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.


Ovarian, Ovarian Cancer: Click to Expand ⟱
Ovarian Cancer


Scientific Papers found: Click to Expand⟱
5459- AF,    Auranofin Induces Lethality Driven by Reactive Oxygen Species in High-Grade Serous Ovarian Cancer Cells
- in-vitro, Ovarian, NA
ROS↑, TrxR↓, MMP↓, Apoptosis↑, eff↓, Casp3↑, Casp7↑, DNAdam↑, eff↑, GSH↓, angioG↓, ChemoSen↑, cl‑PARP↑, eff↑,
1381- BBR,  Rad,    Berberine enhances the sensitivity of radiotherapy in ovarian cancer cell line (SKOV-3)
- in-vitro, Ovarian, SKOV3
RadioS↑, ROS↑, GSH↓, Apoptosis↑,
1585- Citrate,    Sodium citrate targeting Ca2+/CAMKK2 pathway exhibits anti-tumor activity through inducing apoptosis and ferroptosis in ovarian cancer
- in-vitro, Ovarian, SKOV3 - in-vitro, Ovarian, A2780S - in-vitro, Nor, HEK293
Apoptosis↑, Ferroptosis↑, Ca+2↓, CaMKII ↓, Akt↓, mTOR↓, Hif1a↓, ROS↑, ChemoSen↑, Casp3↑, Casp9↑, BAX↑, Bcl-2↓, Cyt‑c↑, GlucoseCon↓, lactateProd↓, Pyruv↓, GLUT1↓, HK2↓, PFKP↓, Glycolysis↓, Hif1a↓, p‑Akt↓, p‑mTOR↓, Iron↑, lipid-P↑, MDA↑, ROS↑, H2O2↑, mtDam↑, GSH↓, GPx↓, GPx4↓, NADPH/NADP+↓, eff↓, FTH1↓, LC3‑Ⅱ/LC3‑Ⅰ↑, NCOA4↑, eff↓, TumCG↓,
5047- erastin,    The ferroptosis inducer erastin irreversibly inhibits system xc− and synergizes with cisplatin to increase cisplatin’s cytotoxicity in cancer cells
- in-vitro, Ovarian, NA
xCT↓, GSH↓, Ferroptosis↑, ChemoSen↑, eff↑,
4951- PEITC,    ROS accumulation by PEITC selectively kills ovarian cancer cells via UPR-mediated apoptosis
- in-vitro, Ovarian, PA1 - in-vitro, Ovarian, SKOV3
ROS↑, TumCP↓, GSH↓, selectivity↑, UPR↑, CHOP↑, ER Stress↑, GRP78/BiP↑, PERK↑, ATF6↑, eff↓, TumCG↓, Apoptosis↑, toxicity↓,
4954- PEITC,    Selective killing of oncogenically transformed cells through a ROS-mediated mechanism by β-phenylethyl isothiocyanate
- vitro+vivo, Ovarian, SKOV3
ROS↑, GSH↓, selectivity↑, mtDam↑, TumCD↑, OS↑, eff↑, *toxicity↓, H2O2↑, NO↑, eff↓, GPx↓, Dose↝, eff↑,
323- Sal,  AgNPs,    Combination of salinomycin and silver nanoparticles enhances apoptosis and autophagy in human ovarian cancer cells: an effective anticancer therapy
- in-vitro, BC, MDA-MB-231 - in-vitro, Ovarian, A2780S
TumCD↑, LDH↓, MDA↑, SOD↓, ROS↑, GSH↓, Catalase↓, MMP↓, P53↑, P21↑, BAX↑, Bcl-2↓, Casp3↑, Casp9↑, Apoptosis↑, TumAuto↑,
1343- SK,    Simple ROS-responsive micelles loaded Shikonin for efficient ovarian cancer targeting therapy by disrupting intracellular redox homeostasis
- in-vitro, Ovarian, A2780S - in-vivo, NA, A2780S
*BioAv↓, ROS↑, GSH↓, TumCG↓,
5330- TFdiG,  Cisplatin,    Theaflavin-3,3′-Digallate Enhances the Inhibitory Effect of Cisplatin by Regulating the Copper Transporter 1 and Glutathione in Human Ovarian Cancer Cells
- in-vitro, Ovarian, A2780S - in-vitro, Ovarian, OVCAR-3
selectivity↑, ChemoSen↑, DNAdam↑, GSH↓, CTR1↑,

Showing Research Papers: 1 to 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

Catalase↓, 1,   Ferroptosis↑, 2,   GPx↓, 2,   GPx4↓, 1,   GSH↓, 9,   H2O2↑, 2,   Iron↑, 1,   lipid-P↑, 1,   MDA↑, 2,   NADPH/NADP+↓, 1,   ROS↑, 8,   SOD↓, 1,   TrxR↓, 1,   xCT↓, 1,  

Metal & Cofactor Biology

FTH1↓, 1,   NCOA4↑, 1,  

Mitochondria & Bioenergetics

MMP↓, 2,   mtDam↑, 2,  

Core Metabolism/Glycolysis

GlucoseCon↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↓, 1,   LDH↓, 1,   PFKP↓, 1,   Pyruv↓, 1,  

Cell Death

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 5,   BAX↑, 2,   Bcl-2↓, 2,   Casp3↑, 3,   Casp7↑, 1,   Casp9↑, 2,   Cyt‑c↑, 1,   Ferroptosis↑, 2,   TumCD↑, 2,  

Kinase & Signal Transduction

CaMKII ↓, 1,  

Protein Folding & ER Stress

ATF6↑, 1,   CHOP↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 1,   PERK↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes

LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair

DNAdam↑, 2,   P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence

P21↑, 1,  

Proliferation, Differentiation & Cell State

mTOR↓, 1,   p‑mTOR↓, 1,   TumCG↓, 3,  

Migration

Ca+2↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature

angioG↓, 1,   Hif1a↓, 2,   NO↑, 1,  

Barriers & Transport

CTR1↑, 1,   GLUT1↓, 1,  

Drug Metabolism & Resistance

ChemoSen↑, 4,   Dose↝, 1,   eff↓, 5,   eff↑, 5,   RadioS↑, 1,   selectivity↑, 3,  

Clinical Biomarkers

LDH↓, 1,  

Functional Outcomes

OS↑, 1,   toxicity↓, 1,  
Total Targets: 68

Pathway results for Effect on Normal Cells:


Drug Metabolism & Resistance

BioAv↓, 1,  

Functional Outcomes

toxicity↓, 1,  
Total Targets: 2

Scientific Paper Hit Count for: GSH, Glutathione
2 Phenethyl isothiocyanate
1 Auranofin
1 Berberine
1 Radiotherapy/Radiation
1 Citric Acid
1 erastin
1 salinomycin
1 Silver-NanoParticles
1 Shikonin
1 Aflavin-3,3′-digallate
1 Cisplatin
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:20  Cells:%  prod#:%  Target#:137  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

Home Page