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.


Lung, Lung Cancer: Click to Expand ⟱
Lung CSC (Cancer Stem Cells) markers (CD133, CD44, ALDHA1, Nanog and Oct4)

Scientific Papers found: Click to Expand⟱
5167- AL,    The Effects of Allicin, a Reactive Sulfur Species from Garlic, on a Selection of Mammalian Cell Lines
- in-vitro, Nor, 3T3 - in-vitro, BC, MCF-7 - in-vitro, Lung, A549 - in-vitro, CRC, HT-29
Thiols↓, tumCV↓, TumCP↓, GSH↓, GSSG↑, ROS↑,
1349- And,    Andrographolide promoted ferroptosis to repress the development of non-small cell lung cancer through activation of the mitochondrial dysfunction
- in-vitro, Lung, H460 - in-vitro, Lung, H1650
TumCG↓, TumMeta↓, Ferroptosis↑, ROS↑, MDA↑, Iron↑, GSH↓, GPx4↓, xCT↓, MMP↓, ATP↓,
1565- Api,    Apigenin-7-glucoside induces apoptosis and ROS accumulation in lung cancer cells, and inhibits PI3K/Akt/mTOR pathway
- in-vitro, Lung, A549 - in-vitro, Nor, BEAS-2B - in-vitro, Lung, H1975
TumCP↓, Apoptosis↑, TumCMig↓, TumCI↓, Cyt‑c↑, MDA↑, GSH↓, ROS↑, PI3K↓, Akt↓, mTOR↓,
2618- Ba,    Baicalein induces apoptosis by inhibiting the glutamine-mTOR metabolic pathway in lung cancer
- in-vitro, Lung, H1299 - in-vivo, Lung, A549
TumCG↓, TumCP↓, Apoptosis↑, GLUT1↓, GLS↓, mTOR↓, *toxicity∅, cl‑Casp9↓, cl‑Casp3↓, GSH↓, GlutMet↓,
5695- BRU,    Brusatol enhances the efficacy of chemotherapy by inhibiting the Nrf2-mediated defense mechanism
- in-vitro, Lung, A549
NRF2↓, ChemoSen↑, Apoptosis↑, TumCP↓, TumCG↓, MRP1↓, GSH↓, cMyc↓,
6131- CHr,  Bor,  Z,    Fabrication of phenyl boronic acid modified pH-responsive zinc oxide nanoparticles as targeted delivery of chrysin on human A549 cells
- in-vitro, Lung, A549
*BioAv↑, ROS↑, TumCD↑, TumCCA↑, MMP2↓, TumMeta↓, TumCI↓, GSH↓, eff↑,
1602- Cu,    A simultaneously GSH-depleted bimetallic Cu(ii) complex for enhanced chemodynamic cancer therapy†
- in-vitro, BC, MCF-7 - in-vitro, BC, 4T1 - in-vitro, Lung, A549 - in-vitro, Liver, HepG2
eff↑, GSH↓, H2O2↑, ROS↑, *BioAv↑, selectivity↑, TumCCA↑, Apoptosis↑, Fenton↑, *toxicity?,
404- CUR,    Curcumin induces ferroptosis in non-small-cell lung cancer via activating autophagy
- vitro+vivo, Lung, A549 - vitro+vivo, Lung, H1299
TumAuto↑, TumCG↓, TumCP↓, Iron↑, GSH↓, lipid-P↑, GPx↓, mtDam↑, autolysosome↑, Beclin-1↑, LC3s↑, p62↓, Ferroptosis↑,
1981- CUR,    Mitochondrial targeted curcumin exhibits anticancer effects through disruption of mitochondrial redox and modulation of TrxR2 activity
- in-vitro, Lung, NA
eff↑, ROS↑, mt-GSH↓, Bax:Bcl2↑, Cyt‑c↑, MMP↓, Casp3↑, Trx2↓, TrxR↓, mt-DNAdam↑,
2587- LT,    Luteolin inhibits Nrf2 leading to negative regulation of the Nrf2/ARE pathway and sensitization of human lung carcinoma A549 cells to therapeutic drugs
- in-vitro, Lung, A549
NRF2↓, GSH↓, ChemoSen↑, HO-1↓,
4803- Lyco,    Enhanced cytotoxic and apoptosis inducing activity of lycopene oxidation products in different cancer cell lines
- in-vitro, Pca, PC3 - in-vitro, BC, MCF-7 - in-vitro, Melanoma, A431 - in-vitro, Liver, HepG2 - in-vitro, Cerv, HeLa - in-vitro, Lung, A549
tumCV↓, GSH↓, MDA↑, ROS↑, Apoptosis↑,
1063- MEL,    HDAC1 inhibition by melatonin leads to suppression of lung adenocarcinoma cells via induction of oxidative stress and activation of apoptotic pathways
- in-vitro, Lung, A549 - in-vitro, Lung, PC9
AntiCan↑, TumCMig↓, GSH↓, Casp3↑, Apoptosis↑, ROS↑, HDAC1↓, Ac-histone H3↑, PUMA↑, BAX↑, PCNA↓, Bcl-2↓,
1204- MET,    Metformin induces ferroptosis through the Nrf2/HO-1 signaling in lung cancer
- in-vitro, Lung, A549 - in-vitro, Lung, H1299
MDA↑, ROS↑, Iron↑, GSH↓, T-SOD↓, Catalase↓, GPx4↓, xCT↓, NRF2↓, HO-1↓,
4956- PEITC,    Inhibition of cancer growth in vitro and in vivo by a novel ROS-modulating agent with ability to eliminate stem-like cancer cells
- vitro+vivo, Lung, A549
GSH↓, ROS↑, mtDam↑, mitResp↓, MMP↓, CSCs↓, OCT4↓, ABC↓, SOX2↓, CD133↓, CD44↓, ALDH↓, Nanog↓, TumCG↓,
1769- PG,    The Anti-Apoptotic Effects of Caspase Inhibitors in Propyl Gallate-Treated Lung Cancer Cells Are Related to Changes in Reactive Oxygen Species and Glutathione Levels
- in-vitro, Lung, Calu-6 - in-vitro, Lung, A549
TumCP↓, eff↑, ROS↑, GSH↓,
1772- PG,    Propyl gallate decreases the proliferation of Calu-6 and A549 lung cancer cells via affecting reactive oxygen species and glutathione levels
- in-vitro, Lung, Calu-6 - in-vitro, Lung, A549
ROS⇅, TumCP↓, GSH↓,
1765- PG,    Enhanced cell death effects of MAP kinase inhibitors in propyl gallate-treated lung cancer cells are related to increased ROS levels and GSH depletion
- in-vitro, Lung, A549 - in-vitro, Lung, Calu-6
TumCD↑, MMP↓, ROS↑, GSH↓, Dose∅, eff↑,
2943- PL,    Piperlongumine Inhibits Thioredoxin Reductase 1 by Targeting Selenocysteine Residues and Sensitizes Cancer Cells to Erastin
- in-vitro, CRC, HCT116 - in-vitro, Lung, A549 - in-vitro, BC, MCF-7
TrxR1?, TumCD↑, ROS↑, GSH↓, eff↑,
2203- SK,    Shikonin suppresses small cell lung cancer growth via inducing ATF3-mediated ferroptosis to promote ROS accumulation
- in-vitro, Lung, NA
TumCP↓, Apoptosis↓, TumCMig↓, TumCI↓, Ferroptosis↑, ERK↓, GPx4↓, 4-HNE↑, ROS↑, GSH↓, ATF3↑, HDAC1↓, ac‑Histones↑,
5090- SSE,    Sodium Selenite Induces Ferroptosis in Non-small Cell Lung Cancer A549 Cells Via Reactive Oxygen Species (ROS)/Glutathione (GSH)/Glutathione Peroxidase4 (GPx4) Axis
- NA, Lung, A549
TumCP↓, ROS↑, GSH↓, MMP↓, GPx4↓, Iron↑,
2110- TQ,    Nigella sativa seed oil suppresses cell proliferation and induces ROS dependent mitochondrial apoptosis through p53 pathway in hepatocellular carcinoma cells
- in-vitro, HCC, HepG2 - in-vitro, BC, MCF-7 - in-vitro, Lung, A549 - in-vitro, Nor, HEK293
P53↑, lipid-P↑, GSH↓, ROS↑, MMP↓, BAX↑, Casp3↑, Casp9↑, Bcl-2↓, tumCV↓, selectivity↑,

Showing Research Papers: 1 to 21 of 21

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 21

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

4-HNE↑, 1,   ATF3↑, 1,   Catalase↓, 1,   Fenton↑, 1,   Ferroptosis↑, 3,   GPx↓, 1,   GPx4↓, 4,   GSH↓, 20,   mt-GSH↓, 1,   GSSG↑, 1,   H2O2↑, 1,   HO-1↓, 2,   Iron↑, 4,   lipid-P↑, 2,   MDA↑, 4,   NRF2↓, 3,   ROS↑, 16,   ROS⇅, 1,   T-SOD↓, 1,   Thiols↓, 1,   Trx2↓, 1,   TrxR↓, 1,   TrxR1?, 1,   xCT↓, 2,  

Mitochondria & Bioenergetics

ATP↓, 1,   mitResp↓, 1,   MMP↓, 6,   mtDam↑, 2,  

Core Metabolism/Glycolysis

Ac-histone H3↑, 1,   cMyc↓, 1,   GLS↓, 1,   GlutMet↓, 1,   ac‑Histones↑, 1,  

Cell Death

Akt↓, 1,   Apoptosis↓, 1,   Apoptosis↑, 6,   BAX↑, 2,   Bax:Bcl2↑, 1,   Bcl-2↓, 2,   Casp3↑, 3,   cl‑Casp3↓, 1,   Casp9↑, 1,   cl‑Casp9↓, 1,   Cyt‑c↑, 2,   Ferroptosis↑, 3,   PUMA↑, 1,   TumCD↑, 3,  

Transcription & Epigenetics

tumCV↓, 3,  

Autophagy & Lysosomes

autolysosome↑, 1,   Beclin-1↑, 1,   LC3s↑, 1,   p62↓, 1,   TumAuto↑, 1,  

DNA Damage & Repair

mt-DNAdam↑, 1,   P53↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence

TumCCA↑, 2,  

Proliferation, Differentiation & Cell State

ALDH↓, 1,   CD133↓, 1,   CD44↓, 1,   CSCs↓, 1,   ERK↓, 1,   HDAC1↓, 2,   mTOR↓, 2,   Nanog↓, 1,   OCT4↓, 1,   PI3K↓, 1,   SOX2↓, 1,   TumCG↓, 5,  

Migration

MMP2↓, 1,   TumCI↓, 3,   TumCMig↓, 3,   TumCP↓, 9,   TumMeta↓, 2,  

Barriers & Transport

GLUT1↓, 1,  

Drug Metabolism & Resistance

ABC↓, 1,   ChemoSen↑, 2,   Dose∅, 1,   eff↑, 6,   MRP1↓, 1,   selectivity↑, 2,  

Functional Outcomes

AntiCan↑, 1,  
Total Targets: 82

Pathway results for Effect on Normal Cells:


Drug Metabolism & Resistance

BioAv↑, 2,  

Functional Outcomes

toxicity?, 1,   toxicity∅, 1,  
Total Targets: 3

Scientific Paper Hit Count for: GSH, Glutathione
3 Propyl gallate
2 Curcumin
1 Allicin (mainly Garlic)
1 Andrographis
1 Apigenin (mainly Parsley)
1 Baicalein
1 brusatol
1 Chrysin
1 Boron
1 Zinc
1 Copper and Cu NanoParticles
1 Luteolin
1 Lycopene
1 Melatonin
1 Metformin
1 Phenethyl isothiocyanate
1 Piperlongumine
1 Shikonin
1 Selenite (Sodium)
1 Thymoquinone
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:15  Cells:%  prod#:%  Target#:137  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

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