Disease relevance of glutathione disulfide

• Dietary selenium markedly increased activity of plasma GSH peroxidase and partially retarded the rates of hemolysis and methomoglobin formation, but it had no significant effect on the erythrocyte levels of GSH, GSH reductase, catalse, G6P dehydrogenase and superoxide dismutase or plasma vitamin E levels of young rats [1].
• We conclude that insulin in patients with type 2 diabetes mellitus can reduce intracellular oxidative stress through increased GSH/GSSG ratio [2].
• 3. With respect to glutathione inhibition of glutathione-disulphide reduction (at constant [NADPH]), the human enzyme was inhibited uncompetitively; the bovine and yeast enzymes displayed apparent mixed hyperbolic inhibition; the E. coli enzyme was inhibited competitively [3].

High impact information on glutathione disulfide

• In these cell lines, levels of DNA polymerase beta, glutathione (GSH), GSH transferase, GSH reductase (NAD(P)H), gamma-glutamyltransferase did not correlate with radiation parameters of sensitivity [4].
• In patients randomized to receive GSH, GSH was given at a dose of 1.5 g/m2 in 100 mL of normal saline solution over a 15-minute period immediately before CDDP administration, and at a dose of 600 mg by intramuscular injection on days 2 to 5 [5].
• Glutathione-glutathione peroxidase (GSH-GSH peroxidase), an extracellular H2O2 scavenger, totally protected neutrophil myeloperoxidase from inactivation by azide plus glucose-glucose oxidase [6].
• To test the hypothesis that DNA damage was being prevented by conjugation of F23Q with GSH, GSH-depleted cells were treated with both quinones [7].
• Although we observed no sex differences for GSH, GSH/hemoglobin ratios were 8-18% greater in women < 55 years old than in older subjects (P < 0.05) [8].

Biological context of glutathione disulfide

• C20 cells did not differ from the parent cell line with respect to cell cycle distribution, doubling time, GSH, GSH peroxidase, GSH reductase or GSH transferase levels [9].
• The objective of this study was to determine the influence of insulin on oxidative stress, defined as a reduced intracellular GSH/GSH disulfide (GSSG) ratio and lipid peroxidation by plasma thiobarbituric acid reactive substances (TBARSs) in patients with type 2 diabetes [2].
• We confirmed that our patients underwent oxidative stress as shown by the significant difference in intracellular GSH/GSSG ratio in diabetic patients as compared to controls (13.56 +/- 3.84 vs 27.89 +/- 8.37, P < .0001) [2].

Anatomical context of glutathione disulfide

• Thus, the results indicate that a GSH-GSH peroxidase-insensitive pool of H2O2 is also generated, presumably at the plasma membrane, and this pool of H2O2 can undergo direct internal diffusion to inactivate myeloperoxidase [6].
• Cisplatin induced a decrease in cytochrome P-450, GSH, GSH S-transferase, GSH reductase and GSH peroxidase activities, and an increase in N-glucuronyl transferase, lipid peroxidation and oxidized glutathione (GSSG) in kidney cortical microsomes and cytosolic fractions [10].

Associations of glutathione disulfide with other chemical compounds

• The constituent amino acids of reduced glutathione (GSH), GSH itself, and D-alpha-tocopherol inhibited 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced ornithine decarboxylase (ODC, L-ornithine carboxy-lyase, EC 4.1.1.17) activity in mouse epidermis in vivo and in vitro [11].
• PH(3) significantly decreased GSH, GSH peroxidase and catalase, while significantly increased lipid peroxidation (as malondialdehyde and 4-hydroxyalkenals), DNA oxidation (as 8-hydroxydeoxyguaonsoine) and superoxide dismutase (SOD) levels in kidney and heart [12].
• Further, the antioxidant components GSH, GSH Px and CuZn SOD and the relationships among them, were affected differently in the liver and blood by diabetes or vitamin E supplementation [13].

Gene context of glutathione disulfide

• The results of the present study indicate that resistance in LoVo/C7 cells cannot be attributed to alterations in P-gp, LRP or GSH/GSH-dependent enzyme levels [14].
• In preterm babies significant correlations were found between G-6-PDH and CAT, GSH, GSH/GSSG ratio, and GSSG (r = -0.67, r = 0.71, r = -0.66, p < 0.01; r = 0.71, p < 0.05, respectively) [15].
• We aimed to investigate serum GSH, GSH-dependent enzymes activities (GSH-Px and GST), XO, CAT, Cu-Zn SOD activity, and NO*, and MDA levels in patients with NSCLC and with SCLC and correlate with the cancer stage [16].

References