| 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: |
| Cytochrome c ** The term "release of cytochrome c" ** an increase in level for the cytosol. Small hemeprotein found loosely associated with the inner membrane of the mitochondrion where it plays a critical role in cellular respiration. Cytochrome c is highly water-soluble, unlike other cytochromes. It is capable of undergoing oxidation and reduction as its iron atom converts between the ferrous and ferric forms, but does not bind oxygen. It also plays a major role in cell apoptosis. The term "release of cytochrome c" refers to a critical step in the process of programmed cell death, also known as apoptosis. In its new location—the cytosol—cytochrome c participates in the apoptotic signaling pathway by helping to form the apoptosome, which activates caspases that execute cell death. Cytochrome c is a small protein normally located in the mitochondrial intermembrane space. Its primary role in healthy cells is to participate in the electron transport chain, a process that helps produce energy (ATP) through oxidative phosphorylation. Mitochondrial outer membrane permeability leads to the release of cytochrome c from the mitochondria into the cytosol. The release of cytochrome c is a pivotal event in apoptosis where cytochrome c moves from the mitochondria to the cytosol, initiating a chain reaction that leads to programmed cell death. On the one hand, cytochrome c can promote cancer cell survival and proliferation by regulating the activity of various signaling pathways, such as the PI3K/AKT pathway. This can lead to increased cell growth and resistance to apoptosis, which are hallmarks of cancer. On the other hand, cytochrome c can also induce apoptosis in cancer cells by interacting with other proteins, such as Apaf-1 and caspase-9. This can lead to the activation of the intrinsic apoptotic pathway, which can result in the death of cancer cells. Overexpressed in Breast, Lung, Colon, and Prostrate. Underexpressed in Ovarian, and Pancreatic. |
| 4557- | AgNPs, | The apoptotic effect of nanosilver is mediated by a ROS- and JNK-dependent mechanism involving the mitochondrial pathway in NIH3T3 cells |
| - | in-vitro, | NA, | NIH-3T3 | - | in-vitro, | CRC, | HCT116 |
| 5977- | AgNPs, | CDT, | Silver Nitroprusside as an Efficient Chemodynamic Therapeutic Agent and a Peroxynitrite nanogenerator for Targeted Cancer Therapy |
| - | in-vivo, | Ovarian, | A2780S | - | NA, | Ovarian, | SKOV3 |
| 5238- | AgNPs, | β-Sitosterol-assisted silver nanoparticles activates Nrf2 and triggers mitochondrial apoptosis via oxidative stress in human hepatocellular cancer cell line |
| - | in-vitro, | HCC, | HepG2 |
| 4417- | AgNPs, | Caffeine-boosted silver nanoparticles target breast cancer cells by triggering oxidative stress, inflammation, and apoptotic pathways |
| - | in-vitro, | BC, | MDA-MB-231 |
| 4415- | AgNPs, | SDT, | CUR, | Examining the Impact of Sonodynamic Therapy With Ultrasound Wave in the Presence of Curcumin-Coated Silver Nanoparticles on the Apoptosis of MCF7 Breast Cancer Cells |
| - | in-vitro, | BC, | MCF-7 |
| 4405- | AgNPs, | Silver nanoparticles defeat p53-positive and p53-negative osteosarcoma cells by triggering mitochondrial stress and apoptosis |
| - | in-vitro, | OS, | NA |
| 4549- | AgNPs, | Silver nanoparticles: Synthesis, medical applications and biosafety |
| - | Review, | Var, | NA | - | Review, | Diabetic, | NA |
| 2288- | AgNPs, | Silver Nanoparticle-Mediated Cellular Responses in Various Cell Lines: An in Vitro Model |
| - | Review, | Var, | NA |
| 397- | AgNPs, | GEM, | Silver nanoparticles enhance the apoptotic potential of gemcitabine in human ovarian cancer cells: combination therapy for effective cancer treatment |
| - | in-vitro, | Ovarian, | A2780S |
| 388- | AgNPs, | Apoptotic efficacy of multifaceted biosynthesized silver nanoparticles on human adenocarcinoma cells |
| - | in-vitro, | BC, | MCF-7 |
| 306- | AgNPs, | Cancer Therapy by Silver Nanoparticles: Fiction or Reality? |
| - | Analysis, | NA, | NA |
| 324- | AgNPs, | CPT, | Silver Nanoparticles Potentiates Cytotoxicity and Apoptotic Potential of Camptothecin in Human Cervical Cancer Cells |
| - | in-vitro, | Cerv, | HeLa |
| 387- | AgNPs, | Silver nanoparticles induce mitochondria-dependent apoptosis and late non-canonical autophagy in HT-29 colon cancer cells |
| - | in-vitro, | Colon, | HT-29 |
| 363- | AgNPs, | Silver nanoparticles induce oxidative cell damage in human liver cells through inhibition of reduced glutathione and induction of mitochondria-involved apoptosis |
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#:77 State#:% Dir#:%
wNotes=0 sortOrder:rid,rpid