GSH/GSSG Cancer Research Results

GSH/GSSG, GSH/GSSG ratio: Click to Expand ⟱
Source:
Type:
Glutathione (GSH) is a ubiquitous tripeptide antioxidant that plays a key role in mitigating oxidative damage. GSH is oxidized by ROS to form a homodimer disulfide (GSSG).
The ratio between GSH and GSSG can be used as a metric to define the redox state of a cell, and imbalances in this ratio leading to excess GSSG can cause cell death.
GSH/GSSG ratio can be altered in various types of cancer, including breast, lung, colon, and prostate cancer. In general, increased GSH levels and decreased GSSG levels are associated with cancer progression and poor prognosis.
Scientific Papers found: Click to Expand⟱
1987- PTL,  Rad,    A NADPH oxidase dependent redox signaling pathway mediates the selective radiosensitization effect of parthenolide in prostate cancer cells
- in-vitro, Pca, PC3 - in-vitro, Nor, PrEC
selectivity↑, parthenolide (PN), a sesquiterpene lactone, selectively exhibits a radiosensitization effect on prostate cancer PC3 cells but not on normal prostate epithelial PrEC cells.
RadioS↑,
ROS↑, oxidative stress in PC3 cells but not in PrEC cells
*ROS∅, oxidative stress in PC3 cells but not in PrEC cells
NADPH↑, In PC3 but not PrEC cells, PN activates NADPH oxidase leading to a decrease in the level of reduced thioredoxin, activation of PI3K/Akt and consequent FOXO3a phosphorylation, which results in the downregulation of FOXO3a targets, MnSOD, CAT
Trx↓,
PI3K↑,
Akt↑,
p‑FOXO3↓, downregulation of FOXO3a targets, antioxidant enzyme manganese superoxide dismutase (MnSOD) and catalase
SOD2↓, MnSOD
Catalase↓,
radioP↑, when combined with radiation, PN further increases ROS levels in PC3 cells, while it decreases radiation-induced oxidative stress in PrEC cells
*NADPH∅, Parthenolide activates NADPH oxidase in PC3 cells but not in PrEC cells
*GSH↑, increases glutathione (GSH) in PrEC cells(normal cells)
*GSH/GSSG↑, GSH/GSSG ratio is not significantly changed by parthenolide in PC3 cells but is increased 2.4 fold in PrEC cells (normal cells)
*NRF2↑, The induction of GSH may be due to the activation of the Nrf2/ARE (antioxidant/electrophile response element) pathway

2134- TQ,    Modulation of Nrf2/HO1 Pathway by Thymoquinone to Exert Protection Against Diazinon-induced Myocardial Infarction in Rats
- in-vivo, Nor, NA
*ALAT↓, CK-MB, ALT, and AST) were shown. DN-treated rats showed significantly elevated enzyme activities as compared with control rats (147.33 ± 20.85, 110.67 ± 9.65, and 407.5 ± 31.3, respectively), and these abnormalities were alleviated in the TQ treatmen
*AST↓,
*MDA↓, TQ treatment to DN intoxicated rats significantly decreased MDA levels when compared with the DN alone group of rats, recommending the protective antioxidant role of TQ
*ROS↓,
*GSSG↓, GSSG that exhibit significant elevation in DN intoxication and normalized levels during TQ treatment.
*GSH↑, Administration of TQ with DN during the experimental period significantly increased GSH (heart and serum), vit-E and vit-C contents to near normal levels in the heart tissues and serum
*VitE↑,
*VitC↑,
*NRF2↑, TQ, significantly increased Nrf2, HO-1, NQO1, and SOD were noticed (22.2 ± 1.41, 37.2 ± 2.6, 33.37 ± 4.28, and 52.7 ± 3.05, respectively), when compared to the DN intoxicated group.
*HO-1↑,
*NQO1↑,
*SOD↑,
*cardioP↑, Restoration of body weight and improvement in heart weight in TQ treatment showed beneficial effects of TQ treatment.
*GSH/GSSG↑, TQ has a significant efficacy to control the levels of oxidized and reduced glutathione pools and able to decrease the GSSG/GSH ratio.
*GPx↑, TQ enhances GSH and GPx activities in DN-intoxicated rats by a beneficial mechanism.


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   ROS↑, 1,   SOD2↓, 1,   Trx↓, 1,  

Core Metabolism/Glycolysis ⓘ

NADPH↑, 1,  

Cell Death ⓘ

Akt↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑FOXO3↓, 1,   PI3K↑, 1,  

Drug Metabolism & Resistance ⓘ

RadioS↑, 1,   selectivity↑, 1,  

Functional Outcomes ⓘ

radioP↑, 1,  
Total Targets: 11

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

GPx↑, 1,   GSH↑, 2,   GSH/GSSG↑, 2,   GSSG↓, 1,   HO-1↑, 1,   MDA↓, 1,   NQO1↑, 1,   NRF2↑, 2,   ROS↓, 1,   ROS∅, 1,   SOD↑, 1,   VitC↑, 1,   VitE↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   NADPH∅, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,  
Total Targets: 18

Scientific Paper Hit Count for: GSH/GSSG, GSH/GSSG ratio
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#:%  Target#:104  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

Home Page