| Features: | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| 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 |
|
| Source: |
| Type: |
| Endonucleases are enzymes that play a crucial role in the maintenance of genome stability by cleaving the phosphodiester backbone of DNA. In the context of cancer, endonucleases can have both tumor-suppressing and tumor-promoting effects. 1. APEX1 (Apurinic/Apyrimidinic Endonuclease 1) Cancers: Breast cancer, lung cancer, colorectal cancer Prognosis: High expression is often associated with poor prognosis due to its role in DNA repair and resistance to chemotherapy. 2. FEN1 (Flap Endonuclease 1) Cancers: Breast cancer, prostate cancer, pancreatic cancer Prognosis: Overexpression is linked to increased tumor aggressiveness and poor survival rates. 3. EXO1 (Exonuclease 1) Cancers: Colorectal cancer, ovarian cancer Prognosis: High levels of EXO1 expression can correlate with poor prognosis and increased risk of metastasis. 4. DNase I (Deoxyribonuclease I) Cancers: Various solid tumors Prognosis: Altered expression levels can be indicative of tumor progression and immune evasion. 5. Caspase-3 (an endonuclease involved in apoptosis) Cancers: Various cancers, including leukemia and solid tumors Prognosis: High levels of active caspase-3 are often associated with increased apoptosis and may correlate with better treatment responses. 6. Rad51 (a recombinase with endonuclease activity) Cancers: Breast cancer, ovarian cancer Prognosis: Elevated expression is often linked to resistance to DNA-damaging therapies and poor prognosis. 7. MRE11 (part of the MRN complex) Cancers: Breast cancer, lung cancer Prognosis: Altered expression can indicate defects in DNA repair mechanisms, influencing treatment outcomes. 8. TDP1 (Tyrosyl-DNA Phosphodiesterase 1) Cancers: Glioblastoma, breast cancer Prognosis: High expression levels may be associated with resistance to certain chemotherapeutic agents. 9. UNG (Uracil-DNA Glycosylase) Cancers: Colorectal cancer, lung cancer Prognosis: Its expression can influence the mutation rate and may correlate with tumor aggressiveness. 10. LIG3 (DNA Ligase III) Cancers: Various cancers, including breast and prostate cancer Prognosis: Overexpression may be linked to enhanced DNA repair capabilities, contributing to treatment resistance. |
| 400- | AgNPs, | MF, | Polyvinyl Alcohol Capped Silver Nanostructures for Fortified Apoptotic Potential Against Human Laryngeal Carcinoma Cells Hep-2 Using Extremely-Low Frequency Electromagnetic Field |
| - | in-vitro, | Laryn, | HEp2 |
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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:153 Target#:635 State#:% Dir#:2
wNotes=0 sortOrder:rid,rpid