The present study examined the effect of nitric oxide (NO) on hydrogen peroxide (H^2O^2) - induced damage in isolated rabbit gastric cells. H^2O^2 was generated by glucose oxidase acting on β-D-glucose. To modulate No synthesis, L-arginine and/or N^G...
The present study examined the effect of nitric oxide (NO) on hydrogen peroxide (H^2O^2) - induced damage in isolated rabbit gastric cells. H^2O^2 was generated by glucose oxidase acting on β-D-glucose. To modulate No synthesis, L-arginine and/or N^G-nitro-L-arginine methyl ester were treated to the cells exposed to glucose/glucose oxidase. Glutathione redox cycle inhibitors (1-chloro-2,4-dinitrobenzene, 1,3-bis-chloroethy-1-nitrosourea, DL-buthionine-S,R-sulfoximine) with or without L-arginine were treated to normal cells. Lipid peroxide production and NO_2 contents in medium as well as glutathione contents and glutathione peroxidase activities of the cells were determined. As a result, concentration - and time - dependent increase in lipid peroxidation and decrease in NO_2 contents in medium as well as glutathione contents and glutathione peroxidase activities were observed in glucose/glucose oxidase - treated cells. Pretreatment of L-arginine, a substrate for No synthase, prevented the increase in lipid peroxide production and the decrease in cellular glutathione contents. NO synthase inhibitor N^G-nitro-Larginine methyl ester did not protect H^2O^2 - induced cell damage. Glutathione redox cycle inhibitors decreased glutathione content and increased lipid peroxidation. L-Arginine inhibited the increase in lipid peroxidation induced by glutathione redox cycle inhibitors. In conclusion, NO protects gastric cells from H^2O^2 by inhibiting lipid peroxidation and by maintaining cellular glutathione stores.