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| 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. |
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| TrxR is an enzyme that reduces Trx, allowing it to perform its reducing functions. It has been shown to have a role in cancer cell metabolism and survival. TrxR is overexpressed in various types of cancer, including breast, lung, colon, and prostate cancer. - Part of the thioredoxin system, which regulates reactive oxygen species (ROS). - TrxR is a major antioxidant systems that maintains the intracellular redox homeostasis. - Inhibition causes an increase in ROS. - TrxR is often upregulated in cancer cells to help manage increased oxidative stress, it is seen as a potential therapeutic target. Inhibiting TrxR may result in increased ROS in cancer cells, pushing them toward apoptosis. - TrxR is a selenoprotein—meaning it incorporates the trace element selenium in the form of the amino acid selenocysteine. TrxR inhibitors: -Piperlongumine -Withania somnifera (Ashwagandha) -Parthenolide -EGCG -Curcumin -Myricetin -Gambogic Acid |
| 1904- | GoldNP, | SNP, | Unveiling the Potential of Innovative Gold(I) and Silver(I) Selenourea Complexes as Anticancer Agents Targeting TrxR and Cellular Redox Homeostasis |
| - | in-vitro, | Lung, | H157 | - | in-vitro, | BC, | MCF-7 | - | in-vitro, | Colon, | HCT15 | - | in-vitro, | Melanoma, | A375 |
| 1907- | SNP, | GoldNP, | Cu, | In vitro antitumour activity of water soluble Cu(I), Ag(I) and Au(I) complexes supported by hydrophilic alkyl phosphine ligands |
| - | in-vitro, | Lung, | A549 | - | in-vitro, | BC, | MCF-7 | - | in-vitro, | Melanoma, | A375 | - | in-vitro, | Colon, | HCT15 | - | in-vitro, | Cerv, | HeLa |
| 1908- | SNP, | Exposure to Silver Nanoparticles Inhibits Selenoprotein Synthesis and the Activity of Thioredoxin Reductase |
| - | in-vitro, | Lung, | A549 |
| 1909- | SNP, | The Antibacterial Drug Candidate SBC3 is a Potent Inhibitor of Bacterial Thioredoxin Reductase |
| - | in-vivo, | Nor, | NA |
| 1903- | SNP, | Novel Silver Complexes Based on Phosphanes and Ester Derivatives of Bis(pyrazol-1-yl)acetate Ligands Targeting TrxR: New Promising Chemotherapeutic Tools Relevant to SCLC Managemen |
| - | in-vitro, | Lung, | U1285 |
| 1906- | SNP, | GoldNP, | Cu, | Current Progresses in Metal-based Anticancer Complexes as Mammalian TrxR Inhibitors |
| - | Review, | Var, | NA |
| 1902- | SNP, | Modulation of the mechanism of action of antibacterial silver N-heterocyclic carbene complexes by variation of the halide ligand |
| - | in-vitro, | NA, | NA |
| 1905- | SNP, | Evaluation of the effect of silver and silver nanoparticles on the function of selenoproteins using an in-vitro model of the fish intestine: The cell line RTgutGC |
| - | in-vivo, | Nor, | NA |
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