Glutathione oxidation products

BSS with the addition of glutathione (oxidized) and dextrose as energy sources, bicarbonate as a physiological buffer, and a phosphate buffer system to maintain the products storage pH in the physiological range [296,297],... 

Alternatively, acrylonitrile is metabolized to 2-cyanoethylene oxide by the microsomal enzyme system. 2-Cyanoethylene oxide can react directly with tissue macromolecules or it can be further metabolized to oxidation products that release cyanide. Cyanide is converted to thiocyanate and excreted in the urine. 2-Cyanoethylene oxide is also conjugated with glutathione and metabolized to 2- hydroxyethylmercapturic acid which is excreted in the urine. 

The capacity of furoxan derivatives to behave as NO-donors was first demonstrated by Feelisch et al. [19], who showed that furoxan derivatives produce nitric oxide when dissolved in physiological solution in the presence of thiols. Among the reaction products, they isolated nitrite and, in lesser amounts, nitrate, which are the final oxidation products of nitric oxide in aerobic water solution, as well as dioxime derivatives, which are the reduction products of the furoxans. They also evidenced a marked p H -dependent production of S-nitrosothiols. Working with N, AF-diisopropylfuroxan-3,4-dicarboxamide (29, Ipramidil) and an excess of glutathione (GSH), the amount of S-nitrosoglutathione formed increased with increasing pH until pH 9, above which it... 

Direct evidence of the reaction of PAN with sulfhydryl compounds has since been obtained (PAN at 115 ppm for 1-10 min). - In the reaction with glutathione, the major products are oxidized glutathione (disulfide) and 5-acetylglutathione. Other sulfhydryl compounds (e.g., coenzyme A, lipoic acid, and cysteine) yield only oxidation products, with no evidence of 5-acetylation. However, acetylation reactions have been observed with alcohols and amines. Sulfur compounds other than thiols can undergo oxidation by PAN methionine is converted to methionine sulfoxide, and oxidized lipoic acid (disulfide) is converted to sulfoxide. 

Oxidant production (e.g., dihydroethidium, dichlorofluor-escein), antioxidant changes (e.g., glutathione = mono-chlorobimane), antioxidant system enzyme, resistance to dye oxidation (e.g., total antioxidant status), macromolec-ular oxidation byproducts (e.g., malondialdehyde, hydro-xynonenal, 8-hydroxyguanosine)... 

The interaction of unspecified catecholamine oxidation products with certain sulfhydryl compounds, including cysteine, glutathione, and coenzyme A, has been studied by Roston.85- 88 It appeared that... 

Oxidation, demethylation, and other alterations are catalyzed by one or more of the nearly 300 cytochrome P450 monooxygenases present in the liver (step c). Oxidation products may be detoxified by glutathione S-transferases, step d (see also Box ll-B).b,c,cc... 

Values are mean SEM. LPO lipid peroxidation NOPs nitric oxide products SOD superoxide dismutase GSH reduced glutathione GSSG oxidized glutathione GR glutathione reductase GSHPx glutathione peroxidase MT metallothionein. p < 0.05 versus untreated control group. (Adapted from Ayaz and Turan, 2006.)... 

Certain oxidation products of proteins, such as oxidation of Cys to cystine, and Met residues to methionine sulfoxide can be repaired by enzymes such as glutathione reductase and methionine sulfoxide (Gabbita et al., 1999 Moskovitz et al.,... 

Kim, Y.B., Lee, Y.S., Choi, D.S., Cha, S.H., Sok, D.E. (1996h). Change in glutathione S-transferase and glyceraldehyde-3-phosphate dehydrogenase activities in the organs of mice treated with 2-chloroethyl ethyl sulfide or its oxidation products. Food Chem. Toxicol. 34 259-65. 

In an earlier study of the effects of imipenem in the rabbit kidney it was shown that imipenem caused a significant decrease of mitochondrial respiration, deplehon of reduced glutathione, increased production of oxidized glutathione and lipid peroxidation [56]. However, these effects were less than those produced by a comparable nephrotoxic dose of cephaloridine [56]. Panipenem induced nephrotoxicity at a dose of 200 mg/kg, i.v., but this was less severe than that caused by a single dose of imipenem [57]. Simultaneous adminis-trahon of p-mipron (N-benzoyl-3-propionic acid) with imipenem and panipenem reduced the nephrotoxicity of these carbapenems by inhibiting the active transport of carbapenems in the renal cortex [57]. 

The oxidative product of ascorbic acid, dehydroascorbic acid, is the preferred form of the vitamin for uptake by neutrophils, erythrocytes, and lymphocytes (27). Once within the erythrocyte, dehydroascorbic acid is reduced to ascorbic acid by a glutathione-dependent, dehydro-ascorbic-acid-reducing enzyme (20,28). However, the reduced form of ascorbic acid is found in most other tissues, that is, liver, lungs, kidneys, skin, and pituitary and adrenal glands (20,29). From these studies, ascorbic acid is taken up by several tissues by an energy-dependent and Na -sensitive process, but the transport of the oxidized vitamin form follows the principles of diflFusion. 

Pu, Y., McCormick, C.C., Roneker, C., and Lei, X.G. (2001). Lipopolysaccharide and interferon-gamma-induced nitric oxide production and protein oxidation in mouse peritoneal macrophages are affected by glutathione peroxidase-1 gene knockout. Free Radic Biol Med 31, 450-9. 

Pullar, J.M., Vissers, M.C., and Winterboum, C.C. (2001). Glutathione oxidation by h3fpochlorous acid in endothelial cells produces glutathione sulfonamide as a major product but not glutathione disulfide. J Biol Chem 276, 22120-5. 

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