Database Query Results : Selenium, , radioP

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)


radioP, RadioProtective: Click to Expand ⟱
Source:
Type:
Protect against the damaging effects of radiation therapy.
Scientific Papers found: Click to Expand⟱
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.

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.

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.

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


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 1,   NRF2↓, 1,   TrxR↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↑, 1,   eff↝, 1,   RadioS↑, 1,   selectivity↑, 2,  

Functional Outcomes ⓘ

chemoP↑, 2,   radioP↑, 3,  
Total Targets: 11

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   GPx↑, 2,   GPx1↑, 1,   GPx4↑, 1,   GSH↑, 2,   lipid-P↓, 1,   NRF2↑, 1,   ROS↓, 2,   selenoP↑, 2,  

DNA Damage & Repair ⓘ

DNAdam↓, 2,  

Drug Metabolism & Resistance ⓘ

Dose↝, 1,  

Functional Outcomes ⓘ

radioP↑, 2,  
Total Targets: 12

Scientific Paper Hit Count for: radioP, RadioProtective
5 Selenium
3 Radiotherapy/Radiation
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

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:149  Target#:1185  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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