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| Silver NanoParticles (AgNPs) Summary: 1.Smaller sizes are generally more bioactive due to increased surface area and enhanced tumor accumulation via the enhanced permeability and retention (EPR) effect. 2.Two relevant forms: particulate silver (AgNPs) and ionic silver (Ag⁺). There is debate regarding oral use, as Ag⁺ can precipitate as AgCl in gastric acid, reducing bioavailability; AgNPs may partially avoid this via particulate uptake and intracellular Ag⁺ release. Gastric pH may influence this equilibrium. 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.” These values reflect experimental or anecdotal contexts and are not established safe or therapeutic doses. 4. Antioxidants such as NAC can counteract AgNP cytotoxicity by restoring glutathione pools and suppressing ROS-mediated mitochondrial damage. 5. In vitro studies commonly show ROS elevation in both cancer and normal cells; however, in vivo, superior antioxidant, NRF2, and repair capacity in normal tissues may confer selectivity. 6. Pathways/mechanisms of action/: -” intracellular ROS was increased...reduction in levels of glutathione (GSH)” - Normal-cell selectivity is partly mediated by NRF2-dependent antioxidant and detoxification responses. - AgNPs impair mitochondrial electron transport, increasing electron leak and amplifying ROS upstream of ΔΨm collapse. -AgNPs inhibit VEGF-driven endothelial signaling and permeability (anti-angiogenic effect) -”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.” Chronic accumulation and long-term systemic effects remain insufficiently characterized. 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. Similar oxidative considerations may apply to selenium compounds, though mechanisms differ. 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. AgNP anticancer effects come from three overlapping mechanisms: -Nanoparticle–cell interaction (uptake, membrane effects) -Intracellular ROS generation -Controlled Ag⁺ release inside cancer cells Comparison adding Citrate Capping | Property | Uncapped AgNPs | Citrate-capped AgNPs | | --------------------- | -------------- | -------------------- | | Stability | Poor | Excellent | | Free Ag⁺ | High | Low | | Normal cell toxicity | Higher | Lower | | Cancer selectivity | Lower | **Higher** | | Mechanism specificity | Crude | **Targeted** | | Storage behavior | Degrades | Stable |
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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. |
| - | in-vitro, | CRC, | HCT116 |
| 4417- | AgNPs, | Caffeine-boosted silver nanoparticles target breast cancer cells by triggering oxidative stress, inflammation, and apoptotic pathways |
| - | in-vitro, | BC, | MDA-MB-231 |
| 4439- | AgNPs, | Anticancer Potential of Green Synthesized Silver Nanoparticles Using Extract of Nepeta deflersiana against Human Cervical Cancer Cells (HeLA) |
| - | in-vitro, | Cerv, | HeLa |
| 1902- | AgNPs, | Modulation of the mechanism of action of antibacterial silver N-heterocyclic carbene complexes by variation of the halide ligand |
| - | in-vitro, | NA, | NA |
| 2287- | AgNPs, | Silver nanoparticles induce endothelial cytotoxicity through ROS-mediated mitochondria-lysosome damage and autophagy perturbation: The protective role of N-acetylcysteine |
| - | in-vitro, | Nor, | HUVECs |
| 2836- | AgNPs, | Gluc, | Glucose capped silver nanoparticles induce cell cycle arrest in HeLa cells |
| - | in-vitro, | Cerv, | HeLa |
| 398- | AgNPs, | Silver nanoparticles induced testicular damage targeting NQO1 and APE1 dysregulation, apoptosis via Bax/Bcl-2 pathway, fibrosis via TGF-β/α-SMA upregulation in rats |
| - | in-vivo, | Testi, | NA |
| 4382- | AgNPs, | Silver nanoparticles induce cytotoxicity by a Trojan-horse type mechanism |
| - | in-vitro, | Nor, | RAW264.7 |
| 4371- | AgNPs, | Effects of Green Silver Nanoparticles on Apoptosis and Oxidative Stress in Normal and Cancerous Human Hepatic Cells in vitro |
| - | in-vitro, | Liver, | HUH7 |
| 344- | AgNPs, | Cytotoxicity and ROS production of manufactured silver nanoparticles of different sizes in hepatoma and leukemia cells |
| - | in-vitro, | Liver, | HepG2 |
| 335- | AgNPs, | PDT, | Biogenic Silver Nanoparticles for Targeted Cancer Therapy and Enhancing Photodynamic Therapy |
| - | Review, | NA, | NA |
| 324- | AgNPs, | CPT, | Silver Nanoparticles Potentiates Cytotoxicity and Apoptotic Potential of Camptothecin in Human Cervical Cancer Cells |
| - | in-vitro, | Cerv, | HeLa |
| 373- | AgNPs, | Cytotoxic Potential and Molecular Pathway Analysis of Silver Nanoparticles in Human Colon Cancer Cells HCT116 |
| - | in-vitro, | Colon, | HCT116 |
| - | in-vitro, | Hepat, | HepG2 |
| 369- | AgNPs, | Silver nanoparticles induce oxidative cell damage in human liver cells through inhibition of reduced glutathione and induction of mitochondria-involved apoptosis |
| - | in-vitro, | Liver, | NA |
| 323- | Sal, | AgNPs, | Combination of salinomycin and silver nanoparticles enhances apoptosis and autophagy in human ovarian cancer cells: an effective anticancer therapy |
| - | in-vitro, | BC, | MDA-MB-231 | - | in-vitro, | Ovarian, | A2780S |
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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