| 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. |
| Liver Cancer |
| 5434- | AG, | Recent Advances in the Mechanisms and Applications of Astragalus Polysaccharides in Liver Cancer Treatment: An Overview |
| - | Review, | Liver, | NA |
| 4371- | AgNPs, | Effects of Green Silver Nanoparticles on Apoptosis and Oxidative Stress in Normal and Cancerous Human Hepatic Cells in vitro |
| - | in-vitro, | Liver, | HUH7 |
| 344- | AgNPs, | Cytotoxicity and ROS production of manufactured silver nanoparticles of different sizes in hepatoma and leukemia cells |
| - | in-vitro, | Liver, | HepG2 |
| 369- | AgNPs, | Silver nanoparticles induce oxidative cell damage in human liver cells through inhibition of reduced glutathione and induction of mitochondria-involved apoptosis |
| - | in-vitro, | Liver, | NA |
| 3384- | ART/DHA, | Dihydroartemisinin triggers ferroptosis in primary liver cancer cells by promoting and unfolded protein response‑induced upregulation of CHAC1 expression |
| - | in-vitro, | Liver, | Hep3B | - | in-vitro, | Liver, | HUH7 | - | in-vitro, | Liver, | HepG2 |
| 727- | Bor, | RSL3, | erastin, | Enhancement of ferroptosis by boric acid and its potential use as chemosensitizer in anticancer chemotherapy |
| - | in-vitro, | Liver, | HepG2 |
| 5919- | Cats, | Cisplatin, | Uncaria tomentosa Leaves Decoction Modulates Differently ROS Production in Cancer and Normal Cells, and Effects Cisplatin Cytotoxicity |
| - | in-vitro, | Liver, | HepG2 |
| 6176- | Cu, | Copper Oxide Nanoparticles Induced Mitochondria Mediated Apoptosis in Human Hepatocarcinoma Cells |
| - | in-vitro, | Liver, | HepG2 |
| 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 |
| 481- | CUR, | CHr, | Api, | Flavonoid-induced glutathione depletion: Potential implications for cancer treatment |
| - | in-vitro, | Liver, | A549 | - | in-vitro, | Pca, | PC3 | - | in-vitro, | AML, | HL-60 |
| 1620- | EA, | Rad, | Radiosensitizing effect of ellagic acid on growth of Hepatocellular carcinoma cells: an in vitro study |
| - | in-vitro, | Liver, | HepG2 |
| 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 |
| 5106- | SSE, | GSH, | Dual role of glutathione in selenite-induced oxidative stress and apoptosis in human hepatoma cells |
| - | in-vitro, | Liver, | HepG2 |
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:14 Cells:% prod#:% Target#:137 State#:% Dir#:1
wNotes=0 sortOrder:rid,rpid