GSSG Cancer Research Results

GSSG, oxidized glutathione: Click to Expand ⟱
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GSSG (oxidized glutathione) is a component of the cellular redox system rather than a protein or signaling molecule produced de novo. Its levels, often evaluated along with its reduced counterpart (GSH), serve as an important index of cellular oxidative stress and redox balance.

– GSSG is generated when glutathione (GSH) neutralizes reactive oxygen species (ROS) by donating electrons; in doing so, GSH is oxidized to GSSG.

– The GSH/GSSG ratio is a sensitive marker of the intracellular redox state. Under conditions of oxidative stress (commonly observed in many cancers), this ratio often shifts toward increased GSSG.

– Elevated GSSG levels (or an increased GSSG/GSH ratio) can indicate that cancer cells are under oxidative stress, which has implications both for cancer progression and for sensitivity to certain treatments.
Scientific Papers found: Click to Expand⟱
3283- ALA,    Alpha-lipoic acid inhibits TNF-alpha-induced NF-kappaB activation and adhesion molecule expression in human aortic endothelial cells
- in-vitro, Nor, NA
*TNF-α↓, LA also strongly inhibited TNF-alpha-induced mRNA expression of monocyte chemoattractant protein-1
*NF-kB↓, LA dose-dependently inhibited TNF-alpha-induced IkappaB kinase activation, subsequent degradation of IkappaB, the cytoplasmic NF-kappaB inhibitor, and nuclear translocation of NF-kappaB.
*antiOx↑, LA in its free, non-protein-bound form has potent antioxidant and metal-chelating properties
*IronCh↑,
*GSSG↓, DHLA/LA couple may chemically reduce glutathione disulfide (GSSG) to GSH
*VCAM-1↓, E-selectin, VCAM-1, ICAM-1, and MCP-1 message levels decreased by 93%, 77%, 67%, and 100%, respectively, when HAEC were pretreated with 0.5mmol/l LA
*E-sel↓,
*ICAM-1↓,
*MCP1↓,
*NF-kB↓, Lipoic acid inhibits TNF-a-induced activation of NF-kB and degradation of IkBs
IKKα↓,

3782- FA,    Ferulic acid ameliorates bisphenol A (BPA)-induced Alzheimer’s disease-like pathology through Akt-ERK crosstalk pathway in male rats
- in-vivo, AD, NA
*cognitive↑, Interestingly, the BPA + FA treated group showed a reversal in the cognitive impairments induced by BPA
*ERK↓, a significant decrease in brain inflammatory cytokines, ERK, and p-Akt levels
*p‑Akt↓,
*AChE↓, brain levels of AChE and BACE were substantially reduced in BPA + FA rats.
*BACE↓,
*neuroP↑, neuroprotective effect of FA was confirmed by restoring the normal architecture of brain tissue, which was associated with decreasing GFAP.
*ROS↓, FA was sufficient to trigger antioxidant capabilities and decrease intracellular reactive oxygen species (ROS
*MDA↓, BPA + FA revealed a substantial reduction in MDA levels compared to rats intoxicated with BPA
*GSH↑, BPA + FA revealed a significant increment of GSH associated with a significant decrease in GSSG
*GSSG↓,
*p‑tau↓, BPA + FA showed a significant decline in the brain level of pTau compared to intoxicated rats.
*lipid-P↓, inhibit lipid peroxidation
*Aβ↓, FA has significantly counteracted the deleterious effect of BPA by decreasing Aβ 1–42, as previously reported

3463- MF,    Pulsed Electromagnetic Fields Alleviates Hepatic Oxidative Stress and Lipids Accumulation in db/db mice
- in-vivo, NA, NA
*hepatoP↑, PEMF exposure could protect the liver from oxidative stress injury by decreasing MDA and GSSG level, promoting reduced GSH level, and increasing GSH-Px activity and expression in comparison with sham group
*MDA↓,
*GSSG↓,
*GSH↑,
*GPx↑,
*antiOx↑, PEMF could increase antioxidant enzymes activity and alleviate lipid accumulation in fatty liver.
*SREBP1↓, PEMF exposure ameliorated hepatic steatosis through reducing the expression of SREBP-1c to regulate the lipid synthesis.

4934- PEITC,    Differential induction of apoptosis in human breast cancer cell lines by phenethyl isothiocyanate, a glutathione depleting agent
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
GSH↓, Phenethyl isothiocyanate (PEITC) is a naturally occurring electrophile which depletes intracellular glutathione (GSH) levels and triggers accumulation of reactive oxygen species (ROS)
ROS↑,
chemoPv↑, PEITC is of considerable interest as a potential chemopreventive/chemotherapeutic agent
Apoptosis↑, PEITC readily induced apoptosis in MDA-MB-231 cells (associated with rapid activation of caspases 9 and 3, and decreased expression of BAX), MCF7 cells were relatively resistant to the apoptosis promoting effects of PEITC.
Casp9↑,
Casp3↑,
eff↓, pre-treatment of MDA-MB-231 cells with NAC rendered these cells relatively resistant to PEITC-induced apoptosis.
TumCG↓, PEITC-induced growth inhibition in human breast cancer cell lines
TumCCA↑, There was also an increase in the proportion of cells in S phase, and cells with sub-G1 DNA content, indicative of cell death, especially after 48 h.
BAX↑, An increase in BAX expression was observed at 2 h after addition of PEITC in MDA-MB-231 cells, and BAX levels further increased at 4 and 6 h (
Nrf1↑, PEITC increased NRF2 expression by ~3-fold in MDA-MB-231 cells at 4 h after treatment with PEITC. By contrast, NRF2 expression in MCF7 cells was not effected by PEITC
GSH↓, Total GSH and GSSG levels were reduced in MCF7 cells at 2 h after treatment with PEITC, but then remained at this level for the remainder of the time course
GSSG↓,
GSH/GSSG↓, By contrast, in MDA-MB-231 cells, total GSH levels decreased up to 6 h and were reduced by ~50% at this time. There was also an increase in the GSSG/GSH ratio, indicative of increasing oxidative stress.

3007- RosA,    Hepatoprotective effects of rosmarinic acid: Insight into its mechanisms of action
- Review, NA, NA
*ROS↓, antioxidant properties as a ROS scavenger and lipid peroxidation inhibitor, anti-inflammatory, neuroprotective and antiangiogenic among others.
*lipid-P↓,
*Inflam↓,
*neuroP↑,
*angioG↓,
*eff↑, The hepatoprotective effects of RA alone and in combination with caffeic acid (CA) was reported in t-BHP-induced oxidative liver damage
*AST↓, significant reduction of indicators of hepatic toxicity, such as AST, ALT, GSSG, lipid peroxidation.
*ALAT↓,
*GSSG↓,
*eNOS↓, It also reduced the liver content of eNOS/iNOS and NO, attenuated NF-κB activation
*iNOS↓,
*NO↓,
*NF-kB↓,
*MMP2↓, It inhibited MMP-2 activity and suppressed ROS generation and lipid peroxidation.
*MDA↓, It also decreased malondialdehyde (MDA) and TNF-α levels while increasing GSH levels as well as SOD and GSH-Px activities in the livers and kidneys.
*TNF-α↓,
*GSH↑,
*SOD↑,
*IL6↓, RA decreased the hepatic level of IL-6, TNF-Alpha, and PGE2, as well as the activity of COX-2 It also decreased hepatic RAGE and sorbitol levels, and GLO-1 activity
*PGE2↓,
*COX2↓,
*mTOR↑, In the study, it was observed that RA stimulated hepatocyte proliferation. Specifically activated the mTOR signaling pathway during liver regeneration and rescued PH-impaired liver functions

3936- RT,    Rutin improves spatial memory in Alzheimer's disease transgenic mice by reducing Aβ oligomer level and attenuating oxidative stress and neuroinflammation
- in-vivo, AD, NA
*memory↑, orally administered rutin significantly attenuated memory deficits in AD transgenic mice, decreased oligomeric Aβ level
*Aβ↓,
*SOD↑, increased super oxide dismutase (SOD) activity and glutathione (GSH)/glutathione disulfide (GSSG) ratio, reduced GSSG and malondialdehyde (MDA) levels, downregulated microgliosis and astrocytosis, and decreased interleukin (IL)-1β and IL-6 levels in
*GSH↑,
*GSSG↓,
*MDA↓,
*IL1β↓,
*IL6↓,
*antiOx↑, rutin is a promising agent for AD treatment because of its antioxidant, anti-inflammatory, and reducing Aβ oligomer activitie
*Inflam↓,

2124- TQ,    Thymoquinone: an emerging natural drug with a wide range of medical applications
- Review, Var, NA
hepatoP↑, Hepatoprotective
Bax:Bcl2↑, A549 non-small cell lung cancer cells exposed to benzo(a)pyrene plus TQ in vitro
cycD1/CCND1↓,
P21↑,
TRAIL↑,
P53↑,
TumCCA↑, G2/M cell cycle arrest
hepatoP↑, Hepatoprotective effects
*ALAT↓, The levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), tissue levels of malondialdehyde (MDA), oxidized glutathione (GSSG), and superoxide dismutase (SOD) activity were found to be lower
*AST↓,
*MDA↓,
*GSSG↓,
*COX2↓, N. sativa and TQ treatment also suppressed the expression of the COX-2 enzyme in the pancreatic tissue
*lipid-P↓, Thymoquinone and thymohydroquinone inhibited in vitro non-enzymatic lipid peroxidation in hippocampal homogenates induced by iron-ascorbate (52)
PPARγ↑, In breast cancer cells TQ was able to increase peroxisome proliferator-activated receptor gamma (PPAR-γ) activity
p38↑, Treatment of human breast carcinoma in both in vitro and in vivo models demonstrated antiproliferative and proapoptotic effects of TQ, which are mediated by its inductive effect on p38 and ROS signaling
ROS↑,
ChemoSen↑, TQ possesses anti-tumor effects in breast tumor xenograft mice and it potentiates the antitumor effect of doxorubicin (64).
selectivity↑, TQ is also a microtubule-targeting agent (MTA), and binds to the tubulin-microtubule network, thus preventing microtubule polymerization and causing mitotic arrest and apoptosis of A549 cells but not of normal HUVEC cells
selectivity↑, No effect on α/β tubulin protein expression was found in normal human fibroblasts used as control cell model. These data indicate that TQ exerts a selective effect on α/β tubulin in cancer cells
*MDA↓, Reduction of tissue MDA levels, and increased SOD levels
*SOD↑,

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 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 2,   GSH/GSSG↓, 1,   GSSG↓, 1,   Nrf1↑, 1,   ROS↑, 2,  

Core Metabolism/Glycolysis ⓘ

PPARγ↑, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   BAX↑, 1,   Bax:Bcl2↑, 1,   Casp3↑, 1,   Casp9↑, 1,   p38↑, 1,   TRAIL↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 1,  

Immune & Inflammatory Signaling ⓘ

IKKα↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↓, 1,   selectivity↑, 2,  

Functional Outcomes ⓘ

chemoPv↑, 1,   hepatoP↑, 2,  
Total Targets: 24

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 3,   GPx↑, 2,   GSH↑, 5,   GSH/GSSG↑, 1,   GSSG↓, 7,   HO-1↑, 1,   lipid-P↓, 3,   MDA↓, 7,   NQO1↑, 1,   NRF2↑, 1,   ROS↓, 3,   SOD↑, 4,   VitC↑, 1,   VitE↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 3,   SREBP1↓, 1,  

Cell Death ⓘ

p‑Akt↓, 1,   iNOS↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   mTOR↑, 1,  

Migration ⓘ

E-sel↓, 1,   MMP2↓, 1,   VCAM-1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   eNOS↓, 1,   NO↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   ICAM-1↓, 1,   IL1β↓, 1,   IL6↓, 2,   Inflam↓, 2,   MCP1↓, 1,   NF-kB↓, 3,   PGE2↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,   p‑tau↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 2,   BACE↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 3,   AST↓, 3,   IL6↓, 2,  

Functional Outcomes ⓘ

cardioP↑, 1,   cognitive↑, 1,   hepatoP↑, 1,   memory↑, 1,   neuroP↑, 2,  
Total Targets: 49

Scientific Paper Hit Count for: GSSG, oxidized glutathione
2 Thymoquinone
1 Alpha-Lipoic-Acid
1 Ferulic acid
1 Magnetic Fields
1 Phenethyl isothiocyanate
1 Rosmarinic acid
1 Rutin
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

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