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• W2016113921 abstract "Recent studies suggest that in some cell types, the activity of nitric oxide (NO) is influenced by the endogenous antioxidant, reduced glutathione (GSH). The present study has examined the role of GSH in NO-induced cytotoxicity in cells harvested from the rat gastric mucosa. Cell integrity was assessed by Trypan blue exclusion and alamar blue dye absorbance. Pretreatment of rats with bacterial endotoxin lipopolysaccharide increased Ca2+-independent NO synthase (iNO synthase) activity (as detected by the radiolabeled conversion of [14C]arginine to [14C]citrulline, lowered GSH content and increased cell injury. Lipopolysaccharide treatment also resulted in a significant increase in the in vitro production of reactive oxygen metabolites as assessed by the fluorescent probe 2′,7′-dichlorofluorescein diacetate. Inhibition of iNO synthase activity by dexamethasone and NG-nitro-l-arginine methyl ester prevented these effects. Similarly, the NO donor, S-nitroso acetyl-penicillamine depleted GSH stores and damaged cells in a dose-dependent manner. The effects of S-nitroso acetyl-penicillamine were diminished by the NO scavenger, 2-phenyl-4,4,5,5,-tetramethylimidazoline-1-oxyl-3-oxide. In contrast, incubating cells with N-acetyl-l-cysteine to augment endogenous GSH synthesis, prevented the effects of S-nitroso acetyl-penicillamine. Reduction of GSH stores by pretreatment of rats with buthionine sulfoximine or incubating cells in vitro with diethyl maleate, increased oxidant production and exacerbated NO-induced cell injury. These results suggest that excessive levels of NO alter GSH homeostasis and increase the generation of oxidants leading to increased gastric cellular injury." @default.
• W2016113921 created "2016-06-24" @default.
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• W2016113921 date "1997-01-01" @default.
• W2016113921 modified "2023-09-27" @default.
• W2016113921 title "Role of glutathione in nitric oxide-mediated injury to rat gastric mucosal cells" @default.
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• W2016113921 doi "https://doi.org/10.1016/s0014-2999(96)00865-5" @default.
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