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

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.

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.

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
"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⟱
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].

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.

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

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.

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.

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↝,

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,

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

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.

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

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.

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↓,

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

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

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%

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.

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

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

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↑,

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↑,

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↓,

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

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)

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.

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.

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

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.

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

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

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

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

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

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↓,

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.

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↓,

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↑,

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

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;

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↑,

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)

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: 85

Results for Effect on Cancer/Diseased Cells:
ALAT↓,1,   ALP↓,1,   angioG↓,2,   AntiCan↑,10,   AntiCan∅,2,   antiOx↑,5,   AntiTum↑,3,   Apoptosis↑,13,   AST↓,1,   BAX↑,2,   BBB↑,1,   Bcl-2↓,3,   BIM↑,1,   Ca+2↝,1,   Casp↑,1,   Casp3↑,3,   cl‑Casp3↑,1,   Casp9↑,4,   cl‑Casp9↑,1,   Catalase↓,1,   chemoP↑,3,   ChemoSen↑,7,   ChemoSideEff↓,2,   CHOP↑,1,   Cyt‑c↑,2,   DNAdam↑,4,   Dose?,1,   Dose↓,3,   Dose↑,3,   Dose↝,10,   Dose∅,3,   eff↓,4,   eff↑,22,   eff↝,1,   eff∅,2,   EPR↑,2,   ER Stress↑,1,   FADD↑,2,   Fas↑,2,   FasL↑,2,   Fenton↑,1,   GADD34↑,1,   Glycolysis↓,1,   GSH↓,2,   H2O2↑,3,   Hif1a↓,1,   IL2↑,1,   Imm↑,1,   INF-γ↑,1,   LDH↓,1,   LDH↑,1,   lipid-P↑,1,   MMP↓,7,   MMP2↓,1,   MMP9↓,1,   mtDam↑,1,   NA↑,2,   NAD↓,1,   NRF2↓,1,   OS↓,1,   OS↑,7,   other?,1,   other↝,3,   other∅,1,   P53↑,1,   PARP↑,1,   PARP↝,1,   PCNA↓,1,   PrxI↓,1,   PUMA↑,1,   RadioS↑,3,   RenoP↑,1,   Risk↓,22,   Risk↑,3,   Risk↝,2,   Risk∅,2,   ROS↑,12,   ROS⇅,2,   selectivity↓,2,   selectivity↑,15,   selenoP↓,1,   selenoP↑,1,   selm↑,1,   selm↝,1,   SOD↓,1,   Th1 response↑,1,   Th2↑,1,   toxicity↓,1,   toxicity↝,1,   TrxR↓,1,   TumCCA↑,6,   TumCD↑,1,   TumCG↓,3,   TumCI↓,1,   TumCMig↓,1,   TumCP↓,1,   tumCV↓,4,   TumMeta↓,2,   VEGF↓,1,  
Total Targets: 99

Results for Effect on Normal Cells:
AChE↓,1,   Akt↑,1,   ALAT↓,6,   Albumin↑,1,   ALP↓,3,   AntiAge↑,1,   AntiCan↑,1,   antiOx↑,13,   AST↓,5,   Bacteria↓,6,   BBB↑,1,   BChE↓,1,   BDNF↑,2,   BioAv↑,8,   BP↓,1,   cardioP↑,2,   Catalase↑,3,   cognitive↑,2,   creat↓,1,   CRP↓,2,   DNAdam↓,2,   Dose?,1,   Dose⇅,1,   Dose↝,15,   eff↑,8,   eff↝,1,   EMT↓,1,   GADD45A↑,1,   glucose↓,1,   GPx↓,1,   GPx↑,10,   GR↑,1,   GSH↑,6,   GutMicro↑,6,   HDL↑,2,   hepatoP↑,7,   HO-1↑,1,   IFN-γ↓,1,   IGF-1↑,1,   IGFBP1↑,1,   IL1↓,1,   IL10↑,1,   IL1β↓,2,   IL2↓,1,   IL2↑,1,   IL4↑,1,   IL6↓,5,   Imm↑,1,   Inflam↓,12,   Keap1↓,1,   LDH↓,1,   LDL↓,2,   lipid-P?,1,   lipid-P↓,3,   MCP1↓,1,   MDA↓,4,   memory↑,3,   neuroP↑,3,   NF-kB↓,4,   NLRP3↓,1,   NRF2↑,4,   other↓,1,   other↑,2,   other↝,7,   other∅,1,   p65↓,1,   PI3K↑,1,   PPARγ↓,1,   QoL↑,1,   RenoP↑,2,   Risk↓,4,   Risk↝,1,   ROS↓,17,   selenoP↑,8,   SOD↑,7,   TGF-β↓,1,   TNF-α↓,8,   toxicity↓,13,   toxicity↑,2,   toxicity↝,1,   TrkB↓,1,   TrkB↑,1,   TrxR↑,1,   VitC↑,1,   VitE↑,1,  
Total Targets: 85

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