR mice by regulating the Nrf2/GPx4 pathway
- in-vivo, Autism, NA
*Ferroptosis↓, Selenium inhibits ferroptosis and ameliorate abnormal behavior via the Nrf2/Gpx4 signaling pathway.
*NRF2↑, Treatment with Se increased levels of Nrf2 and GPX4.
*GPx4↑,
*other↝, Se exhibited a beneficial effect on autism-relevant behaviors and inhibited ferroptosis in the BTBR mouse model of ASD, possibly through modulation of the Nrf2/GPX4 signaling pathway.

4731- Se,    Dietary selenium mitigates cadmium-induced apoptosis and inflammation in chicken testicles by inhibiting oxidative stress through the activation of the Nrf2/HO-1 signaling pathway
- in-vivo, Nor, NA
*ROS↓, Se effectively suppressed the Cd-induced elevation in ROS, MDA, and H2O2 levels, while also preventing the downregulation of CAT, GSH, and T-AOC levels.
*MDA↓,
*H2O2↓,
*Catalase↑,
*GSH↑,
*NRF2↑, Se administration ameliorated the reduction in the expression levels of Nrf2, HO-1, and Bcl-2 induced by Cd
*HO-1↑,
*Bcl-2↑,
*other↝, this study elucidated that Se might mitigate Cd-induced oxidative stress in chicken testicles through the stimulation of the Nrf2/HO-1 signaling pathway,

4730- Se,    Association between plasma selenium level and NRF2 target genes expression in humans
- Human, Nor, NA
*NRF2↑, NRF2 mRNA level was positively correlated with expression of investigated NRF2-target genes.
*GSTP1/GSTπ↓, plasma Se level was significantly inversely associated only with expression of GSTP1 (β-coef. = −0.270, p = 0.009), PRDXR1 (β-coef. = −0.245, p = 0.017) and SOD2 with an inverse trend toward significance
*SOD2↓,

4729- Se,    Selenium regulates Nrf2 signaling to prevent hepatotoxicity induced by hexavalent chromium in broilers
*ROS↓, Studies have reported that selenium (Se), which is one of the essential trace elements of the poultry and participates in the oxidative metabolism, can alleviate Cr(Ⅵ)-induced organ damage by inhibiting oxidative stress,
*NRF2↑, levels of Nrf2, glutathione peroxidase 1 (GPx-1), NAD(P)H: quinone oxidoreductase 1 (NQO1), and mechanistic target of rapamycin (mTOR) in the Se&Cr group was upregulated
*GPx1↑,
*NQO1↑,
*mTOR↑,
*Beclin-1↓, along with decreased expression of Beclin 1, ATG5 and LC3 compared to the Cr group.
*ATG5↓,
*LC3s↓,
*hepatoP↑,

4728- Se,    Selective Impact of Selenium Compounds on Two Cytokine Storm Players
- NA, Covid, NA
*IL6↓, MSeA was found to be the most potent selenium form among the four selenium compounds tested that reduced the levels of IL-6 and TNF-α secreted by THP-1 macrophages.
*TNF-α↓,
*NRF2↑, In addition, an increase in Nrf2 and decrease in pIκBα in human macrophages was observed following MSeA treatment.
*other↑, Alternatively, selenium levels in populations could be improved by supplementing soil with selenium-enriched fertilizers that kept mortality rates due to COVID-19 low in Finland
*eff↑, Moreover, it is important to consider selenium as a cofactor to achieve a more effective immune response to COVID-19 vaccination

4727- Se,    Selenium inhibits ferroptosis in ulcerative colitis through the induction of Nrf2/Gpx4
- in-vivo, Col, NA
*Ferroptosis↓, Selenium can relieve DSS-induced colitis and inhibit IECs ferroptosis by up-regulating the expression of Nrf2/Gpx4.
*NRF2↑,
*GPx4↑,
*eff↑, The in vivo results showed that selenium treatment could improve IECs colitis induced by DSS and inhibit ferroptosis.
*other↓, The serum selenium content of UC patients was lower than that of healthy subjects.
*antiOx↑, Selenium, an essential micronutrient of human, which has the functions of anti-oxidation, immune regulation, anti-inflammatory and anti-tumor
*Inflam↓,
AntiTum↑,

4615- Se,  Rad,    Selenium as an adjuvant for modification of radiation response
- Review, Nor, NA
*antiOx↑, Selenium is a trace element in the body that has shown potent antioxidant and radioprotective effects for many years
*radioP↑,
*GSH↑, via upregulation of glutathione (GSH) level and glutathione peroxidase activity
*GPx↑,
*Dose↝, recent years have shown that selenium is able to mitigate radiation toxicity when administered after exposure.
selectivity↑, selenium protects different normal cells against radiation, while it may sensitize tumor cells.
RadioS↑, its radiosensitive effect on cancer cells.

4725- Se,    Targeting the Nrf2-Prx1 Pathway with Selenium to Enhance the Efficacy and Selectivity of Cancer Therapy
- in-vitro, Lung, A549 - in-vitro, CRC, HT29
AntiCan↑, anti-cancer activity of selenium may in part be mediated by suppressing the Nrf2-Prx1 pathway of a tumor.
NRF2↓, Our study showed that seleni-um suppressed Nrf2 activation and reduced the up-regulation of prx1 in tumor tissues obtained from humanlung cancer A549 and colon cancer HT-29
Prx↓,
ChemoSen↑, how selenium modulation of the Nrf2-Prx1 pathway may enhance the efficacy and selectivity of cancer therapy in both pre-clinical and clinical settings.
*Prx↑, Conversely, increased expression of Prx1 and several other Nrf2 target genes was observed in some normal tissues in the tumor-bearing mice.
*NRF2↑,

4724- Se,    Chapter Four - Selenium in the Redox Regulation of the Nrf2 and the Wnt Pathway
- Review, Var, NA
Risk↓, Selenium deficiency is known to increase cancer risk by so far unclear mechanisms.
*selenoP↑, Selenium exerts its biological effects via selenocysteine as an integral part of selenoproteins.
other↝, A moderate Se deficiency activates the Nrf2 and the Wnt pathways
Risk↓, not only healthy cells but also malignant ones benefit from intact Keap1/Nrf2 signaling, making a dysregulated hydroperoxide signaling a plausible explanation for the increased cancer risk in selenium deficiency.

4723- Se,    Selenium Induces Ferroptosis in Colorectal Cancer Cells via Direct Interaction with Nrf2 and Gpx4
- in-vitro, CRC, HCT116
TumCP↓, In vitro experiments using HCT116 cells showed that Na₂SeO₃ treatment inhibited proliferation, increased intracellular Fe2⁺, MDA, and ROS levels, and reduced mitochondrial membrane potential.
Iron↑,
MDA↑,
ROS↑,
MMP↓,
NRF2↓, Western blotting further revealed the downregulation of Nrf2 and Gpx4 proteins upon selenium treatment
GPx4↓,
Ferroptosis↑, Our research findings indicate that sodium selenite may induce ferroptosis by regulating the Nrf2/Gpx4 axis, highlighting its potential as a dual nutrient and pharmacological drug for the treatment of CRC.

4722- Se,    The Yin and Yang of Nrf2-Regulated Selenoproteins in Carcinogenesis
- Review, Var, NA
Risk↓, Selenium deficiency is associated with a higher cancer risk making also this essential trace element a promising candidate for cancer prevention.
*NRF2↓, Selenium deficiency activates Nrf2 as does a TrxR1 knockout making a synergism between both systems plausible. Although this might hold true for healthy cells, the interplay may turn into the opposite in cancer cells
NRF2↑, The induction of the detoxifying and antioxidant enzymes by Nrf2 will make cancer cells chemoresistant and will protect them against oxidative damage.
*NRF2↓, Selenium exerts its effects mainly as part of selenoproteins with redox functions, and Nrf2 upregulates enzymes of the adaptive response.
OS↑, selenium, vitamin E, and β-carotene, called factor D, significantly reduced total mortality, total cancer mortality, and most significantly mortality from gastric cancer. selenium ... according to subsequent studies it appeared to have the most effic
eff↝, Considering age, the effect of factor D was much stronger in individuals younger than 55 but almost absent in subjects older than 55 years.
eff↝, selenium appears to prevent initiation of cancer in healthy cells at young age, in the elderly it may be harmful and rather support tumor growth of already initiated cells
NRF2↝, “dark” side of Nrf2. Its upregulation in cancer cells provides an advantage for these cells to grow and, in addition, makes them resistant against chemotherapy

4721- Se,    A review on selenium nanoparticles and their biomedical applications
- Review, AD, NA - Review, Diabetic, NA - Review, Arthritis, NA
*antiOx↑, SeNPs have attractive antioxidant and anti-inflammatory properties
*Inflam↓,
*eff↝, SeNPs-based drug delivery in Alzheimer, diabetes, infectious disease, Rheumatoid arthritis, and cancer is being investigated.
*selenoP↑, Selenium is incorporated into Selenoproteins such as selenocysteine (Sec)
*Bacteria↓, efficacy against various cancer cells, microbial pathogens, viral infections, neuroprotective properties, diabetic control, oxidative stress, and inflammation-mediated illnesses such as rheumatoid arthritis.
*neuroP↑,
*ROS↓,
ChemoSen↑, Selenium nanoparticles (SeNPs) have been utilized with drugs like 5-Fluorouracil (5-FU) and irinotecan, displaying enhanced anticancer activity.

4720- Se,    Selenium Nanoparticle in the Management of Oxidative Stress During Cancer Chemotherapy
- Review, Var, NA
*toxicity↓, Selenium nanoparticles have shown much less toxicity toward normal cells than other selenium compounds while displaying excellent antioxidant properties.
*antiOx↑,
chemoP↑, The trace element selenium is present in different selenoenzymes in mammals including humans which act as antioxidant and tissue protectant.

4719- Se,    Selenium nanoparticles are more efficient than sodium selenite in producing reactive oxygen species and hyper-accumulation of selenium nanoparticles in cancer cells generates potent therapeutic effects
- in-vivo, Var, NA
ROS↑, ROS production by SeNPs in above systems is more efficient than by selenite.
selenoP↑, (SeNPs) administered via oral route possess similar capacities of increasing selenoenzyme activities as the extensively examined sodium selenite, selenomethionine and methylselenocysteine, and yet display the lowest toxicity among these selenium comp
*toxicity↓,

4718- Se,    High-Dose Selenium Induces Ferroptotic Cell Death in Ovarian Cancer
- in-vitro, Ovarian, NA
TumCP↑, Here, we observed that high-dose sodium selenite (SS) significantly decreased the proliferation and increased the death of ovarian cancer cells, mediated by an increased generation of reactive oxygen species.
ROS↑,
GPx↓, high-dose SS decreased the levels of glutathione peroxidase (GPx), a selenoprotein with antioxidant properties, without altering other selenoproteins.
lipid-P↑, Furthermore, high-dose SS triggered lipid peroxidation and ferroptosis, a type of iron-dependent cell death, due to dysregulated GPx4 pathways.
Ferroptosis↑,
Dose↑, effective dose (1000–2000 μg/kg) of SS for anticancer effects in an ovarian cancer mouse model through tail injection three times per week for 2 weeks

4717- Se,    A systematic review of Selenium as a complementary treatment in cancer patients
- Review, Var, NA
*antiOx↑, Selenium, a trace element with antioxidant properties, has been widely studied for its benefits in cancer treatment.
eff↝, clear statement regarding the effectiveness of Se supplementation is not possible
radioP↑, whereas cancer patients with a Se deficiency could profit from a Se supplementation during radio- or chemotherapy.
chemoP↑,
*selenoP↑, Se is crucial for the biosynthesis of selenoproteins and essential enzymes (glutathione peroxidases (GSH-PPX), thioredoxin reductase, and selenoprotein P
*GPx↑,
TrxR↑,
*ROS↓, Glutathione peroxidase, an enzyme within this group, directly neutralizes reactive oxygen species, which can be detrimental to cells.

4716- Se,    Selenium Substitution During Radiotherapy of Solid Tumours – Laboratory Data from Two Observation Studies in Gynaecological and Head and Neck Cancer Patients
- in-vivo, HNSCC, NA
Dose↝, Conclusion: The used dosage of 500 μg sodium selenite per day is sufficient to treat selenium deficiency during radiotherapy.
*GPx↑, Selenium is known as an essential cofactor for the activity of glutathione peroxidase (1), which is an important enzyme system for scavenging of free radicals in the human body.
*ROS↓,

4715- Se,    The Interaction of Selenium with Chemotherapy and Radiation on Normal and Malignant Human Mononuclear Blood Cells
chemoP↑, Selenium, a trace element with anticancer properties, can reduce harmful toxicities of chemotherapy and radiotherapy without compromising efficacy.
radioP↑,
selectivity↑, MSA, at lower concentrations, induced protective responses in normal cells but cytotoxic effects in malignant cells, alone and in conjunction with chemotherapy or radiation.
ChemoSen↑, potentially improve efficacy of anticancer treatments.
GSH↓, Furthermore, the depletion of GSH by MSA in malignant THP1 cells was still significantly reduced at 24 h after radiation and chemotherapy treatment, again without the advantage of higher MSA concentrations
*GSH↑, The GSH increase in normal PBMCs was maintained at 24 h when cells were also treated with 2 Gy radiation, cytosine arabinoside (AraC) or doxorubicin (Dox), though the maximum benefit was achieved with 2.5 µM MSA
*DNAdam↓, MSA Reduces DNA Damage in Normal Cells While Increasing DNA Damage in Malignant Cells
DNAdam↑,
eff↑, The simultaneous increase in GSH in normal cells and depletion of GSH in malignant cells may contribute to improving the therapeutic ratio of cancer treatment by reducing normal tissue toxicities while increasing the anticancer efficacy.

4714- Se,    Selenium in cancer management: exploring the therapeutic potential
- Review, Var, NA
Risk↓, Prolonged selenium deficiency has been conclusively linked to an elevated risk of various diseases, including but not limited to cancer, cardiovascular disease, inflammatory bowel disease, Keshan disease, and acquired immunodeficiency syndrome.
*BioAv↑, compounds such as selenite, selenate, and selenium-enriched amino acid analogs are more amenable to absorption, particularly when synergized by vitamins A, D and E
eff↝, Based on current research, selenium supplementation alone has not shown favorable results in prostate cancer treatment.
*ROS↓, It is a well-established fact that selenium demonstrates its anticancer capabilities primarily through its antioxidant attributes. These attributes help maintain the cellular redox balance and shield healthy cells from ROS
MMP↓, Sodium selenite, the most abundant inorganic selenium compound in nature, reduces mitochondrial membrane potential and enhances the antiproliferative and apoptosis-inducing effects of polyene paclitaxel on prostate cancer cell PC3
ROS↑, The above studies also suggest that ROS generation, upregulation of p53, and reduction of mitochondrial membrane potential play important roles in selenium-assisted anti-tumor processes.
P53↑,
*toxicity↓, selenium-containing nanoparticles an attractive avenue for research, with the potential to revolutionize cancer treatment by offering targeted, effective therapies with reduced toxicity.
TumCP↓, SeNPs effectively curbed the proliferation of these cancer cells by triggering a cascade of caspase-mediated apoptosis
Casp↑,
Apoptosis↑,

4713- Se,  VitC,  VitK3,    Selenium supplementation protects cancer cells from the oxidative stress and cytotoxicity induced by the combination of ascorbate and menadione sodium bisulfite
- in-vitro, GBM, NA
eff↓, selenium supplementation significantly protected cancer cells from VC/VK3 treatment concomitantly with enhanced expression levels and enzymatic activity of antioxidant selenoproteins, including thioredoxin reductases (TXNRDs) and glutathione reductas

4712- Se,    Selenium and selenoproteins: key regulators of ferroptosis and therapeutic targets in cancer
- Review, Var, NA
selenoP↑, Selenium (Se) and selenoproteins regulate ferroptosis, a lipid peroxidation–driven form of cell death
Ferroptosis↑,
lipid-P↑,

4711- Se,    Association of selenium status and blood glutathione concentrations in blacks and whites
- Human, Nor, NA
Risk↓, Selenium deficiency has been linked with increased cancer risk and, in some studies, selenium supplementation was protective against certain cancers.
chemoP↑, Previous studies suggest that selenium chemoprevention may involve reduced oxidative stress through enhanced glutathione (GSH).
*GSH↑, selenium concentrations were associated with increased blood GSH concentration and GCL activity (P<0.05).

1701- Se,    An Assessment of Serum Selenium Concentration in Women with Ovarian Cancer
- Human, Ovarian, NA
Risk↓, The mean concentration of selenium was lower among diseased ones than among controls (53.31 μg/L vs. 78.99 μg/L). A decrease in selenium concentration was noticed with the advancement of ovarian cancer.
Risk↓, a clear relationship between low selenium concentration and the occurrence of ovarian cancer was found
Dose∅, average concentration of selenium in the SELECT and Nutritional Prevention of Cancer Trial was approximately 135 [47] and 114 µg/L [75], respectively.

4443- Se,    Bioogenic selenium and its hepatoprotective activity
- in-vivo, LiverDam, NA
*hepatoP↑, Biogenic selenium and its hepatoprotective activity
*AST↓, pretreatment with BioSeNPs inhibiting the elevation of activities of various enzymes significantly which included aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase and liver lipid peroxide
*ALAT↓,
*LDH↓,
*lipid-P?,

4441- Se,    The Role of Selenium Nanoparticles in the Treatment of Liver Pathologies of Various Natures
- Review, Nor, NA
*ROS↓, liver is the depot for most selenoproteins, which can reduce oxidative stress, inhibit tumor growth, and prevent other liver damage.
*hepatoP↑, their hepatoprotective properties
*selenoP↑,
*ALAT↓, (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (AP). However, the introduction of SeNPs significantly reduced the change in the level of these enzymes
*AST↓,
*GSH↑, significant increase in the content of glutathione and glutathione peroxidase in the liver
*GPx↑,
*TNF-α↓, In addition, the expression level of TNF-α, IL-6, NF-kB, and p65 genes was significantly increased in the cadmium-treated group (compared with the control), co-treatment of SeNPs and lacto-SeNPs led to a decrease in the expression of these genes.
*IL6↓,
*NF-kB↓,
*p65↓,
*Dose⇅, lactobacilli were used to restore Se from sodium selenite, while the synthesized nanoparticles had a size of 42.4 ± 10.5 nm and a zeta potential of −36.6 mV.

4440- Se,  SNP,    Selenium, silver, and gold nanoparticles: Emerging strategies for hepatic oxidative stress and inflammation reduction
- Review, NA, NA
*hepatoP↑, This review focuses on the hepatoprotective potential of selenium (SeNPs), silver (AgNPs), and gold nanoparticles (AuNPs), emphasizing their antioxidant, anti-inflammatory, and immunomodulatory mechanisms.
*antiOx↑,
*Inflam↓,
*ROS↓, SeNPs enhance antioxidant defenses by scavenging reactive oxygen species (ROS) and upregulating key enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPx).
*SOD↑,
*GPx↑,
*lipid-P↓, AgNPs exhibit anti-inflammatory effects by modulating cytokine expression, reducing lipid peroxidation, and preserving hepatic architecture.

4216- Se,    Selenium ameliorates mercuric chloride-induced brain damage through activating BDNF/TrKB/PI3K/AKT and inhibiting NF-κB signaling pathways
- in-vitro, NA, NA
*BDNF↑, In summary, Na2SeO3 ameliorated HgCl2-induced brain injury via inhibiting apoptosis and inflammation through activating BDNF/TrKB/PI3K/AKT and suppressing NF-κB pathways.
*TrkB↓,
*PI3K↑,
*Akt↑,
*neuroP↑, Se has neuroprotective effects and antagonize the toxicity of heavy metals

4214- Se,    Selenium ameliorates cognitive impairment through activating BDNF/TrkB pathway
- in-vivo, NA, NA
*memory↑, selenium supplementation can improve spatial learning and memory deficiencies in 3 × Tg-AD mice.
*other↑, Selenium supplementation increased selenium and GSH-Px levels in the brain tissue of 3 × Tg-AD mice and significantly enhanced neuronal conditions
*BDNF↑, the expression levels of proteins related to the BDNF/TrkB pathway significantly increased following selenium supplementation.
*TrkB↑,

4085- Se,    Role of micronutrients in Alzheimer's disease: Review of available evidence
- Review, AD, NA
*AChE↓, selenium inhibits ACHE and butylcholinesterase, which has a positive effect on the treatment of AD
*BChE↓,
*antiOx↑, Selenium is a central component of many antioxidant enzymes (glutathione peroxidase) that regulate redox levels in the body and have a positive effect on the immune system
*memory↑, Chondroitin sulfate selenium has been shown to improve spatial learning and memory impairment in mice with AD
*cognitive↑, Higher blood selenium levels in older people were shown to be associated with higher cognitive scores;

2142- Se,    A U-shaped association between selenium intake and cancer risk
- Review, NA, NA
*Risk↝, We observed a U-shaped association between selenium intake and cancer risk.
Dose↝, A safe intake ranged from 110.8 to 124.4 µg/day (mean 117.8 µg/day).
*Risk↓, individuals with the lowest intake (i.e., 27.8–77.2 µg/day) were associated with an increased risk of cancer (ie higher levels means lower risk)

2141- Se,    Selenium and cancer risk: Wide-angled Mendelian randomization analysis
- Review, NA, NA
Dose↝, Nonetheless, a nutrition survey in US people indicated that a trivial proportion of the population had serum levels of selenium >170 ng/mL
Risk↝, Evidence on the association between selenium and cancer risk is inconclusive

2140- Se,    Selenium Exposure and Cancer Risk: an Updated Meta-analysis and Meta-regression
- Review, Var, NA
Risk↓, High selenium exposure- It decreased the risk of breast cancer, lung cancer, esophageal cancer, gastric cancer and prostate cancer, but it was not associated with colorectal cancer, bladder cancer and skin cancer.
antiOx↑, The major positive effect may be contributed by the antioxidant function of GPxs and selenoprotein P
eff↑, High selenium exposure could decrease cancer risk, especially high plasma/serum selenium and toenail selenium.
eff↝, High selenium exposure may have dissimilar effects on specific types of cancer.

1707- Se,    A Diet Lacking Selenium, but Not Zinc, Copper or Manganese, Induces Anticancer Activity in Mice with Metastatic Cancers
- in-vivo, Ovarian, NA - in-vivo, BC, NA
OS↓, A significant improvement in mice survival was observed when the normal diet was replaced with the selenium-free diet. (ie OS down with selenium)

1706- Se,    Selenium in Prostate Cancer: Prevention, Progression, and Treatment
- Review, Pca, NA
Risk∅, randomized controlled studies have shown that selenium supplementation does not prevent prostate cancer (HR: 0.95; 95% CI 0.80–1.13).
ChemoSen↑, In the context of combinatorial therapy, selenium has demonstrated promising synergistic potential in the treatment of prostate cancer.
Risk↓, Moreover, there is increasing evidence suggesting that selenium can serve as a preventive agent, and the levels of selenium in the bloodstream may be linked to the development of prostate cancer
toxicity↝, Interestingly, both low and high levels of selenium have shown potential implications.
Risk↑, Generally, lower serum selenium status has been correlated with an increased risk of cancer.
eff↑, Furthermore, foundational studies have proposed that antioxidants, such as vitamin E and lycopene [50], may enhance the effectiveness of selenium in preventing the formation of mammary tumors.
*toxicity↑, selenium supplementation after diagnosis and found that supplementation of 140 μg/day or more following a nonmetastatic prostate cancer diagnosis increased prostate cancer mortality.
RadioS↑, Sodium selenite, for instance, has demonstrated a significant enhancement of the radiosensitizing effect in both HI–LAPC-4 and PC-3 xenograft tumors
eff↓, Additionally, another study [59] provided valuable evidence indicating that prostate cancer patients with low levels of selenium and lycopene are more susceptible to DNA damage induced by ionizing radiation.
eff↑, Husbeck et al. highlighted that selenite increases sensitivity to gamma radiation in prostate cancer by reducing the ratio of GSH:GSSG
ChemoSen↑, while selenium supplementation alone did not demonstrate a positive effect on prostate cancer progression, it shows promise in enhancing the efficacy of chemotherapy and radiotherapy while mitigating their associated side effects during cancer treatm
ChemoSideEff↓,

1705- Se,    Serum Selenium Level and 10-Year Survival after Melanoma
- Study, Melanoma, NA
OS↑, The subgroup with low selenium levels had a significant lower survival rate in relation to patients with high selenium levels, HR = 8.42; p = 0.005 and HR = 5.83; p = 0.02, for uni- and multivariable models, respectively.

1704- Se,    Prospective study of toenail selenium levels and cancer among women
- Study, Var, NA
Risk∅, No inverse association was observed between selenium levels in toenails and cancer risk

1703- Se,    An Assessment of Serum Selenium Concentration in Women with Endometrial Cancer
- Study, EC, NA
Risk↓, The mean concentration of selenium was lower in patients with endometrial cancer than in healthy controls (60.63 µg/L (0.77 µmol/L) vs. 78.74 µg/L (0.99 µmol/L), respectively). strong correlation between lower selenium levels and the incidence of EC
selm↝, A strong correlation between the level of selenium in the blood serum and the risk of endometrial cancer indicates that patients with low levels should be a candidate group requiring appropriate preventive examinations.

1702- Se,    Supplemental Selenium May Decrease Ovarian Cancer Risk in African-American Women
- Human, Ovarian, NA
Risk↓, Women with the highest intakes of supplemental selenium (>20 μg/d) had an ∼30% lower risk of ovarian cancer than those with no supplemental intake
eff∅, There was also no association of dietary or supplemental zinc or copper intake with ovarian cancer.

4484- Se,  Chit,  PEG,    Anti-cancer potential of selenium-chitosan-polyethylene glycol-carvacrol nanocomposites in multiple myeloma U266 cells
- in-vitro, Melanoma, U266
tumCV↓, SCP-Car-NCs decreased the viability of U266 cells while having no impact on the proliferation of Vero cells.
selectivity↑,
ROS↑, SCP-Car-NCs significantly boosted ROS production, decreased the MMP level, and promoted apoptosis
MMP↓,
Apoptosis↑,
BAX↑, Bax, caspase-3, and −9 activities had increased while the Bcl-2 level had decreased.
Casp3↑,
Casp9↑,
Bcl-2↓,

1700- Se,    Metabolism of Selenium, Selenocysteine, and Selenoproteins in Ferroptosis in Solid Tumor Cancers
- Review, Var, NA
Dose↝, In humans, the optimal range of Se in the serum is around 125 μg/L
Risk↑, Additionally, serum Se levels > 150 μg/L were associated with a modest increase in cancer mortality among adults in the United States.
Dose↝, same study also noticed a rise in cancer mortality with serum Se levels below 130 μg/L, which could be considered optimal
Risk↓, other side of the curve, inadequate amounts of Se or Se deficiency are also linked to an elevated risk of several diseases.

1699- Se,    Vegetarianism and colorectal cancer risk in a low-selenium environment: effect modification by selenium status? A possible factor contributing to the null results in British vegetarians
- Analysis, CRC, NA
Dose↑, a food-based recommendation is desirable and Brazil nuts have been shown to improve Se status
eff↓, undoubtedly Se is a micronutrient of concern in plant-based diets in Se-poor areas
Dose↓, A dramatic decrease in the Se status in the UK had been observed over the 1980s in longitudinal studies on same subjects

1698- Se,    Association between Dietary Zinc and Selenium Intake, Oxidative Stress-Related Gene Polymorphism, and Colorectal Cancer Risk in Chinese Population - A Case-Control Study
- Human, CRC, NA
Risk↓, Intake of selenium was found to be inversely associated with CRC risk, while zinc was not associated with CRC risk.

1697- Se,  Calc,    Calcium intake may explain the reduction of colorectal cancer odds by dietary selenium - a case-control study in Poland
- Human, CRC, NA
Risk↓, dietary selenium was associated with the decrease of colorectal cancer odds by 8% (OR = 0.92, 95%CI: 0.84–0.99 for every 10μg Se/day increase).
Risk↓, In individuals with lower (< 1000 mg/day) calcium content the odds of CRC was decreased by 13%(for every 10μg Se/day) and by 44% and 66% depending on the categories of selenium intake (60 to < 80 μg/day and ≥ 80 μg/day, respectively).
Dose∅, These authors, however, considered higher doses of selenium, and they observed a decrease in the CRC odds ratio across 81–99 μg/day, 100–118 μg/day, and 119–145 μg/day intake categories with no effect among higher than 145 μg/day doses.
AntiCan↑, protective effect of selenium has been observed also in the North Carolina Colon Cancer Study-Phase II by Williams [12], with the risk reduction estimate of 45% in the highest quartile of dietary selenium category

1696- Se,    Selenium dietary intake and survival among CRC patients
- Human, CRC, NA
OS↑, a decrease in the risk of death from colorectal cancer was observed in the group with higher dietary selenium intake (≥48.8 μg/day, group mean: 63.9 μg/day) compared to the group with lower dietary selenium intake (<48.8 μg/day, mean: 38.5 μg/day)

1695- Se,    Serum Selenium Concentration as a Potential Diagnostic Marker for Early-Stage Colorectal Cancer: A Comparative Study
- Trial, CRC, NA
Risk↓, Selenium deficiency is an established risk factor for colorectal cancer. It is believed that selenium supplementation and eating fish or foods rich in selenium and folic acid are factors modifying the incidence and development of colorectal cancer.
selm↑, Colorectal cancer patients had significantly lower serum selenium concentration than the comparison patients (67.24±15.55 μg/L vs 78.81±12.93 μg/L; P<0.001), and selenium concentration was below the reference range in a high percentage of colorectal
Dose↓, Mean selenium concentration differed significantly between both groups; 67.24±15.55 μg/L in the study group vs 78.81±12.93 μg/L in the comparison group (Figure 1; P<0.001). Selenium concentrations in the CRC patients were seldom within the reference
antiOx↑, Selenium has a strong antioxidant effect, although its excess causes toxic effects.
Dose↑, Therefore, selenium supplementation can be justified in people whose microelement concentration is in the lowest tertile (≤105.2 ng/mL)
Dose↝, arod et al showed that selenium supplementation in the Polish population should be considered in people with serum selenium concentration below 70 μg/L, with the aim of maintaining the concentration in the range of 70–90 μg/L

1694- Se,    Expression of Selenoprotein Genes and Association with Selenium Status in Colorectal Adenoma and Colorectal Cancer
- Analysis, CRC, NA
AntiCan↑, Dietary selenium (Se) intake is essential for synthesizing selenoproteins that are important in countering oxidative and inflammatory processes linked to colorectal carcinogenesis.
selenoP↓,

1693- Se,    Prediagnostic selenium status, selenoprotein gene variants and association with breast cancer risk in a European cohort study
- Analysis, BC, NA
Risk↓, Selenium (Se) may help prevent breast cancer (BC) development.
other∅, Higher Se status does not appear to be associated with BC risk, although activity of the selenoenzyme GPX3 may be inversely associated with premenopausal BC risk, and SNPs in the Se pathway alone or in combination with suboptimal Se status may influe

1692- Se,    Association of Selenoprotein and Selenium Pathway Genotypes with Risk of Colorectal Cancer and Interaction with Selenium Status
- Analysis, CRC, NA
Risk↓, study suggests that SNPs in the Se pathway alone or in combination with suboptimal Se status may contribute to CRC development.

1691- Se,    The influence of selenium and selenoprotein gene variants on colorectal cancer risk
- Analysis, CRC, NA
Risk↓, Low intake of the micronutrient selenium (Se) has been implicated as a risk factor in CRC

1690- Se,    Selenium and cancer: a story that should not be forgotten-insights from genomics
- Review, Var, NA
Dose↓, low Se intake is associated with increased risk of various cancers, the results of supplementation trials have been confusing
other↝, Se supply modulates protein synthesis, unfolded protein response, Wnt, Nrf2 and inflammatory pathways

1689- Se,    Selenium and breast cancer - An update of clinical and epidemiological data
- Analysis, BC, NA
OS↑, Clinical and epidemiological studies summarized here clearly demonstrate that Se status correlates with breast cancer survival
eff↑, one way to curb breast cancer mortality would be via Se supplementation, especially in patients with severely deplete Se status
Dose∅, A sufficient serum Se level is a prerequisite for adequate immune response and an appropriate serum Se level is identified to be around 125 μg/L [40].
*toxicity↝, Any serum Se level lower or higher than this is where health concerns arise.
eff↑, Se levels consistently correlate with survival, indicating that for a subset of breast cancer patients with low Se, Se supplementation can be used for therapeutic purpose.

1688- Se,    Potential Role of Selenium in the Treatment of Cancer and Viral Infections
- Review, Var, NA
IL2↑, in mice promoted T cell receptor signaling that pushed T cell differentiation toward a Th1 phenotype by increasing interleukin -2 (IL-2) and interferon gamma (INF-γ) production
INF-γ↑,
Th1 response↑, 18 human subjects treated with 200 μg selenium-enriched broccoli daily for three days showed that selenium supplementation resulted in substantially higher levels of both Th1 and Th2 cytokines secreted by peripheral blood mononuclear cells
Th2↑,
Dose↑, Wang et al. on hens supplemented selenium (5 mg/kg, 10 mg/kg, and 15 mg/kg) orally for three time periods (15, 30, and 45 days) found that excessive selenium intake leads to a substantial reduction in the amount of IFN-γ and IL-2 cytokines
AntiCan∅, after 5.5 years, the results of this study revealed no relationship between selenium supplementation and prostate cancer risk reduction in men with low selenium levels
Risk↑, instead, they discovered that taking selenium supplements raised the high-grade prostate cancer risk in men who had high selenium levels
chemoP↑, selenium provided protection of normal tissues from drug-induced toxicity
Hif1a↓, Selenium down-regulates HIFs,
VEGF↓, leading to the subsequent down-regulation in expression of several genes including those involved in angiogenesis such as vascular endothelial growth factor (VEGF)
selectivity↑, Selenium also helps with DNA repair in response to DNA-damaging agents, which improves the effectiveness of chemotherapeutic agents by protecting normal cells from their toxicity.
*GADD45A↑, selenium protected WT-MEF from DNA damage in a p53-dependent manner by increasing the expression of p53-dependent DNA repair proteins such as XPC, XPE, and Gadd45a. Thus, cells lacking p53, such as tumor cells, did not receive the same protection
NRF2↓, a defined dose and schedule of selenium down-regulates and up-regulates Nrf2 in tumor tissue and normal tissue, respectively
*NRF2↑, a defined dose and schedule of selenium up-regulates Nrf2 in normal tissue
ChemoSen↑, These differential effects were associated with selective sensitization of tumor tissues to subsequent treatment with chemotherapy. Overactivation of Nrf2 increases the expression of MRPs, consequently decreasing the effectiveness of chemotherapy .
angioG↓, The inhibition of hypoxia-induced activation of HIF-1α and VEGF by knocking down Nrf2 suppresses angiogenesis, demonstrating a crosstalk mechanism between Nrf2 and HIF-1α in angiogenesis
PrxI↓, Selenium was shown to reduce drug detoxification and increase cytotoxic effects of anti-cancer drugs in tumor cells through suppression of the Nrf2/Prx1 pathway,
ChemoSideEff↓, showed that selenium supplementation attenuated the cardiotoxic effects of doxorubicin by decreasing oxidative stress and inflammation through Nrf2 pathway activation
eff↑, combination of niacin and selenium reduced the reactive oxygen species generated by sepsis and diminished the resultant lung injury by upregulating Nrf2 signaling

1687- Se,    Selenium for preventing cancer
- Analysis, Var, NA
eff∅, Two RCTs with 19,009 participants indicated that colorectal cancer was unaffected by selenium administration
AntiCan∅, Well‐designed and well‐conducted RCTs have shown no beneficial effect of selenium supplements in reducing cancer risk

4445- Se,  DFE,    A comparative study on the hepatoprotective effect of selenium-nanoparticles and dates flesh extract on carbon tetrachloride induced liver damage in albino rats
- in-vivo, LiverDam, NA
*hepatoP↑, This study suggests that CCL4-induced liver damage in rats can be protected by administration whether the costly SeNPs or the economical DFE.
*antiOx↑, Selenium (Se) is considered as one of the most beneficial elements on the human health, such as performing as antioxidant and anticancer supplement it regulates the functions of selenoproteins which could reduce the tissue oxidation and balancing the
*AntiCan↑,
*BioAv↑, Selenium nanoparticles (SeNPs) have a high bioavailability and proper biological activities, as its greater surface area, better absorption, minimal toxicity and increasing bioactivity so it is used widely in biomedicine
*toxicity↓,
*ROS↓, The fact that Se has a hepatoprotective effect is usually attributed to its antioxidant ability to limit the tissue oxidation by decreasing the ROS.
*MDA↓, significantly reduced in the SeNPs and DFE groups to levels comparable to the control group.
*ALAT↓, in the current study by consumption of SeNPs or DFE showed a significant decrease in the ALT and increase in albumin blood levels indicating their hepatoprotective properties
*Albumin↑,
*GSH↑, In the current study, the SeNPs group showed a statistically increased in the tissue antioxidants GSH and SOD while in DFE group there was a moderate increas
*SOD↑,
*RenoP↑, dates have anti-inflammatory, immune-stimulating, anti-hyperglycemic, anti-cholesterol, antioxidant, and reno-protective characteristics

4485- Se,    Selenium stimulates the antitumour immunity: Insights to future research
- Review, NA, NA
*antiOx↑, At nutritional low doses, selenium, depending on its form, may act as an antioxidant, protecting against oxidative stress, supporting cell survival and growth, thus, plays a chemo-preventive role
chemoP↑,
ROS↑, at supra-nutritional higher pharmacological doses, selenium acts as pro-oxidant inducing redox signalling and cell death
Imm↑, selenium stimulates the immune system against cancer
selenoP↑, anti-oxidant through selenoproteins
*IL2↑, consumption of Se-enriched foods (200 μg per serving for 3 days) increases the levels of interleukin IL-2, IL-4, IL-5, IL-13 and IL-22, indicating an activated Th2-type response
*IL4↑,
*TNF-α↓, taking selenised yeast (300 μg.day−1) downregulates the gene expression of tumour necrosis factor (TNF)α and transforming growth factor (TGF)β; thus, consequently inhibit the epithelial-to-mesenchymal transition (EMT) in non-malignant prostate tissue
*TGF-β↓,
*EMT↓,
Risk↓, immune-enhancing effects of Se may reduce the risk of cancer
*GPx↑, chemo-preventive effects of Se are mainly mediated by the anti-oxidant function of selenoenzymes such as GPxs and TXNRDs [68] because Se supplementation increases both GPx1 and GPx4 activity in humans
*TrxR↑,

4483- Se,  Chit,    Anti-cancer potential of chitosan-starch selenium Nanocomposite: Targeting osteoblastoma and insights of molecular docking
- in-vitro, OS, NA
AntiCan↑, CS/S/SeNC acts as a potential anti-cancer agent, specifically targeting osteoblastoma cells was evaluated for anti-cancer activity using in-vitro studies MTT assay
TumCP↓, strong ability to inhibit cancer cell proliferation in a dose-dependent manner, and induce apoptosis via ROS- mediated mechanism
Apoptosis↑,
ROS↑,
eff↑, biocompatibility of CS/S/SeNC was confirmed through its interaction with the endogenous protein Decorin, thereby augmenting its potential as a therapeutic agent for the treatment of bone cancer.
other↝, The utilization of chitosan composite materials and their applications in bone tissue engineering have gained a lot of interest lately due to evidence that chitosan accelerates the development of extracellular matrix and formation
eff↑, major advantage of selenium nanoparticles is that they have improved efficacy against cancer cells and their unique function is that they are highly effective at targeted drug delivery
TumCCA↑, function as a pro – oxidants and raise ROS levels in cancer cells, which causes apoptosis and cell cycle arrest
NA↑,
NA↑,

4480- Se,  Chit,    Biogenic synthesized selenium nanoparticles combined chitosan nanoparticles controlled lung cancer growth via ROS generation and mitochondrial damage pathway
- in-vitro, Lung, A549 - in-vitro, Nor, HK-2
selectivity↑, (MCF-10) were not significantly cytotoxically affected by SeNPs and Se-chitosan NPs.
*toxicity↓,
ROS↑, SeNP and Se-chitosan NP treatment resulted in increased ROS generation and caused mitochondrial dysfunction
mtDam↑,
Apoptosis↑, Chito-NPs, SeNPs, and Se-chitosan NPs cause apoptosis and death in A549 cells.
LDH↑, Chito-NPs, SeNPs, and Se-chitosan NPs increase the LDH release

4474- Se,    In vitro growth of gut microbiota with selenium nanoparticles
*GutMicro↑, increased abundance of some beneficial bacteria, for example Lactobacillus sp. and Faecalibacterium prausnitzii, however, without significant pathogen reduction. The quantity of butyric acid in different gut sections was increased. Butyric acid is a

4473- Se,    Anti-cancerous effect and biological evaluation of green synthesized Selenium nanoparticles on MCF-7 breast cancer and HUVEC cell lines
- in-vitro, BC, MCF-7 - in-vitro, Nor, HUVECs
AntiCan↑, Se NPs demonstrated a non-toxic effect on the Human Umbilical Vein Endothelial Cells (HUVEC) normal cell line and anticancer activity on the MCF-7 breast cancer cell line.
selectivity↓,
*Bacteria↓, As a result, Se NPsexhibit outstanding antibacterial, antioxidant, ROSscavenging (i.e., anticancer), and enzyme inhibitionactivities
*antiOx↑,
*toxicity↓, lower toxicity comparedto other conventional organic and inorganicselenium compounds
ROS↑, Selenium nanoparticles have the unique abilityto generate Reactive Oxygen Species (ROS), thus exhibiting pro-oxidant effects.
tumCV↓, In the MCF-7 breast cancer cell line, cell viability decreased to approximately 70% after treatment with 200 μg/mL of Se nanoparticle

4472- Se,    Therapeutic potential of selenium nanoparticles
- Review, Var, NA
*ROS↓, Moreover, it is a cofactor of anti-oxidant enzymes (glutathione peroxidase and thioredoxin reductase) that safeguards our human body from reactive oxygen species (ROS).
*BioAv↑, SeNPs have displayed stupendous properties which have resulted in their maximum utilization for various crucial applications. They are biocompatible and exhibit excellent bioavailability, high affinity, biological activity, good permeability, and int
*antiOx↑, and intestinal absorption, as well as anti-oxidant activities
toxicity↓, NPs have lower toxicity than inorganic Se and other organoselenium compound
eff↑, This is because only a single-step reduction from the elemental selenium atom to selenide anion is required to activate redox cycling with oxygen to produce ROS while multiple-step reduction is necessary for selenite
*other↝, SeNPs are normally unstable in the liquid phase and extremely easy to aggregate which results in the formation of gray or black selenium with a large particle size.
EPR↑, It has been discovered that NPs of sizes ranging between 10 and 100 nm can penetrate deep into the tumor tissues and destroy cancer cells without affecting healthier ones, an effect termed as “enhanced permeation and retention”
selectivity↑,
eff↑, Amidst the efficient nanoparticle family, SeNPs have excelled in proving to be one of the best NPs available for cancer therapy.
RadioS↑, SeNPs (act as a radiosensitizer) were not affected by radiation instead a greater concentration of intracellular Se ions was induced, leading to an increase in its toxicity by rapid generation of free radicals.
eff↑, Small-sized SeNPs exhibited greater inhibition of cancer cell progression through the ROS-mediated system, and no side effects were observed on increasing selenoenzyme activities.
*Bacteria↓, Reports have demonstrated the exemplary features of SeNPs that enable them to be a powerful anti-microbial agent

4471- Se,    Green synthesis of selenium nanoparticles with extract of hawthorn fruit induced HepG2 cells apoptosis
- in-vitro, Liver, HepG2
eff↑, hawthorn fruit extract (HE) was chosen as a reductant to prepare SeNPs.
ROS↑, treatment of HE-SeNPs up-regulated intracellular ROS levels and reduced the MMP
MMP↓,
Casp9↑, HE-SeNPs induced the up-regulation of caspase-9 and down-regulation of Bcl-2.
Bcl-2↓,
selectivity↑, Furthermore, the results in Figure 3(B) suggested that He-SeNPs were almost non-cytotoxic to HL02 cells (healthy hepatic cells).
Apoptosis↑, HE-SeNPs induced apoptosis of HepG2 cells

4470- Se,  Chit,    Synthesis and cytotoxic activities of selenium nanoparticles incorporated nano-chitosan
- in-vitro, CRC, HCT116 - in-vitro, Liver, HepG2 - in-vitro, BC, MCF-7
Dose↝, average size 20 nm and chitosan nanoparticles with an average size 207 and 250 nm for neat nano-chitosan and chitosan incorporated 5-fluorouracil/selenium nanoparticles, respectively.
AntiCan↑, The results indicated the potent cytotoxic activities of all nanocomposite toward the tested cells with enhanced anticancer activity rather than the single drug or neat selenium nanoparticle.
eff↑, It is worth to mention that the above data demonstrated that SeNPs synthesized without a stabilizer was unstable and easily agglomerate, which confirmed the important role of Ch for further 5-Flu encapsulation.

4469- Se,    Selenium Nanoparticles in Cancer Therapy: Unveiling Cytotoxic Mechanisms and Therapeutic Potential
- Review, Var, NA
antiOx↑, SeNPs demonstrate intrinsic antioxidant properties that counteract oxidative stress commonly observed in cancer cells.
selectivity↑, They modulate critical cellular pathways and exhibit selective toxicity, damaging cancer cells while sparing healthy tissues.
eff↑, Additionally, their biocompatibility and capacity to deliver therapeutic agents contribute to improved safety and efficacy compared to other nanoparticle platforms.
AntiCan↑, Additionally, SeNPs modified with ferulic acid showed promising anticancer effects against HepG2 cells, triggering apoptosis via mitochondrial pathways through the generation of intracellular reactive oxygen species and disruption of mitochondrial m
Apoptosis↑,
ROS↑,
MMP↓,
Casp3↑,
Casp9↑,
AntiTum↑, Furthermore, in vivo experiments using zebrafish models confirmed the inhibitory effects of SeNPs on tumor growth, migration, and angiogenesis.
TumCG↓,
TumMeta↓,
angioG↓,
Cyt‑c↑, leading to the release of cytochrome C from mitochondria into the cytoplasm, culminating in cell death and the induction of permanent DNA damage.
DNAdam↑,
RadioS↑, Interestingly, the caspase expression was enhanced under X-ray exposure compared to absence, suggesting a synergistic effect between SeNPs and radiation therapy
BBB↑, SeNPs have shown promise in glioblastoma treatment by significantly reducing cell viability in a dose-dependent manner, indicating their potential to cross the BBB and serve as an alternative therapeutic approach for gliomas
*toxicity↓, However, at proper concentrations, SeNPs are nontoxic to healthy cells, unlike other chemotherapeutic drugs
ChemoSen↑, Anticancer Activity of SeNPs via Autophagy, ROS, and Chemosensitization

4467- Se,  VitC,  Chit,    Nano-chitosan-coated, green-synthesized selenium nanoparticles as a novel antifungal agent against Sclerotinia sclerotiorum in vitro study
- Study, NA, NA
*Dose↝, CS NPs with a tiny particle size of an average diameter of 6.43 ± 0.2 nm
*Dose↝, L.P. -Se NPs with small particle size and good dispersion due to the presence of extract biomolecules that serve as capping agents providing stabilization and reduced particle size with an average diameter of 42.8 ± 18.5 nm

4466- Se,    Synthesis and Characterization of Selenium Nanoparticles and its Effects on in vitro Rumen Feed Degradation, Ruminal Parameters, and Total Gas Production
- Study, NA, NA
other?, see above for synethsis notes

4465- Se,  VitC,    Selenium nanoparticles: Synthesis, in-vitro cytotoxicity, antioxidant activity and interaction studies with ct-DNA and HSA, HHb and Cyt c serum proteins
- Study, NA, NA
*other↝, The aim of this study was the synthesis of selenium nanoparticles (SeNPs) employing vitamin C as a biocompatible and low toxic reducing agent.
*eff↑, ynthesized nano-selenium can bind to the most important blood proteins such as human serum albumin (HSA), human hemoglobin (HHb), and Cytochrome c (Cyt c).
AntiCan↑, reported that Nano-selenium demonstrates anti-tumor and anticancer activity through induction of cancer cell apoptosis with minimal side effects on normal cells
*Dose↝, adequate selenium intake has been reported to be between 55 and 75 μg /day with an upper limit of ∼400 μg
*BioAv↑, Nano-selenium has high biological activity, better bioavailability and low toxicity compared to organic and inorganic Se-compounds such as Se(IV) and Se(VI) [9]
*other↝, synthesis listed in description

4464- Se,    Antioxidant Properties of Selenium Nanoparticles Synthesized Using Tea and Herb Water Extracts
- Study, NA, NA
*eff↑, The smallest nanoparticles were obtained from the synthesis using mint; they had a size of 54.8 nm.
*eff↝, The size of SeNPs, especially, is crucial if they are to be used in medicine; they should be smaller than 100 nm.

4463- Se,  VitC,    Selenium nanoparticles: Synthesis, characterization and study of their cytotoxicity, antioxidant and antibacterial activity
- Study, Nor, NA
Dose↝, see description for synthesis

4462- Se,  VitC,    Selenium nanoparticles: influence of reducing agents on particle stability and antibacterial activity at biogenic concentrations
- Study, Nor, NA
*Dose↝, see description for synthesis method
*Bacteria↓,

4460- Se,  VitC,    Ascorbic acid-mediated selenium nanoparticles as potential antihyperuricemic, antioxidant, anticoagulant, and thrombolytic agents
Dose?, see description for method for synthesis

4444- Se,    Antioxidant and Hepatoprotective Efficiency of Selenium Nanoparticles Against Acetaminophen-Induced Hepatic Damage
- in-vivo, LiverDam, NA
*hepatoP↑, hepatoprotective role of selenium nanoparticles (Nano-Se) against APAP-induced hepatic injury.
*ROS↓, Nano-Se exhibits a protective effect against APAP-induced hepatotoxicity through improved liver function and oxidative stress mediated by catalase, SOD, and GSH and decreases hepatic DNA fragmentation,
*Catalase↑,
*SOD↑,
*GSH↑,
*DNAdam↓,

4446- Se,    Antioxidant and Hepatoprotective Effects of Moringa oleifera-mediated Selenium Nanoparticles in Diabetic Rats.
- in-vivo, Diabetic, NA
*glucose↓, MO-SeNPs treatment significantly reduced blood glucose levels (p < 0.05) and restored insulin resistance, with lower dose demonstrating better glycaemic control than larger dose.
*antiOx↑, MO-SeNPs also increased hepatic antioxidant enzyme activity, including GSH-Px, CAT, and T-SOD, which neutralise oxidative stress
*GPx↑,
*Catalase↑,
*SOD↑,
*ROS↓,
*cardioP↑, MO-SeNPs also improves cardiovascular health by raising HDL and lowering LDL.
*HDL↑,
*LDL↓,
*hepatoP↑, MO-SeNPs showed hepatoprotective benefits by lowering inflammatory markers such TNF-α, IL-6, IL-1β, iNOS, and AGEs, and reduced lipid peroxidation.
*TNF-α↓,
*IL6↓,
*IL1β↓,
*lipid-P↓,
*Inflam↓, The reduction in these indicators shows MO-SeNPs reduce liver inflammation and protect the liver.
*ALAT↓, The normalisation of liver enzyme levels (ALT, AST, ALP) showed improved liver function.
*AST↓,
*ALP↓,
*Dose↝, For the aqueous extract, 20 g of powdered leaves were homogenized in 800 mL of boiling distilled water, shaken at 150 rpm for 4 hours, centrifuged at 4000 rpm for 20 minutes, and filtered using Whatman filter paper No. 1 (Cat No. 1001 125) from GE H
*Dose↝, Selenium nanoparticles (MO-SeNPs) were synthesized by adding 5 mL of a 50 mM sodium selenite solution dropwise to 20 mL of Moringa oleifera extract under magnetic stirring, followed by incubation at 37 °C for 48 hours at pH 8 to facilitate the green

4448- Se,    Selenium Nanoparticles: A Comprehensive Examination of Synthesis Techniques and Their Diverse Applications in Medical Research and Toxicology Studies
- Review, Nor, NA
*toxicity↓, Selenium is non-toxic, and colorless, depending on the oxidation state, and acts as the redox center for several antioxidant enzymes
*toxicity↓, This statement has also been proven: selenium nanoparticles have less toxicity than selenomethionine
selectivity↑, Se nanoparticles have shown better selectivity between normal and cancer cells
*antiOx↑, Se nanoparticles have a potent antioxidant property in comparison to selenium species, which makes them a potent compound
*cognitive↑, figure 1
*other↝, The chemical method for the reduction in inorganic selenium into precursors is the most widely used approach for producing SeNPs. Ascorbic acid, glutathione, cysteine, sodium meta sulfite, and ionic liquid 1-ethyl-3-methylimidazolium thiocyanate, glu
TumCCA↑, SeNPs’ anticancer effects are mediated by their capacity to stop cancer cells from growing by inducing cell cycle arrest in the S phase

4449- Se,    PEG-nanolized ultrasmall selenium nanoparticles overcome drug resistance in hepatocellular carcinoma HepG2 cells through induction of mitochondria dysfunction
- in-vitro, Liver, HepG2
MMP↓, depletion of mitochondrial membrane potential and generation of superoxide anions contributed to PEG-SeNPs-induced apoptotic cell death in R-HepG2 cells.
selectivity↑, Despite this potency, PEG-SeNPs showed much lower cytotoxicity toward normal cells (human kidney HK-2 cells)
Apoptosis↑, PEG-SeNPs inhibit R-HepG2 cell growth though induction of apoptosis
ROS↑, The results showed that treatments of PEG-SeNPs led to dose- and time-dependent increases in intracellular superoxide anion level

4450- Se,    Functionalized selenium nanoparticles with nephroprotective activity, the important roles of ROS-mediated signaling pathways
- in-vitro, Kidney, NA
antiOx↑, (trolox) surface-functionalized selenium nanoparticles (Se@Trolox) with enhanced antioxidant activity have been prepared by self-assembly of trolox on the surface of the nanoparticles, and their nephroprotective effects have been investigated
*ROS↓, Se@Trolox effectively blocked the cisplatin-induced reactive oxygen species (ROS) accumulation
RenoP↑, Taken together, our findings suggest that Se@Trolox is a promising Se species with potential application in prevention of cisplatin-induced renal injury.

4451- Se,    Effects of chitosan-stabilized selenium nanoparticles on cell proliferation, apoptosis and cell cycle pattern in HepG2 cells: comparison with other selenospecies
- in-vitro, Liver, HepG2
*antiOx↑, excellent antioxidant properties
Apoptosis↑, cell proliferation, apoptosis and cell cycle pattern on HepG2 cells has shown the unique properties of this relatively novel compound that support and complete prior evidences for future applications as chemotherapeutic agent.
TumCCA↑,

4452- Se,  Chit,    Antioxidant capacities of the selenium nanoparticles stabilized by chitosan
- in-vitro, Nor, 3T3
*toxicity↓, Our work could demonstrate the CS-SeNPs hold a lower toxicity
*antiOx↑, Selenium (Se) is involved in the antioxidant defense systems of the liver and plays an important role in protecting against oxidative stress.
*GPx↑, Se supplementation can increase the level of enzymes such as GPx etc
*ROS↓, The inhibition of the intracellular ROS by CS-SeNPs was examined in the BABLC-3T3 and Caco-2 cell lines, designed as skin or viscera cell models, respectively.

4453- Se,    Selenium Nanoparticles: Green Synthesis and Biomedical Application
- Review, NA, NA
*toxicity↓, “Green” synthesis has special advantages due to the growing necessity for environmentally friendly, non-toxic, and low-cost methods.
*Bacteria↓, SeNPs are active against both Gram-positive and Gram-negative microorganisms
ROS↑, The cancer cells exhibit an acidic pH and an imbalanced redox state. These conditions in cancer cells initiate the pro-oxidant conversion of SeNPs and trigger the development of free radicals in malignant cells
MMP↓, mitochondrial membrane destruction
ER Stress↑, on the other hand, to stress in the endoplasmic reticulum (ER)
P53↑, Selenium nanoparticles can stimulate p53 expression in cancer cells, leading to caspase-9 activation, mitochondrial membrane potential depletion, and the induction of apoptosis.
Apoptosis↑,
Casp9↑,
DNAdam↑, In addition, in cellular processes, DNA structure is damaged, causing the cell cycle to stop and, ultimately, cell death.
TumCCA↑,
eff↑, positively charged SeNPs may have a strong affinity for breast cancer cells, causing the enhanced anticancer efficacy of SeNPs
Catalase↓, was accompanied by a decrease in antioxidant marker levels (CAT, SOD, GPx activity and GSH levels) in MCF-7 cells exposed to green SeNPs
SOD↓,
GSH↓,
selectivity↓, in contrast to control cells
selectivity↑, SeNPs selectively affect LDH leakage and membrane disruption in cancer cells because the SeNP concentration required to influence LDH leakage in normal cells is much higher compared to that in cancer cells
PCNA↓, SeNPs reduced the PCNA expression level in MCF-7 cells, showing their role in suppressing oncogenesis and proliferation in breast cancer by inhibiting PCNA gene expression
eff↑, Nanoparticle capping can enhance their absorption via accumulation by endocytosis in cancer cells, which can therefore lead to ROS generation induction
*ALAT↓, SeNPs could significantly decrease hepatic (serum ALT, AST, and ALP) and renal (serum uric acid, urea, and creatinine) function markers, total lipid, total cholesterol, triglyceride and low-density lipoprotein cholesterol levels, and glucose-6-phosph
*AST↓,
*ALP↓,
*creat↓,
*Inflam↓, selenium nanoparticles appear to be a possible anti-inflammatory agent.
*toxicity↓, Most studies confirm that SeNPs are less toxic than sodium selenite
selectivity↑, despite affecting cancer cells and causing their death, SeNPs do not harm normal cells,

4457- Se,    Selenium nanoparticles: a review on synthesis and biomedical applications
- Review, Var, NA - NA, Diabetic, NA
*BioAv↑, Recently, selenium nanoparticles (SeNPs) attracted the interest of many researchers due to their biocompatibility, bioavailability, and low toxicity.
*toxicity↓,
*eff↑, synthesized SeNPs demonstrate greater compatibility with human organs and tissues
chemoP↑, They can also act as chemopreventive agents, anti-inflammatory agents, and antioxidants.
*Inflam↓,
antiOx↑,
*selenoP↑, Selenium, a part of selenoproteins and selenocompounds within the human body, plays a critical role in reproduction, DNA synthesis, thyroid hormone, metabolism, and protection from infections and oxidative damage.
*ROS↓, also figure 6
*Dose↝, The United Kingdom group of vitamins and minerals recommended the daily intake of selenium by women and men should be 60 μg and 70 μg, respectively.3 A daily intake of more than 400 μg could be toxic
AntiCan↑, Several studies have supported their anticancer,22 antioxidant,21 antimicrobial,23–25 and anti-biofilm properties
*Bacteria↓,
eff↑, Tran et al.65 reduced sodium selenite by ascorbic acid using polyvinyl alcohol (PVA) as the stabilising agent, resulting in an average particle size of 70 nm . The absorption was observed in the wavelength range 250 to 450 nm
DNAdam↑, figure 6
selectivity↑, figure 6
*eff↑, At a concentration of 2.0 mg kg−1 body weight, chitosan stabilized SeNPs resulted in improved antidiabetic activity.

4458- Se,    Selenium Nanoparticles for Antioxidant Activity and Selenium Enrichment in Plants
*Dose↝, By dissolving selenium powder in ethylenediamine (EDA) to create a homogeneous Se–EDA solution, SeNPs can be easily formed by adding this solution to water.
*eff↑, Our findings indicate that SeNPs exert a minimal effect on the growth of bean sprouts while substantially boosting the levels of seleno-amino acids within them.
*Dose↝, At a SeNP concentration of 20 mg/L, the concentration of seleno-amino acids in the bean sprouts can increase to as much as 0.182 μg/g.

4459- Se,  VitC,    Nano and mesosized selenium and its synthesis using the ascorbic acid route
*eff↑, The most commonly used reducing agent is ascorbic acid because the reaction may be performed at ambient temperature in water and the ascorbic acid is affordable and non-harmful.
*Dose↝, Sodium selenite (Schuchardt Munchen, Germany), ascorbic acid, and hydrochloric acid (Penta, Czech Repubic) were used. All chemicals were used without further purification. Demineralized water was used for the preparation of all solutions
*Dose↝, 200 ml of the solution of 6 mM sodium selenite was mixed with 40 ml of ascorbic acid solution at different concentrations. The molar quantity ratios in which individual samples were mixed are shown in Table 1.

4461- Se,  VitC,    Synthesis, Characterization, and Cytotoxic Evaluation of Selenium Nanoparticles
*Dose?, see description for manufacturing SeNPs

4743- Se,    Selenium for alleviating the side effects of chemotherapy, radiotherapy and surgery in cancer patients
- Review, Var, NA
eff↝, To date, research findings do not provide a basis for any recommendation in favour or against selenium supplementation in cancer patients.
chemoP↝, There is insufficient evidence at present that selenium supplementation alleviates the side effects of tumour specific chemotherapy or radiotherapy treatments
radioP↝,

4744- Se,  Chemo,  antiOx,    Ingestion of selenium and other antioxidants during prostate cancer radiotherapy: A good thing?
- Review, Pca, NA
Risk↓, A large body of epidemiological evidence, including observational, trials, and randomized controlled clinical trials, support the proposition that selenium may prevent prostate cancer in humans
chemoP↑, This systematic review provides the first evidence that antioxidant supplementation during chemotherapy holds potential for reducing dose-limiting toxicities.

4745- Se,  Chemo,    Translational Selenium Nanoparticles Promotes Clinical Non-small-cell Lung Cancer Chemotherapy via Activating Selenoprotein-driven Immune Manipulation
- Study, NSCLC, NA
Risk↓, In this study, it is found that selenium (Se) depletion and immune dysfunction are present in patients with advanced NSCLC compared with healthy volunteers
TumCD↑, translational SeNPs can promote the proliferation of NK cells and enhance its cytotoxicity against cancer cells by activating mTOR signaling pathway
mTOR↑,
AntiTum↑, driven by GPXs to regulate the secretion of cytokines to achieve an antitumor response.
ChemoSen↑, Investigator-initiated Trial shows that translational SeNPs supplementation in combination with bevacizumab/cisplatin/pemetrexed exhibits enhanced therapeutic efficacy with an objective response rate of 83.3% and a disease control rate of 100%

4747- Se,  Chemo,  antiOx,    Phase I trial of selenium plus chemotherapy in gynecologic cancers
- Trial, Ovarian, NA
*toxicity↓, The maximum tolerated dose of selenium was not reached
ChemoSen∅, Selenium had no effect on carboplatin pharmacokinetics.
RAD51↓, Correlative studies showed post-treatment downregulation of RAD51AP1, a protein involved in DNA repair, in both cancer cell lines and patient tumors.
other↝, Overall, the addition of selenium to carboplatin/paclitaxel chemotherapy is safe and well tolerated, and does not alter carboplatin pharmacokinetics. A 5000 μg dose of elemental selenium as selenious acid is suggested as the dose to be evaluated in a

4748- Se,  Chemo,  antiOx,    Efficacy and safety of intravenous administration of high-dose selenium for preventing chemotherapy-induced peripheral neuropathy in gastric cancer patients receiving adjuvant oxaliplatin and capecitabine after gastrectomy: a retrospective pilot study
- Trial, GC, NA
toxicity↓, No adverse events related to high-dose selenium administration were observed.
chemoP∅, There were no significant differences in chemotherapy-related adverse events, such as hand-foot syndrome, nausea, vomiting, diarrhea, and loss of appetite, between the two groups.
*neuroP↑, by the end of chemotherapy, the selenium group exhibited significantly lower by the end of chemotherapy, the selenium group exhibited significantly lower paresthesia severity compared to the non-selenium groseverity compared to the non-selenium group
*Dose↝, Several studies in cancer patients undergoing chemotherapy have failed to demonstrate a protective effect with low-dose oral selenium supplementation

4749- Se,  Chemo,  antiOx,    Selenium as an element in the treatment of ovarian cancer in women receiving chemotherapy
- Trial, Ovarian, NA
*GSH↑, patients with ovarian cancer undergoing chemotherapy and receiving Se showed a significant increase in the activity of GSH-P(x) in erythrocytes after 2 months' (P < 0.0015) and 3 months' (P < 0.0038) supplementation.
*MDA↑, An increase of the concentration of malondialdehyde (MDA) following the administration of Se after 2 months (P < 0.0363) and 3 months (P < 0.0489) was found to be significant.
*other?, Se administration for 3 months resulted in the significant increase of white blood cells (WBC) (P < 0.0001)
*other?, After 2 and 3 months of Se administration, a significant decrease of hair loss
*chemoP↑, As a result of this clinical trial, we conclude that there are beneficial effects caused by ingesting selenium, as a supportive element in chemotherapy.

4750- Se,  Rad,    Selenium in Radiation Oncology—15 Years of Experiences in Germany
- Review, Var, NA
RadioS∅, Survival data imply that Se supplementation did not interfere with radiation success.
radioP↑, Some positive effects of supplemental Se in the prevention of ageusia (loss of taste) and dysphagia due to radiotherapy were noted in a second randomized trial in patients with head and neck cancer.
eff↑, Se supplementation yielded promising results concerning radioprotection in tumor patients and should be considered as a promising adjuvant treatment option in subjects with a relative Se deficit.

4751- Se,  Chemo,    Selenium Protects Against Toxicity Induced by Anticancer Drugs and Augments Antitumor Activity: A Highly Selective, New, and Novel Approach for the Treatment of Solid Tumors
- in-vivo, Var, NA
Dose↝, Studies in mice have documented that the minimum effective dose of MSC when combined with irinotecan is 0.01 mg daily.
ChemoSen↑, Results from this laboratory have demonstrated that MSC and SLM are highly effective modulators of irinotecan cure rates in de novo sensitive and resistant human tumor xenografts.
chemoP↑, Selenium Protects Against Toxicity Induced by Anticancer Drugs

4752- Se,  CUR,  Chemo,    Curcumin-Modified Selenium Nanoparticles Improve S180 Tumour Therapy in Mice by Regulating the Gut Microbiota and Chemotherapy
- in-vitro, Cerv, HeLa - in-vitro, sarcoma, S180
tumCV↓, Cur/Se nanoparticles showed higher cytotoxicity against HeLa and S180 tumour cells.
ROS↑, Cur/Se nanoparticles significantly delivered more curcumin into the HeLa tumour cells and induced greater ROS production.
*GutMicro↑, Cur and Cur/Se nanoparticles significantly reduced the relative abundances of Rikenellaceae_RC9_gut_group, Enterorhabdus and Bilophila and increased the relative abundance of Lachnospiraceae_UCG-006.
BioAv↑, Cur/Se nanoparticles could increase the bioactivity of curcumin and improve cancer therapy by regulating the gut microbiota.
other↝, The Cur/Se nanoparticles were prepared by reducing sodium selenite with curcumin in one step
Dose↝, The IC50 values of Cur and Cur/Se nanoparticles were 33.0 μg/mL and 8.4 μg/mL, respectively, against S180

4753- Se,  Chemo,    Selenium and Lung Cancer: A Systematic Review and Meta Analysis
- Review, Lung, NA
Risk⇅, Selenium supplementation may reduce risk of lung cancers in populations with lower baseline selenium status (serum<106 ng/mL), but increase risk of lung cancers in those with higher selenium (≥121.6 ng/mL).
chemoP↑, In the treatment of lung cancers, selenium may reduce cisplatin-induced nephrotoxicity and side effects associated with radiation therapy.
radioP↑,

4754- Se,  Chemo,    The effect of selenium yeast in the prevention of adverse reactions related to platinum-based combination therapy in patients with malignant tumors
- Trial, Var, NA
chemoP↑, Patients with selenium yeast treatment after chemotherapy had better appetites and more stable body weights than those without selenium yeast
QoL↑, quality of life of the patients, as evidenced by the elevated Karnofsky Performance Status (KPS) scores of the two groups, and selenium yeast treatment potentiated this improvement
chemoP↑, Selenium yeast treatment significantly reduced the incidence of adverse reactions in patients after chemotherapy by 23.26% (p<0.05), and patients also experienced milder adverse reactions after selenium yeast administration
Pain↓, Chemotherapy with selenium yeast treatment provided better pain mitigation for patients vs. without selenium yeast administration

4755- Se,  Chemo,    Selenium Prevention of Alopecia, Bladder and Kidney Toxicity Induced by Chemotherapeutic Agents
- in-vitro, Var, NA
chemoP↑, Researchers at Roswell Park Comprehensive Cancer Center have demonstrated that selenium containing compounds are highly effective in preventing alopecia and severe bladder toxicity associated with cyclophosphamide as well as in preventing kidney toxi
creat↓, significant increase in creatinine and blood urea nitrogen (BUN) following treatment with cisplatin were restored to normal values in animals that were treated.
BUN↓,

4756- Se,    Selenium‐Containing Nanoparticles Combine the NK Cells Mediated Immunotherapy with Radiotherapy and Chemotherapy
ChemoSen↑, These results indicate that the selenium‐containing NPs would be a potential approach to achieve simultaneous treatments of immunotherapy, chemotherapy, and radiotherapy by a simple but effective method.
RadioS↓,

4757- Se,  Chemo,    The protective role of selenium on the toxicity of cisplatin-contained chemotherapy regimen in cancer patients
- Trial, NA, NA
Dose↝, The 400 μg per day of Se as Seleno-Kappacarrageenan were administered from 4 before to 4 d after chemotherapy for study cases.
*ALP↓, The urine enzymes NAG, GGT, AAP, and ALP after chemotherapy for cases were significantly lower than the controls.
chemoP↑, No toxicity of Seleno-Kappacarrageenan was noted. The above results suggest that the Se can be used as an agent for reducing the nephrotoxicity and bone marrow suppression induced by cisplatin.

4434- SNP,  Se,    Sodium Selenite Ameliorates Silver Nanoparticles Induced Vascular Endothelial Cytotoxic Injury by Antioxidative Properties and Suppressing Inflammation Through Activating the Nrf2 Signaling Pathway
- vitro+vivo, Nor, NA
*ROS↓, Se showed the capacity against AgNP with biological functions in guiding the intracellular reactive oxygen species (ROS) scavenging and meanwhile exhibiting anti-inflammation effects
*Inflam↓,
*NLRP3↓, Se supplementation decreased the intracellular ROS release and suppressed NOD-like receptor protein 3 (NLRP3) and nuclear factor kappa-B (NF-κB
*NF-kB↓,
*NRF2↑, by activating the Nrf2 and antioxidant enzyme (HO-1) signal pathway
*HO-1↑,
*toxicity↓, Several studies have reported that Se was capable of protection against the toxicity of heavy metals, including its role against AgNP-induced toxication.

3406- TQ,  Se,    A study to determine the effect of nano-selenium and thymoquinone on the Nrf2 gene expression in Alzheimer’s disease
- in-vivo, AD, NA
*NRF2↑, Nrf2 mean expression levels in the nano-selenium-treated rats, the thymoquinone-treated rats, and the rats that were given both treatments all increased significantly compared to AD rats with no treatment.
*GSH↑, TQ and SeNPs demonstrated improvement in the levels of different biomarkers (Nrf2, Aβ-42, TNF-α, GSH & MDA) reversing them toward the normal levels.
*MDA↓, the mean brain tissue MDA levels in groups 3, 4, and 5 (27.37 ± 9.42, 29.23 ± 12.18, and 23.28 ± 4.89 nmol/mg protein, respectively) were significantly lower than those in group 2
*TNF-α↓, mean serum levels of TNF-α in groups 3, 4, and 5 (63.03 ± 11.07, 66.05 ± 9.96, and 36.41 ± 10.53 pg/ml) were found to be considerably lower than those in group 2

4468- VitC,  Se,    Selenium modulates cancer cell response to pharmacologic ascorbate
- in-vivo, GBM, U87MG - in-vitro, CRC, HCT116
eff↓, In vivo, dietary selenium deficiency resulted in significant enhancement of ascorbate activity against glioblastoma xenografts
TumCD↑, pharmacologic ascorbate raises the serum ascorbate concentration into the millimolar range, a concentration at which ascorbate has been shown to kill cancer cells in vitro
ChemoSen↑, Pharmacologic ascorbate has been shown to synergize with multiple chemotherapeutic agents in animal models and is well-tolerated in human patients [1,4], motivating ongoing clinical trials.
ROS⇅, Indeed, the role of ascorbate as either a pro- or anti-oxidant has been suggested to depend on concentration, with low doses mitigating ROS and high doses generating them
DNAdam↑, H2O2 generation by ascorbate has been associated with DNA damage and subsequent PARP activation, which can deplete NAD and thereby inhibit glycolysis
PARP↑,
NAD↓,
Glycolysis↓,
Fenton↑, Ascorbate cytotoxicity depends on the intracellular labile iron pool (Fig 1a) [3,9]. One explanation for this phenomenon is that ascorbate-generated H2O2 causes toxicity through Fenton chemistry
lipid-P↑, extensive lipid peroxidation
eff↓, More generally, they establish dietary selenium depletion as a potential means of sensitizing tumors to free radical stress.
H2O2↑, High concentrations (mM) of ascorbate have been shown to generate H2O2 in vitro
other↝, Selenium supplementation has been shown to protect cells against iron-dependent cell death by supporting increased expression of selenoproteins, including GPX4, which defend against oxidative stress

609- VitC,  ALA,  VitK3,  Se,    Vitamin C and Cancer: Is There A Use For Oral Vitamin C?
OS↑,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 147

Results for Effect on Cancer/Diseased Cells:
ALAT↓,1,   ALP↓,1,   angioG↓,4,   AntiCan↑,14,   AntiCan∅,2,   antiOx↑,5,   AntiTum↑,7,   Apoptosis↑,18,   AST↓,1,   BAX↑,2,   BBB↑,1,   Bcl-2↓,3,   BIM↑,1,   BioAv↑,1,   BUN↓,1,   Ca+2↝,1,   Casp↑,4,   Casp3↑,3,   cl‑Casp3↑,1,   Casp9↑,4,   cl‑Casp9↑,1,   Catalase↓,2,   chemoP↑,19,   chemoP↝,1,   chemoP∅,1,   chemoR↓,1,   ChemoSen↓,1,   ChemoSen↑,16,   ChemoSen∅,1,   ChemoSideEff↓,2,   CHOP↑,1,   creat↓,1,   CSCs↓,1,   Cyt‑c↑,2,   DNAdam↑,7,   Dose?,1,   Dose↓,3,   Dose↑,6,   Dose⇅,1,   Dose↝,16,   Dose∅,3,   eff↓,6,   eff↑,30,   eff↝,7,   eff∅,3,   EPR↑,2,   ER Stress↑,3,   FADD↑,2,   Fas↑,2,   FasL↑,2,   Fenton↑,1,   Ferroptosis↑,3,   GADD34↑,1,   Glycolysis↓,1,   GPx↓,1,   GPx4↓,1,   GSH↓,3,   H2O2↑,3,   Hif1a↓,1,   HO-1↓,1,   IL2↑,1,   Imm↑,2,   INF-γ↑,1,   Inflam↓,1,   Iron↑,1,   LDH↓,1,   LDH↑,1,   lipid-P↑,3,   MAPK↑,1,   MDA↑,1,   MMP↓,10,   MMP2↓,2,   MMP9↓,2,   mtDam↑,1,   mTOR↑,1,   NA↑,2,   NAD↓,1,   NRF2↓,6,   NRF2↑,1,   NRF2↝,2,   OS↓,1,   OS↑,8,   other?,1,   other↝,9,   other∅,1,   p‑p38↑,1,   P53↑,3,   Pain↓,1,   PARP↑,1,   PARP↝,1,   PCNA↓,1,   pH∅,1,   e-pH↓,1,   Prx↓,1,   PrxI↓,1,   PUMA↑,1,   QoL↑,2,   RAD51↓,1,   radioP↑,8,   radioP↝,1,   RadioS↓,2,   RadioS↑,4,   RadioS∅,1,   RenoP↑,1,   Risk↓,38,   Risk↑,3,   Risk⇅,1,   Risk↝,2,   Risk∅,2,   ROS↑,26,   ROS⇅,2,   selectivity↓,2,   selectivity↑,22,   selenoP↓,1,   selenoP↑,3,   selm↑,1,   selm↝,1,   Sepsis↓,1,   SOD↓,2,   Th1 response↑,1,   Th2↑,1,   toxicity↓,3,   toxicity↝,2,   TrxR↓,1,   TrxR↑,1,   TumCCA↑,8,   TumCD↑,2,   TumCG↓,4,   TumCI↓,2,   TumCMig↓,1,   TumCP↓,4,   TumCP↑,1,   tumCV↓,5,   TumMeta↓,4,   TumVol↓,1,   VEGF↓,1,  
Total Targets: 136

Results for Effect on Normal Cells:
AChE↓,1,   Akt↑,1,   ALAT↓,7,   Albumin↑,1,   ALP↓,4,   AMPK↓,1,   AntiAg↑,1,   AntiAge↑,1,   AntiCan↑,1,   AntiDiabetic↑,1,   antiOx↓,1,   antiOx↑,23,   Apoptosis↓,1,   AST↓,6,   ATG3↓,1,   ATG5↓,1,   Aβ↓,1,   Bacteria↓,10,   BBB↑,1,   BChE↓,1,   Bcl-2↑,1,   BDNF↑,2,   Beclin-1↓,1,   BioAv↑,13,   BP↓,1,   BUN↓,1,   cardioP↑,3,   Catalase↑,6,   chemoP↑,1,   cognitive↑,2,   creat↓,1,   CRP↓,4,   DNAdam↓,8,   Dose?,1,   Dose↓,1,   Dose⇅,1,   Dose↝,28,   eff↑,17,   eff↝,2,   EMT↓,1,   Ferroptosis↓,2,   GADD45A↑,1,   glucose↓,1,   GPx↓,1,   GPx↑,15,   GPx1↑,3,   GPx4↑,3,   GR↑,1,   GSH↑,14,   GSTP1/GSTπ↓,1,   GSTs↑,1,   GutMicro↑,8,   H2O2↓,3,   Half-Life↓,1,   HDL↑,2,   hepatoP↑,9,   HO-1↑,2,   IFN-γ↓,1,   IGF-1↑,1,   IGFBP1↑,1,   IL1↓,1,   IL10↑,1,   IL1β↓,2,   IL2↓,1,   IL2↑,1,   IL4↑,1,   IL6↓,6,   Imm↑,3,   Inflam↓,21,   Keap1↓,1,   LC3s↓,1,   LDH↓,1,   LDL↓,2,   lipid-P?,1,   lipid-P↓,6,   MCP1↓,1,   MDA↓,6,   MDA↑,1,   memory↑,3,   mTOR↑,1,   neuroP↑,5,   NF-kB↓,4,   NLRP3↓,2,   NQO1↑,1,   NRF2↓,3,   NRF2↑,16,   other?,2,   other↓,4,   other↑,3,   other↝,12,   other∅,1,   p65↓,1,   Pain↓,1,   PI3K↑,1,   PPARγ↓,1,   Prx↑,1,   QoL↑,2,   radioP↑,7,   RadioS↑,1,   RenoP↑,3,   Risk↓,4,   Risk↝,1,   ROCK1↓,1,   ROS↓,28,   selenoP↑,20,   Sepsis↓,1,   SOD↑,11,   SOD2↓,1,   TAC↑,1,   TGF-β↓,1,   TNF-α↓,10,   toxicity↓,23,   toxicity↑,2,   toxicity↝,3,   toxicity∅,1,   TrkB↓,1,   TrkB↑,1,   Trx↑,1,   TrxR↑,1,   TrxR1↑,1,   VitC↑,1,   VitE↑,1,  
Total Targets: 122

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:149  Target#:%  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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