Database Query Results : Selenium, , ROS

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."
ROS, Reactive Oxygen Species: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Melavonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day
-Dipyridamole typically 200mg 2x/day
-Lycopene typically 100mg/day range

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy

Scientific Papers found: Click to Expand⟱
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].

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

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.

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.

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.

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.

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

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.

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.

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

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.

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,

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↑,

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.

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.

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↓,

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↑,

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.

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↓,

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

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

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

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

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.

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.

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

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.

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


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 52

Results for Effect on Cancer/Diseased Cells:
angioG↓,3,   AntiCan↑,8,   antiOx↑,3,   AntiTum↑,4,   Apoptosis↑,11,   BAX↑,2,   BBB↑,1,   Bcl-2↓,3,   BioAv↑,1,   Casp↑,2,   Casp3↑,2,   cl‑Casp3↑,1,   Casp9↑,4,   cl‑Casp9↑,1,   Catalase↓,1,   chemoP↑,5,   ChemoSen↑,5,   CSCs↓,1,   Cyt‑c↑,2,   DNAdam↑,6,   Dose↑,2,   Dose⇅,1,   Dose↝,4,   eff↓,2,   eff↑,15,   eff↝,2,   eff∅,1,   EPR↑,1,   ER Stress↑,3,   FADD↑,1,   Fas↑,1,   FasL↑,1,   Fenton↑,1,   Ferroptosis↑,2,   Glycolysis↓,1,   GPx↓,1,   GPx4↓,1,   GSH↓,2,   H2O2↑,3,   Imm↑,2,   Inflam↓,1,   Iron↑,1,   LDH↑,1,   lipid-P↑,2,   MDA↑,1,   MMP↓,10,   MMP2↓,1,   MMP9↓,1,   mtDam↑,1,   NA↑,2,   NAD↓,1,   NRF2↓,1,   OS↑,2,   other↝,4,   P53↑,2,   PARP↑,1,   PCNA↓,1,   QoL↑,1,   radioP↑,3,   RadioS↑,2,   RenoP↑,1,   Risk↓,13,   ROS↑,26,   ROS⇅,2,   selectivity↓,2,   selectivity↑,14,   selenoP↑,2,   Sepsis↓,1,   SOD↓,1,   toxicity↓,1,   toxicity↝,1,   TrxR↓,1,   TrxR↑,1,   TumCCA↑,5,   TumCD↑,1,   TumCG↓,2,   TumCI↓,1,   TumCP↓,4,   TumCP↑,1,   tumCV↓,3,   TumMeta↓,4,  
Total Targets: 81

Results for Effect on Normal Cells:
ALAT↓,4,   Albumin↑,1,   ALP↓,2,   AMPK↓,1,   AntiAg↑,1,   AntiAge↑,1,   AntiCan↑,1,   AntiDiabetic↑,1,   antiOx↓,1,   antiOx↑,14,   AST↓,3,   ATG3↓,1,   ATG5↓,1,   Aβ↓,1,   Bacteria↓,7,   Bcl-2↑,1,   Beclin-1↓,1,   BioAv↑,10,   BP↓,1,   cardioP↑,2,   Catalase↑,4,   creat↓,1,   CRP↓,3,   DNAdam↓,5,   Dose⇅,1,   Dose↝,13,   eff↑,11,   eff↝,1,   EMT↓,1,   glucose↓,1,   GPx↓,1,   GPx↑,10,   GPx1↑,2,   GPx4↑,1,   GSH↑,5,   GSTs↑,1,   GutMicro↑,5,   H2O2↓,2,   Half-Life↓,1,   HDL↑,2,   hepatoP↑,6,   HO-1↑,2,   IGF-1↑,1,   IGFBP1↑,1,   IL1↓,1,   IL1β↓,1,   IL2↑,1,   IL4↑,1,   IL6↓,4,   Imm↑,3,   Inflam↓,17,   LC3s↓,1,   LDL↓,2,   lipid-P↓,5,   MCP1↓,1,   MDA↓,4,   memory↑,1,   mTOR↑,1,   neuroP↑,3,   NF-kB↓,3,   NLRP3↓,1,   NQO1↑,1,   NRF2↓,1,   NRF2↑,3,   other↓,3,   other↑,1,   other↝,6,   other∅,1,   p65↓,1,   Pain↓,1,   QoL↑,2,   radioP↑,4,   RenoP↑,3,   Risk↓,3,   ROS↓,28,   selenoP↑,16,   Sepsis↓,1,   SOD↑,7,   TGF-β↓,1,   TNF-α↓,6,   toxicity↓,16,   toxicity↑,1,   toxicity↝,1,   toxicity∅,1,   TrxR↑,1,  
Total Targets: 85

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
52 Selenium
6 chitosan
4 Radiotherapy/Radiation
4 Silver-NanoParticles
2 Vitamin C (Ascorbic Acid)
2 Chemotherapy
1 Chrysin
1 Coenzyme Q10
1 EGCG (Epigallocatechin Gallate)
1 Gold NanoParticles
1 polyethylene glycol
1 Date Fruit Extract
1 Curcumin
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:149  Target#:275  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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