Database Query Results : Selenium, ,

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

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

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

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

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

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

Other common form is Selenomethionine, as it is better absorbed (found in brazil nuts), but might be less effective?
| Category                             | Role in cancer                                                                                  |
| -------------------------------- | ----------------------------------------------------------------------------------------------- |
| Sodium Selenium (selenite)       | Direct cytotoxic redox poison                                                                   |
| Selenium (organic / nutritional) | **Redox buffer & immune modulator** (generally *anti-therapy* when oxidative stress is desired) |
| SeNPs                            | Tunable redox-signaling anticancer platform                                                     |

Selenium (Organic / Nutritional) — Cancer-Relevant Pathways
Rank Pathway / Target Axis Direction Primary Effect Notes / Cancer Relevance Ref
1 Selenoprotein antioxidant systems (GPX1–4, TXNRD) ↑ antioxidant capacity ROS buffering Dietary selenium increases glutathione peroxidase and thioredoxin reductase activity, lowering oxidative stress (ref)
2 Glutathione redox cycling (GSH/GSSG) ↑ GSH recycling Redox homeostasis Selenium supports GPX-mediated peroxide detoxification and preserves cellular GSH pools (ref)
3 Ferroptosis suppression (GPX4 axis) ↓ ferroptosis susceptibility Lipid peroxide detoxification GPX4 is a selenoprotein; adequate selenium suppresses lipid peroxidation and ferroptotic death (ref)
4 NRF2 antioxidant response ↔ / ↑ (supportive) Stress adaptation Selenium status influences NRF2 target gene expression indirectly via redox tone (ref)
5 DNA damage prevention / repair environment ↓ oxidative DNA damage Genomic stability Selenium sufficiency reduces oxidative DNA lesions and supports repair capacity (ref)
6 p53 redox regulation ↔ stabilized (context-dependent) Checkpoint fidelity Redox balance maintained by selenium supports normal p53 signaling rather than triggering apoptosis (ref)
7 NF-κB inflammatory signaling ↓ chronic activation Anti-inflammatory bias Selenium supplementation suppresses NF-κB activation under inflammatory/oxidative conditions (ref)
8 Immune competence (T-cell, NK-cell function) ↑ immune function Improved immune surveillance Selenium supports cytotoxic lymphocyte activity and cytokine balance (ref)
9 Angiogenesis signaling (VEGF) ↔ / mild ↓ Vascular normalization Nutritional selenium does not strongly inhibit angiogenesis but may modestly reduce VEGF under stress (ref)
10 PI3K–AKT survival signaling ↔ (homeostatic) Cell survival maintenance Unlike selenite or SeNPs, organic selenium does not directly suppress PI3K–AKT at nutritional doses (ref)
11 Autophagy (baseline maintenance) ↔ Cellular homeostasis Selenium supports basal autophagy via redox balance but does not drive cytotoxic autophagy (ref)
12 Cancer risk modulation (epidemiologic) ↓ risk in deficient populations Prevention (not treatment) Protective effects are context-dependent; excess selenium may be neutral or adverse in replete populations (ref)


Scientific Papers found: Click to Expand⟱
4746- antiOx,  Chemo,  VitA,RetA,  VitC,  Se  Using Supplements During Chemo: Yes or No?
- Review, Var, NA
eff↓, Taking antioxidants in supplement form (again, remember that antioxidants in food are fine) may actually “protect” cancer cells during treatment.
ChemoSen↓, In other words, antioxidants in pill form have the potential to counteract the effects of chemotherapy or radiation therapy.
RadioS↓,
other↝, Common antioxidant supplements taken by patients include vitamins A, C, and E, carotenoids (such as beta-carotene and lycopene) as well as selenium and Coenzyme Q10.

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

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].

72- QC,  Se,    Selenium- or quercetin-induced retardation of DNA synthesis in primary prostate cells occurs in the presence of a concomitant reduction in androgen-receptor activity
- in-vitro, Pca, PECs - in-vitro, Pca, LNCaP - in-vitro, Pca, NIH-3T3
AR↓, In LNCaP cells transfected with an androgen-receptor (AR)-reporter gene coupled to luciferase, selenomethionine or quercetin reduced AR activity

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

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

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.

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.

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

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.

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

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

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

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

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

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

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

4714- Se,  SSE,  SeNPs,    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↑,

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

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.

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

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

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

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

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↑,

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

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

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

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

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

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

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.

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.

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

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

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.

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

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↓,

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

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)

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.

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

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.

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.

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.

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.

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

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.

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.

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

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)

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;

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↑,

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

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↓,

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
chemoPv↑,
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↑,

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↑,

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

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.

5089- SSE,  Se,    Redox-mediated effects of selenium on apoptosis and cell cycle in the LNCaP human prostate cancer cell line
- in-vitro, Pca, LNCaP
ROS↑, Our results demonstrated that oxidative stress was induced by sodium selenite at high concentrations in both acute and chronic treatments, but outcomes were different.
mtDam↑, After acute exposure to selenite, cells exhibited mitochondrial injury and cell death, mainly apoptosis.
TumCD↑,
Apoptosis↑,
TumCCA↑, After chronic exposure to selenite, cells showed growth inhibition caused by cell cycle arrest, increased numbers of mitochondria and levels of mitochondrial enzymes, and only minimal induction of apoptosis
Trx↓, production of ROS, regulation of the Trx redox system, regulation of the cell cycle, and inhibition of angiogenes
angioG↓,
GSH⇅, intracellular levels of GSH were increased at doses of 0.5 and 1.5 uM selenite and decreased at doses of 2 and 2.5 uM selenite
NADPH↓, In addition, GSH and NADPH are consumed
GPx↑, GPX activities in the selenite-adapted cells were significantly increased (2- to 3-fold induction

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: 64

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   Catalase↓, 1,   Ferroptosis↑, 1,   GPx↑, 1,   GSH↓, 2,   GSH⇅, 1,   H2O2↑, 2,   HO-1↓, 1,   lipid-P↑, 1,   NRF2↓, 3,   NRF2↑, 1,   NRF2↝, 2,   Prx↓, 1,   ROS↑, 8,   ROS⇅, 1,   selenoP↓, 1,   selenoP↑, 2,   SOD↓, 1,   Trx↓, 1,   TrxR↓, 1,   TrxR↑, 1,  

Metal & Cofactor Biology ⓘ

selm↑, 1,   selm↝, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 4,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   BUN↓, 1,   LDH↓, 1,   NADPH↓, 1,  

Cell Death ⓘ

Apoptosis↑, 8,   BAX↑, 2,   Bcl-2↓, 2,   Casp↑, 2,   Casp3↑, 1,   cl‑Casp3↑, 1,   Casp9↑, 1,   cl‑Casp9↑, 1,   Cyt‑c↑, 1,   FADD↑, 2,   Fas↑, 2,   FasL↑, 2,   Ferroptosis↑, 1,   MAPK↑, 1,   p‑p38↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

other↝, 6,   other∅, 1,   tumCV↓, 3,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 1,   RAD51↓, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 1,  

Migration ⓘ

TumCP↓, 2,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,  

Immune & Inflammatory Signaling ⓘ

Imm↑, 1,  

Cellular Microenvironment ⓘ

pH∅, 1,   e-pH↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↓, 1,   ChemoSen↑, 3,   ChemoSen∅, 1,   Dose↓, 3,   Dose↑, 2,   Dose↝, 10,   Dose∅, 2,   eff↓, 3,   eff↑, 10,   eff↝, 6,   eff∅, 1,   RadioS↓, 1,   RadioS↑, 1,   selectivity↑, 5,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   ALP↓, 1,   AR↓, 1,   AST↓, 1,   creat↓, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 4,   AntiTum↑, 1,   chemoP↑, 9,   chemoPv↑, 1,   OS↑, 7,   Pain↓, 1,   QoL↑, 1,   radioP↑, 3,   Risk↓, 21,   Risk↑, 1,   Risk↝, 2,   Risk∅, 1,   toxicity↓, 1,   TumVol↓, 1,  
Total Targets: 94

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 6,   Catalase↑, 1,   GPx↑, 5,   GPx1↑, 2,   GPx4↑, 1,   GSH↑, 7,   GSTP1/GSTπ↓, 1,   H2O2↓, 1,   HDL↑, 1,   Keap1↓, 1,   lipid-P↓, 2,   MDA↓, 1,   MDA↑, 1,   NQO1↑, 1,   NRF2↓, 2,   NRF2↑, 7,   Prx↑, 1,   ROS↓, 6,   selenoP↑, 4,   SOD↑, 3,   SOD2↓, 1,   TrxR↑, 1,   TrxR1↑, 1,   VitC↑, 1,   VitE↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   LDL↓, 1,   PPARγ↓, 1,  

Transcription & Epigenetics ⓘ

other?, 2,   other↑, 2,   other↝, 1,   other∅, 1,  

Autophagy & Lysosomes ⓘ

ATG5↓, 1,   Beclin-1↓, 1,   LC3s↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 3,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   IGF-1↑, 1,   IGFBP1↑, 1,   mTOR↑, 1,  

Migration ⓘ

TGF-β↓, 1,  

Immune & Inflammatory Signaling ⓘ

IFN-γ↓, 1,   IL10↑, 1,   IL1β↓, 1,   IL2↓, 1,   IL2↑, 1,   IL4↑, 1,   IL6↓, 2,   Inflam↓, 2,   NF-kB↓, 1,   TNF-α↓, 4,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,   BChE↓, 1,   BDNF↑, 1,   TrkB↑, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Hormonal & Nuclear Receptors ⓘ

GR↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 2,   Dose↝, 3,   eff↑, 2,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   ALP↓, 2,   AST↓, 1,   BP↓, 1,   IL6↓, 2,  

Functional Outcomes ⓘ

AntiAge↑, 1,   cardioP↑, 2,   chemoP↑, 1,   cognitive↑, 1,   hepatoP↑, 2,   memory↑, 2,   neuroP↑, 1,   QoL↑, 1,   radioP↑, 2,   RenoP↑, 1,   Risk↓, 1,   Risk↝, 1,   toxicity↓, 3,   toxicity↑, 1,   toxicity↝, 1,  
Total Targets: 80

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

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