GSH Cancer Research Results

GSH, Glutathione: Click to Expand ⟱
Source:
Type:
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.
Scientific Papers found: Click to Expand⟱
5098- JG,    Effects of Juglone on Antioxidant Status in Pancreatic Cancer Cell Lines
- in-vitro, PC, Bxpc-3 - in-vitro, PC, PANC1
tumCV↓, Juglone reduced the cell viability of human pancreatic cancer cells in a concentration-dependent manner
ROS↑, At now, it is found that juglone could inhibit cell proliferation and induce ROS production in pancreatic cancer cells
GSH⇅, In our study, it was observed that the application of juglone exposed in different hours caused variability in the antioxidant activity of cells.

897- QC,    Anti- and prooxidant effects of chronic quercetin administration in rats
- in-vivo, Nor, NA
*MDA↓, in rat livers (decrease was more pronounced in vitamin E-deprived rats)
*GSH⇅, in liver
*ROS⇅, results suggest that quercetin may act not only as an antioxidant, but also as a prooxidant in rats.

5089- SSE,  Se,    Redox-mediated effects of selenium on apoptosis and cell cycle in the LNCaP human prostate cancer cell line
- in-vitro, Pca, LNCaP
ROS↑, Our results demonstrated that oxidative stress was induced by sodium selenite at high concentrations in both acute and chronic treatments, but outcomes were different.
mtDam↑, After acute exposure to selenite, cells exhibited mitochondrial injury and cell death, mainly apoptosis.
TumCD↑,
Apoptosis↑,
TumCCA↑, After chronic exposure to selenite, cells showed growth inhibition caused by cell cycle arrest, increased numbers of mitochondria and levels of mitochondrial enzymes, and only minimal induction of apoptosis
Trx↓, production of ROS, regulation of the Trx redox system, regulation of the cell cycle, and inhibition of angiogenes
angioG↓,
GSH⇅, intracellular levels of GSH were increased at doses of 0.5 and 1.5 uM selenite and decreased at doses of 2 and 2.5 uM selenite
NADPH↓, In addition, GSH and NADPH are consumed
GPx↑, GPX activities in the selenite-adapted cells were significantly increased (2- to 3-fold induction


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GPx↑, 1,   GSH⇅, 2,   ROS↑, 2,   Trx↓, 1,  

Mitochondria & Bioenergetics ⓘ

mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

NADPH↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,  
Total Targets: 11

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

GSH⇅, 1,   MDA↓, 1,   ROS⇅, 1,  
Total Targets: 3

Scientific Paper Hit Count for: GSH, Glutathione
1 Juglone
1 Quercetin
1 Selenite (Sodium)
1 Selenium
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#:137  State#:%  Dir#:3
  wNotes=on  sortOrder:rid,rpid

 

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