| 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: |
| Silver NanoParticles Summary: 1. Smaller sizes desirable due to greater surface area, and cell penetration (enhanced permeability and retention (EPR) effect) 2. Two main types: AgNP and silver ions (big debate on uses: Ag+ turning to AgCl in stomach but AgCl also effective. Take sodium-bicarbonate? 3. Dose example 80kg person: 1.12-2mg/day, which can be calculated based on ppm and volume taken (see below) target < 10ppm and 120mL per day (30ppm and 1L per day caused argyria 30mg/day ) (Case Report: 9‐15 ppm@120mL, i.e. 1.1mg/L to 1.8mg/L per day) Likely 10ppm --> 10mg/L, hence if take 100mL, then 1mg/day? (for Cancer) The current Rfd for oral silver exposure is 5 ug/kg/d with a critical dose estimated at 14 ug/kg/d for the average person. Seems like the Cancer target range is 14ug/kg/day to 25ug/kg/day. 80Kg example: 1.12mg to 2mg “1.4µg/kg body weight. If I would have 70kg, I would want to use 100µg/day. However, for fighting active disease, I would tend to explore higher daily dose, as I think this may be too low.” 4. AntiOxidants/NAC can counter act the effect of Silver NanoParticles from producing reactive oxygen species (ROS) and mitochondrial damage . NAC is a supplement form of cysteine, an amino acid that helps make glutathione, a powerful antioxidant. 5. In vitro most reports indicate AgNPs increase ROS in both cancer and normal cell (but in vivo improved antioxidant system of normal may create selectivity) 6. Pathways/mechanisms of action/: -” intracellular ROS was increased...reduction in levels of glutathione (GSH)” -”AgNPs affect the function of the vascular endothelial growth factor (VEGF)” (likely reducing levels) -”expression of BAX and BCL2 genes was increased” -”upregulation of proapoptotic genes (p53, p21, Bax, and caspases) and downregulation of antiapoptotic genes (Bcl-2)” -” upregulation of AMPK and downregulation of mTOR, MMP-9, BCL-2, and α-SMA” -”p53 is a key player...proapoptotic genes p53 and Bax were significantly increased... noticeable reduction in Bcl-2 transcript levels” -” p53 participates directly in the intrinsic apoptosis pathway by regulating the mitochondrial outer membrane permeabilization” - “Proapoptotic markers (BAX/BCL-XL, cleaved poly(ADP-ribose) polymerase, p53, p21, and caspases 3, 8 and 9) increased.” -”The antiapoptotic markers, AKT and NF-kB, decreased in AgNP-treated cells.” Silver NanoParticles and Magnetic Fields Summary: 1. “exposure to PMF increased the ability of AgNPs uptake” 2. 6x improvement from AgNPs alone could glucose capping of SilverNPs work as trojan horse? Sodium selenite might protect against toxicity of AgNPs in normal cells. -uncoated AgNPs can degrade the gut microbiome. PVP, citrate, green-synthesized, chitosan coating, may reduce the effect. Also may be true for Selenium(Sodium selenite) becuase of antioxidant properties, slowing oxidation of Ag0 to Ag+. co-ingestion with food (higher pH) favors reduction and lower Ag+ levels. -action mechanisms of AgNPs: the release of silver ions (Ag+), generation of reactive oxygen species (ROS), destruction of membrane structure. |
| 4440- | Se, | SNP, | Selenium, silver, and gold nanoparticles: Emerging strategies for hepatic oxidative stress and inflammation reduction |
| - | Review, | NA, | NA |
| 4601- | Se, | SNP, | Antioxidant and hepatoprotective role of selenium against silver nanoparticles |
| - | in-vivo, | Nor, | NA |
| 4602- | Se, | SNP, | GoldNP, | Advances in nephroprotection: the therapeutic role of selenium, silver, and gold nanoparticles in renal health |
| - | NA, | Nor, | NA |
| 4604- | Se, | SNP, | Chit, | The ameliorative effect of selenium-loaded chitosan nanoparticles against silver nanoparticles-induced ovarian toxicity in female albino rats |
| - | in-vivo, | Nor, | NA |
| 4607- | Se, | SNP, | A Review on synthesis and their antibacterial activity of Silver and Selenium nanoparticles against biofilm forming Staphylococcus aureus |
| - | Review, | NA, | NA |
| - | vitro+vivo, | Nor, | NA |
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