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| 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
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| Glutathione (GSH) is a thiol antioxidant that scavenges reactive oxygen species (ROS), resulting in the formation of oxidized glutathione (GSSG). Decreased amounts of GSH and a decreased GSH/GSSG ratio in tissues are biomarkers of oxidative stress. Glutathione is a powerful antioxidant found in every cell of the body, composed of three amino acids: cysteine, glutamine, and glycine. It plays a crucial role in protecting cells from oxidative stress, detoxifying harmful substances, and supporting the immune system. cancer cells can have elevated levels of glutathione, which may help them survive in the oxidative environment created by the immune response and chemotherapy. This can make cancer cells more resistant to treatment. While glutathione can be obtained from certain foods (like fruits, vegetables, and meats), its absorption from supplements is debated. Some people take N-acetylcysteine (NAC) or other precursors to boost glutathione levels, but the effects on cancer prevention or treatment are still being studied. Depleting glutathione (GSH) to raise reactive oxygen species (ROS) is a strategy that has been explored in cancer research and therapy. Many cancer cells have altered redox states and may rely on GSH to survive. Increasing ROS levels can induce stress in these cells, potentially leading to cell death. Certain drugs and compounds can deplete GSH levels. For example, agents like buthionine sulfoximine (BSO) inhibit the synthesis of GSH, leading to its depletion. Cancer cells tend to exhibit higher levels of intracellular GSH, possibly as an adaptive response to a higher metabolism and thus higher steady-state levels of reactive oxygen species (ROS). "...intracellular glutathione (GSH) exhibits an astounding antioxidant activity in scavenging reactive oxygen species (ROS)..." "Cancer cells have a high level of GSH compared to normal cells." "...cancer cells are affluent with high antioxidant levels, especially with GSH, whose appearance at an elevated concentration of ∼10 mM (10 times less in normal cells) detoxifies the cancer cells." "Therefore, GSH depletion can be assumed to be the key strategy to amplify the oxidative stress in cancer cells, enhancing the destruction of cancer cells by fruitful cancer therapy." The loss of GSH is broadly known to be directly related to the apoptosis progression. |
| 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 |
| 4715- | Se, | The Interaction of Selenium with Chemotherapy and Radiation on Normal and Malignant Human Mononuclear Blood Cells |
| 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 |
| 4615- | Se, | Rad, | Selenium as an adjuvant for modification of radiation response |
| - | Review, | Nor, | NA |
| 4711- | Se, | Association of selenium status and blood glutathione concentrations in blacks and whites |
| - | Human, | Nor, | NA |
| 4749- | Se, | Chemo, | antiOx, | Selenium as an element in the treatment of ovarian cancer in women receiving chemotherapy |
| - | Trial, | Ovarian, | NA |
| 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 |
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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