Disease relevance of reduced glutathione

• CONCLUSIONS: Acute hyperglycemia in newly diagnosed type 2 diabetic patients causes significant hemodynamic changes that are independent of endogenous insulin and are prevented by glutatione and reversed by L-arginine, suggesting an interference with endogenous NO availability [1].
• The cobalt-induced H2O2 decrease seems to be caused by an increased activity of the glutathion peroxidase that is also induced under hypoxia [2].
• To study the rescue effect of antioxidants on retinal degeneration, rd1 retinas were studied in vitro and in vivo using lutein, zeaxanthin, alpha lipoic acid and reduced l-glutathione [3].
• Glutathion S-transferase (class mu) phenotype in Parkinson's disease [4].
• This study examined the effect of simulated ischemia (deprivation of both oxygen and substrate) on astrocyte reduced-glutathione (GSH) [5].

Psychiatry related information on reduced glutathione

• Oxygen-derived free radicals are controlled by various cellular defense mechanisms consisting of enzymatic such as superoxide dismutase, catalase, glutathion peroxidase and nonenzymatic scavenger components [6].

High impact information on reduced glutathione

• Topical administration of diethyl maleate (DEM) and L-methionine sulfoximine (MS) reduced the L-glutathione (GSH) levels in kidneys, livers, and skin of inbred BALB/c mice [7].
• Generation of hydrogen peroxide after stimulation of erythrocytes with methylene blue was evaluated by the catalase-aminotriazole trapping technique, [14C]formate oxidation, and oxidation of reduced glutatione [8].
• Tissue pH, ATP, the antioxidant enzymes superoxide dismutase, catalase, and glutathion peroxidase, lipid peroxidation products, carbonyls, and aromatic hydroxylation were also tested [9].
• Two different in vitro qualitative assays-yeast two-hybrid and glutathion S-transferase pull-down competition-were performed in order to investigate functional changes in Tcap's interaction with MLP, titin, and calsarcin-1 caused by the identified mutations and a reported DCM-associated mutation, R87Q [10].
• Our previous studies have shown that glutathione is an essential metabolite in the yeast Saccharomyces cerevisiae because a mutant deleted for GSH1, encoding the first enzyme in gamma-l-glutamyl-l-cysteinylglycine (GSH) biosynthesis, cannot grow in its absence [11].

Chemical compound and disease context of reduced glutathione

• Clofibrate seems to stabilize glutathion content and this might contribute to the prevention of liver steatosis [12].
• A 50-year-old woman suffered from a diffuse skin rash, high fever and jaundice immediately after a second injection of glutathion and Stronger Neo-minophagen C which contains glycyrrhizin [13].
• The mutagenic effect of 1,2-dichloroethane on Salmonella typhimurium I. Activation through conjugation with glutathion in vitro [14].

Biological context of reduced glutathione

• Previous work showed that the susceptibility of oligodendroglial progenitors to oxidative stress is related to their low reduced-glutathione (GSH) and high iron contents [15].
• Results showed that N-acetylcysteine and glutathion can protect astrocytes against ROS accumulation and caspase-3 activation, whereas 0.1 mM melatonin can inhibit H2O2-induced apoptosis by regulating Bax expression and by inhibiting caspase-3 activation [16].
• The identified genes can be grouped into two functional groups: Group 1: genes involved in cell protection (i.e. glycosyltransferases, glutathion S-transferases), and Group 2: genes involved in signal transduction (protein kinases and transcription factors) [17].
• The L-glutathione conjugate of 1,2-dibromo-3-chloropropane was chemically synthesized and used to alkylate DNA: following incubations of the conjugate with calf thymus DNA and neutral thermal hydrolysis (to release N7-guanyl adducts) four major fluorescent products were observed [18].
• The method showed that most enzymes of glycolysis and hexose monophosphate shunt were localized in the cytosol except for hexokinase (96% particle bound), phosphoglucose isomerase (10% bound) and glutathion reductase (26% bound) [19].

Anatomical context of reduced glutathione

• Furthermore, addition of the antioxidants l-cystine and l-glutathione to cytokine/LPS-stimulated adipocytes mimicked the lipolytic effect of iNOS inhibition [20].
• The carotid artery was then introduced into a glutide pipe-splint [21].
• This reflected artery wall and the glutide were covered by the freed-up jugular vein [21].
• Glutatione peroxidase in bovine semen [22].
• As tert-butyl hydroperoxide is metabolized by the glutatione peroxidase--glutathione reductase enzyme system present in liver mitochondria, rapid and extensive oxidation of NADH and slow NADPH oxidation are observed [23].

Associations of reduced glutathione with other chemical compounds

• Vitamin E depletion decreased the cellular vitamin E content, but did not change the activity of antioxidant enzymes (catalase, superoxide dismutase) and the glutathion (GSH)/oxidized glutathion (GSSG) ratio in alveolar type II cells [24].
• The structural analysis of the intermediates formed during the refolding of RNase A showed for the first time that Grx is actually able to catalyze both formation and reduction of mixed disulfides involving glutatione [25].
• S-Methylglutathione was hydrolyzed at a slightly higher rate than glutatione by liver gamma-glutamyltransferase [26].
• Catalase activity and malondialdehyde levels were increased but glutathion levels were unchanged in rats fed HFD plus clofibrate [12].
• Lymphoblastoid cells grown in the presence of 20 microM indirect methyltransferase inhibitor adenosine dialdehyde (AdOx) for 72 h appeared to accumulate high levels of hypomethylated proteins for the endogenous protein methyltransferase or recombinant glutathion S-transferase-fused yeast arginine methyltransferase (RMT1) [27].

Gene context of reduced glutathione

• However, unlike par1 mutants, which showed diminished activities of oxidative-stress enzymes and glutathion level, the pos9 mutants did not reveal any such changes [28].
• Superoxide dismutases, catalase, and glutathion peroxidase are proteins involved in the endogenous antioxidant defence system [29].
• In the present studies, the effect of 24 and 72 h administration of ethanol (50 mM). acetaldehyde (175 microM), and LPS (1 microg/ml) were studied on the expression and secretion of TNF-alpha, IL-1beta, IL-6, and TGF-beta3, lipid peroxidation damage and glutathion content in HepG2 cell cultures [30].
• In order to quantify the redox properties of the different complexes consisting of Abeta/alphaB-crystallin/copper, we suggest an NMR assay which allows to estimate the electrochemical properties indirectly by monitoring the rate of glutathion (GSH) auto-oxidation [31].
• Malondialdehyde, TNF-alpha, and IL-6 levels decreased in NTG and L-NTG groups, whereas catalase and glutathion levels increased in NTG, L and L-NTG groups compared to control group (p < 0.05) [32].

Analytical, diagnostic and therapeutic context of reduced glutathione

• We assessed in a mouse model the efficiency of a combined therapy, based on the combination of PZQ chemotherapy with Schistosoma mansoni 28-kDa glutathion S-transferase (Sm28GST) DNA vaccination, designed to limit the pathology [33].
• The expressed proteins, fused to glutathion S-transferase, were purified by glutathion-Sepharose 4B affinity chromatography and cleaved with thrombin, followed by gel filtration chromatography [34].
• Optimization and characterization studies of the biosensor were carried out and a linearity in the gamma-L-glutamyl-L-cysteinyl-glycine (GSH) concentration range 0.1-2 microM was obtained when 600 microM ascorbic acid was used as a substrate [35].
• The intracellular fluorescence level of cells stained continuously with monochlorobimane was monitored by flow cytometry in order to assess the initial rate of glutatione to monochlorobimane conjugation as a measure of glutathione S-transferase activity [36].
• Brain ischemic preconditioning is abolished by antioxidant drugs but does not up-regulate superoxide dismutase and glutathion peroxidase [37].

References