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.
Diabetic, Diabetic: Click to Expand ⟱
Diabetic
Scientific Papers found: Click to Expand⟱
6002- CGA,    Chlorogenic Acid: A Systematic Review on the Biological Functions, Mechanistic Actions, and Therapeutic Potentials
- Review, Var, NA - Review, Diabetic, NA - Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*neuroP↑, *Inflam↓, *antiOx↑, *cardioP↑, *NRF2↑, *AMPK↑, *SOD↑, *Catalase↑, *GSH↑, *GPx↑, *ROS↓, *TNF-α↓, *IL6↓, *NF-kB↓, *COX2↓, *glucose↓, *TRPC1↓, *Ca+2↓, *HO-1↑, *NF-kB↓, *PPARα↝, *Hif1a↓, *JNK↓, *BP↓, *AntiDiabetic↑, *hepatoP↑, *TLR4↓, *NRF2↑, *Casp↓, *neuroP↑, *Aβ↓, *LDH↓, *MDA↓, *memory↑, *AChE↓, *eff↑, EMT↝, N-cadherin↓, E-cadherin↑, TumCCA↑, ROS↑, p‑P53↑, HO-1↑, NRF2↑, ChemoSen↑, mtDam↑, Casp3↑, Casp9↑, PARP↑, Bax:Bcl2↑, TumCG↓, cycD1/CCND1↓, cMyc↓, CDK2↓, mitResp↓, Glycolysis↓, Hif1a↓, PCNA↓, p‑GSK‐3β↓, VEGF↓, PI3K↓, Akt↓, mTOR↓, OS↑,
3251- PBG,    The Antioxidant and Anti-Inflammatory Effects of Flavonoids from Propolis via Nrf2 and NF-κB Pathways
- Review, AD, NA - Review, Diabetic, NA - Review, Var, NA - in-vitro, Nor, H9c2
*antiOx↑, *Inflam↓, *ROS↓, *SOD↑, *Catalase↑, *HO-1↑, *NO↓, *NOS2↓, *NF-kB↓, *NRF2↑, *hepatoP↑, *MDA↓, *mtDam↓, *GSH↑, *p65↓, *TNF-α↓, *IL1β↓, *NRF2↑, *NRF2↓, *ROS⇅, *BioAv↓, *BioAv↑,
5904- TV,    Pharmacological Properties and Molecular Mechanisms of Thymol: Prospects for Its Therapeutic Potential and Pharmaceutical Development
- Review, Var, NA - Review, Stroke, NA - Review, Diabetic, NA - Review, Obesity, NA - Review, AD, NA - Review, Arthritis, NA
*antiOx↑, *ROS↓, *Inflam↓, *Bacteria↓, AntiTum↑, IronCh↑, *HDL↑, *LDL↓, *BioAv↝, *Half-Life↝, *BioAv↑, *SOD↑, *GPx↑, *GSTs↑, *eff↑, radioP↑, *MDA↓, *other↑, *COX1↓, *COX2↓, *AntiAg↑, *RNS↓, *NO↓, *H2O2↓, *NOS2↓, *NADH↓, *Imm↑, Apoptosis↑, TumCP↓, angioG↓, TumCMig↓, Ca+2↑, TumCCA↑, DNAdam↑, BAX↑, Casp9↑, Casp8↑, Casp3↑, cl‑PARP↑, AIF↑, i-ROS↑, MMP↓, Cyt‑c↑, APAF1↑, Ca+2↑, MMP9↓, MMP2↓, PKCδ↓, ERK↓, H2O2↑, BAX↑, Bcl-2↓, DNAdam↑, lipid-P↑, ChemoSen↑, chemoP↑, *cardioP↑, *SOD↑, *Catalase↑, *GPx↑, *GSH↑, *BP↓, *AntiDiabetic↑, *Obesity↓, RenoP↑, *GastroP↑, hepatoP↑, *AChE↓, *cognitive↑, *BChE↓, *other↓, *BioAv↑,

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 ⓘ

H2O2↑, 1,   HO-1↑, 1,   lipid-P↑, 1,   NRF2↑, 1,   ROS↑, 1,   i-ROS↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   mitResp↓, 1,   MMP↓, 1,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   Glycolysis↓, 1,  

Cell Death ⓘ

Akt↓, 1,   APAF1↑, 1,   Apoptosis↑, 1,   BAX↑, 2,   Bax:Bcl2↑, 1,   Bcl-2↓, 1,   Casp3↑, 2,   Casp8↑, 1,   Casp9↑, 2,   Cyt‑c↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   p‑P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   cycD1/CCND1↓, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

EMT↝, 1,   ERK↓, 1,   p‑GSK‐3β↓, 1,   mTOR↓, 1,   PI3K↓, 1,   TumCG↓, 1,  

Migration ⓘ

Ca+2↑, 2,   E-cadherin↑, 1,   MMP2↓, 1,   MMP9↓, 1,   N-cadherin↓, 1,   PKCδ↓, 1,   TumCMig↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 2,  

Functional Outcomes ⓘ

AntiTum↑, 1,   chemoP↑, 1,   hepatoP↑, 1,   OS↑, 1,   radioP↑, 1,   RenoP↑, 1,  
Total Targets: 55

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 3,   Catalase↑, 3,   GPx↑, 3,   GSH↑, 3,   GSTs↑, 1,   H2O2↓, 1,   HDL↑, 1,   HO-1↑, 2,   MDA↓, 3,   NADH↓, 1,   NRF2↓, 1,   NRF2↑, 4,   RNS↓, 1,   ROS↓, 3,   ROS⇅, 1,   SOD↑, 4,  

Mitochondria & Bioenergetics ⓘ

mtDam↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   glucose↓, 1,   LDH↓, 1,   LDL↓, 1,   PPARα↝, 1,  

Cell Death ⓘ

Casp↓, 1,   JNK↓, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,   other↑, 1,  

Migration ⓘ

AntiAg↑, 1,   Ca+2↓, 1,   TRPC1↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,   NO↓, 2,  

Barriers & Transport ⓘ

GastroP↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 1,   COX2↓, 2,   IL1β↓, 1,   IL6↓, 1,   Imm↑, 1,   Inflam↓, 3,   NF-kB↓, 3,   p65↓, 1,   TLR4↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission ⓘ

AChE↓, 2,   BChE↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 3,   BioAv↝, 1,   eff↑, 2,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

BP↓, 2,   IL6↓, 1,   LDH↓, 1,   NOS2↓, 2,  

Functional Outcomes ⓘ

AntiDiabetic↑, 2,   cardioP↑, 2,   cognitive↑, 1,   hepatoP↑, 2,   memory↑, 1,   neuroP↑, 2,   Obesity↓, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 62

Scientific Paper Hit Count for: GSH, Glutathione
1 Chlorogenic acid
1 Propolis -bee glue
1 Thymol-Thymus vulgaris
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:61  Cells:%  prod#:%  Target#:137  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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