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| 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. |
| 2113- | TQ, | Potential role of Nigella sativa (NS) in abating oxidative stress-induced toxicity in rats: a possible protection mechanism |
| - | in-vivo, | Nor, | NA |
| 2134- | TQ, | Modulation of Nrf2/HO1 Pathway by Thymoquinone to Exert Protection Against Diazinon-induced Myocardial Infarction in Rats |
| - | in-vivo, | Nor, | NA |
| 2137- | TQ, | Gastroprotective activity of Nigella sativa L oil and its constituent, thymoquinone against acute alcohol-induced gastric mucosal injury in rats |
| - | in-vivo, | Nor, | NA |
| 2086- | TQ, | Cardioprotective effects of Nigella sativa oil on cyclosporine A-induced cardiotoxicity in rats |
| - | in-vivo, | Nor, | NA |
| 2092- | TQ, | Dissecting the Potential Roles of Nigella sativa and Its Constituent Thymoquinone on the Prevention and on the Progression of Alzheimer's Disease |
| - | Review, | AD, | NA |
| 2111- | TQ, | MTX, | Effect of Nigella sativa (black seeds) against methotrexate-induced nephrotoxicity in mice |
| - | in-vivo, | Nor, | NA |
| 2100- | TQ, | Dual properties of Nigella Sative: Anti-oxidant and Pro-oxidant |
| - | Review, | NA, | NA |
| 2106- | TQ, | Cancer: Thymoquinone antioxidant/pro-oxidant effect as potential anticancer remedy |
| - | Review, | Var, | NA |
| 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 |
| 1934- | TQ, | Studies on molecular mechanisms of growth inhibitory effects of thymoquinone against prostate cancer cells: role of reactive oxygen species |
| - | in-vitro, | Pca, | PC3 | - | in-vitro, | Pca, | C4-2B |
| 3409- | TQ, | Thymoquinone therapy remediates elevated brain tissue inflammatory mediators induced by chronic administration of food preservatives |
| - | in-vivo, | Nor, | NA |
| 3407- | TQ, | Thymoquinone and its pharmacological perspective: A review |
| - | Review, | NA, | NA |
| 3406- | TQ, | SeNPs, | A study to determine the effect of nano-selenium and thymoquinone on the Nrf2 gene expression in Alzheimer’s disease |
| - | in-vivo, | AD, | NA |
| 3404- | TQ, | The Neuroprotective Effects of Thymoquinone: A Review |
| - | Review, | Var, | NA | - | Review, | AD, | NA | - | Review, | Park, | NA | - | Review, | Stroke, | NA |
| 3400- | TQ, | Chemo, | Thymoquinone Ameliorates Carfilzomib-Induced Renal Impairment by Modulating Oxidative Stress Markers, Inflammatory/Apoptotic Mediators, and Augmenting Nrf2 in Rats |
| - | in-vitro, | Nor, | NA |
| 3399- | TQ, | Anticancer Effects of Thymoquinone through the Antioxidant Activity, Upregulation of Nrf2, and Downregulation of PD-L1 in Triple-Negative Breast Cancer Cells |
| - | in-vitro, | BC, | MDA-MB-231 | - | NA, | BC, | MDA-MB-468 |
| 3432- | TQ, | Thymoquinone: Review of Its Potential in the Treatment of Neurological Diseases |
| - | Review, | AD, | NA | - | Review, | Park, | NA |
| 3422- | TQ, | Thymoquinone, as a Novel Therapeutic Candidate of Cancers |
| - | Review, | Var, | NA |
| 3554- | TQ, | Neuroprotective efficacy of thymoquinone against amyloid beta-induced neurotoxicity in human induced pluripotent stem cell-derived cholinergic neurons |
| - | in-vitro, | AD, | NA |
| - | in-vivo, | AD, | NA |
| 3559- | TQ, | Molecular signaling pathway targeted therapeutic potential of thymoquinone in Alzheimer’s disease |
| - | Review, | AD, | NA | - | Review, | Var, | NA |
| 3571- | TQ, | The Role of Thymoquinone in Inflammatory Response in Chronic Diseases |
| - | Review, | Var, | NA | - | Review, | Stroke, | NA |
| 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 |
| 2411- | UA, | Ursolic acid in health and disease |
| - | Review, | Var, | NA |
| 4876- | Uro, | Urolithin A in Health and Diseases: Prospects for Parkinson’s Disease Management |
| - | Review, | Park, | NA | - | Review, | AD, | NA |
| 4037- | VitB12, | FA, | Mechanistic Link between Vitamin B12 and Alzheimer’s Disease |
| - | Review, | AD, | NA |
| 580- | VitC, | MF, | Extremely low frequency magnetic field induces oxidative stress in mouse cerebellum |
| - | in-vivo, | Nor, | NA |
| 635- | VitC, | VitK3, | The combination of ascorbate and menadione causes cancer cell death by oxidative stress and replicative stress |
| - | in-vitro, | NA, | NA |
| 2592- | VitC, | Ascorbic acid restores sensitivity to imatinib via suppression of Nrf2-dependent gene expression in the imatinib-resistant cell line |
| - | in-vitro, | CLL, | NA |
| 1215- | VitC, | immuno, | Metabolomics reveals ascorbic acid inhibits ferroptosis in hepatocytes and boosts the effectiveness of anti-PD1 immunotherapy in hepatocellular carcinoma |
| - | ex-vivo, | HCC, | NA | - | in-vivo, | HCC, | NA |
| 1216- | VitC, | Ascorbic acid induces ferroptosis via STAT3/GPX4 signaling in oropharyngeal cancer |
| - | in-vitro, | Laryn, | FaDu | - | in-vitro, | SCC, | SCC-154 |
| 4090- | VitK2, | ProBio, | Vitamin K2 Holds Promise for Alzheimer's Prevention and Treatment |
| - | Review, | AD, | NA |
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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