| 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. also here In the chemical synthesis of selenium nanoparticles, a precursor such as sodium selenite (Na₂SeO₃) is dissolved in water to form a homogenous solution. A reducing agent, like ascorbic acid or sodium borohydride (NaBH₄), is then added to the solution. The reducing agent donates electrons to the selenium ions (SeO32−SeO32), reducing them to elemental selenium (Se0Se^0). This reduction process leads to the nucleation of selenium atoms, which subsequently grow into nanoparticles through controlled aggregation. Se NPs might be hepatoprotective. (chemoprotective) (radioprotective) (radiosensitizer)
Selenium nanoparticles (SeNPs) are a biocompatible, less-toxic,
and more controllable form of selenium compared to inorganic salts (like sodium selenite).
Major SeNPs hepatoprotective mechanisms
Mechanism Description Key markers affected
1. Antioxidant activity SeNPs boost antioxidant enzyme ↓ ROS, ↓ MDA, ↑ GSH, ↑ GPx
systems (GPx, SOD, CAT) and scavenge
ROS directly.
2. Anti-inflammatory effect Downregulate NF-κB, TNF-α, ↓ TNF-α, ↓ IL-1β, ↓ IL-6
IL-6, and COX-2 pathways.
3. Anti-apoptotic action Balance between Bcl-2/Bax and reduce ↑ Bcl-2, ↓ Bax, ↓ Caspase-3
caspase-3 activation in hepatocytes.
4. Metal/toxin chelation SeNPs can bind or transform toxic ↓ liver metal accumulation
metals (Cd²⁺, Hg²⁺, As³⁺)
into less harmful complexes.
5. Mitochondrial protection Maintain membrane potential, Preserved ΔΨm, ↑ ATP
prevent mitochondrial ROS burst,
and ATP loss.
6. Regeneration support Stimulate hepatocyte proliferation ↑ PCNA, improved histology
and repair via redox signaling
and selenoproteins.
Comparison: SeNPs vs. Sodium Selenite
Property SeNPs Sodium Selenite
Toxicity Low Moderate–high
Bioavailability Controlled, often slow- Rapid, less controllable
release
ROS balance Adaptive, mild antioxidant Can flip to pro-oxidant easily
Safety margin Wide Narrow
Hepatoprotection Strong, sustained Protective at low dose,
toxic at high dose
"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." |
| Features: |
| High-dose vitamin C: Some studies have suggested that high-dose vitamin C may be effective in treating certain types of cancer, such as ovarian cancer and pancreatic cancer. Symptoms of vitamin C deficiency include fatigue, weakness, poor wound healing, ecchymoses, xerosis, lower extremity edema, and musculoskeletal pain—most of them are often observed in end-stage cancer patients. -Vitamin C is an essential nutrient involved in the repair of tissue, the formation of collagen, and the enzymatic production of certain neurotransmitters. It is required for the functioning of several enzymes and is important for immune system function. -Ascorbic Acid, Different levels in different Organs Homeostasis ranging from about 0.2 mM in the muscle and heart, and up to 10 mM in the brain and adrenal gland. -(Note the Oncomagnetic success in the brain also was then under conditions of high Vitamin C) -Ascorbic acid is an electron donor Ascorbic Acid, can be a Pro-oxidant "The pro-oxidative activity of ascorbic acid (Figure 2) is associated with the interaction with transition metal ions (especially iron and copper). Under conditions of high, millimolar ascorbate concentration, vitamin C catalyzes the reduction of free transition metal ions, which causes the formation of oxygen radicals." Ascorbic Acid, formation of H2O2 (Hydrogen Peroxide) Many studies indicate the toxicity of ascorbate to cancer cells. Much evidence indicates that the underlying phenomenon is the pro-oxidative activity of ascorbate, which induces the formation of H2O2 and oxidative stress. "ascorbate at concentrations achieved only by i.v. administration may be a pro-drug for formation of H(2)O(2)" -High dose VitC therapy may not be for those with kidney problems -Oral supplement up to 10g/day? -Direct regulator of TET↑ -caution for (G6PD-) deficient patients receiving vitamin C infusions -Note plasma half-life 30mins to 1hr, 1.5-2hr elimination half-life. oral BioAv water soluble, but has limitiations as 100mg yeilds 60uM/L in plasma, but 1000mg only yeilds 85uM/L. mM concentration are required for effectiveness on cancer cells. Hence why IV administration is common. Boosting HIF increases the intracellular uptake of oxidized VitC Pathways: - high dose induces ROS production in cancer cells. Otherwise well known antioxidant in normal cells. - ROS↑ related: MMP↓(ΔΨm), ER Stress↑, Caspases↑, DNA damage↑, cl-PARP↑, - Lowers AntiOxidant defense in Cancer Cells: NRF2↓, TrxR↓**, SOD↓, GSH↓ Catalase↓ HO1↓ GPx↓ - Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑, - lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓ - inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, TIMP2, IGF-1↓, VEGF↓, NF-κB↓, - reactivate genes thereby inhibiting cancer cell growth : P53↑, TET↑ - cause Cell cycle arrest : TumCCA↑, cyclin D1↓, CDK2↓, - inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, ERK↓, EMT↓, TET1↓, - inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, ECAR↓, GRP78↑, Glucose↓, GlucoseCon↓ - inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, - Others: PI3K↓, AKT↓, STAT↓, AMPK, ERK↓, JNK, - Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Hepatoprotective, - Selectivity: Cancer Cells vs Normal Cells Selenium supplementation may protect cells against iron-dependent cell death by supporting increased expression of selenoproteins, including GPX4, which defend against oxidative stress. Meaning it may decrease effectiveness of high dose VitC.(#4468) |
| 4459- | Se, | VitC, | Nano and mesosized selenium and its synthesis using the ascorbic acid route |
| 4460- | Se, | VitC, | Ascorbic acid-mediated selenium nanoparticles as potential antihyperuricemic, antioxidant, anticoagulant, and thrombolytic agents |
| 4461- | Se, | VitC, | Synthesis, Characterization, and Cytotoxic Evaluation of Selenium Nanoparticles |
| 4462- | Se, | VitC, | Selenium nanoparticles: influence of reducing agents on particle stability and antibacterial activity at biogenic concentrations |
| - | Study, | Nor, | NA |
| 4463- | Se, | VitC, | Selenium nanoparticles: Synthesis, characterization and study of their cytotoxicity, antioxidant and antibacterial activity |
| - | Study, | Nor, | NA |
| 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 |
| 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 |
| 4491- | Se, | Chit, | VitC, | Synthesis of a Bioactive Composition of Chitosan–Selenium Nanoparticles |
| - | Study, | NA, | NA |
| 4606- | Se, | VitC, | Antibacterial and anti-biofilm efficacy of selenium nanoparticles against Pseudomonas aeruginosa: Characterization and in vitro analysis |
| - | in-vitro, | NA, | NA |
| 609- | VitC, | ALA, | VitK3, | Se, | Vitamin C and Cancer: Is There A Use For Oral Vitamin C? |
| 4468- | VitC, | Se, | Selenium modulates cancer cell response to pharmacologic ascorbate |
| - | in-vivo, | GBM, | U87MG | - | in-vitro, | CRC, | HCT116 |
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