condition found tbRes List
SNP, Silver-NanoParticles: Click to Expand ⟱
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?
TrxR, Thioredoxin Reductase: Click to Expand ⟱
Source:
Type:
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
Scientific Papers found: Click to Expand⟱
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
TrxR↓, selectivity↑, eff↑, eff↝, ROS↑, MMP↓, Apoptosis↑, eff↑,
1909- SNP,    The Antibacterial Drug Candidate SBC3 is a Potent Inhibitor of Bacterial Thioredoxin Reductase
- in-vivo, Nor, NA
TrxR↓,
1908- SNP,    Exposure to Silver Nanoparticles Inhibits Selenoprotein Synthesis and the Activity of Thioredoxin Reductase
- in-vitro, Lung, A549
TrxR↓, TrxR1↓, ROS↑, ER Stress↑, TumCP↓, selenoP↓,
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
TrxR↓, eff↓, eff↓, other∅,
1906- SNP,  GoldNP,  Cu,    Current Progresses in Metal-based Anticancer Complexes as Mammalian TrxR Inhibitors
- Review, Var, NA
TrxR↓, eff↓, eff↓,
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
*TrxR↓, *ROS∅, GPx↑,
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
TrxR↓, eff↝, ROS↑,
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
TrxR↓, GSR↓, GSH↓,

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Results for Effect on Cancer/Diseased Cells:
Apoptosis↑,1,   eff↓,4,   eff↑,2,   eff↝,2,   ER Stress↑,1,   GPx↑,1,   GSH↓,1,   GSR↓,1,   MMP↓,1,   other∅,1,   ROS↑,3,   selectivity↑,1,   selenoP↓,1,   TrxR↓,7,   TrxR1↓,1,   TumCP↓,1,  
Total Targets: 16

Results for Effect on Normal Cells:
ROS∅,1,   TrxR↓,1,  
Total Targets: 2

Scientific Paper Hit Count for: TrxR, Thioredoxin Reductase
8 Silver-NanoParticles
3 Gold NanoParticles
2 Copper and Cu NanoParticlex
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:153  Target#:825  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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