Gatric mucosa is exposed to toxic, reactive oxygen species generated within the lumen. Nitric oxide protected acetaminophen-induced hepatotoxicity by maintaining glutathione homeostasis. The present study examined the role of nitric oxide in mediating hydrogen peroxide-induced damage to gastric cells. Hydrogen peroxide was generated by glucose oxidase acting on β-D-glucose. L-arginine, N(G)-nitro-L-arginine methyl ester, or N(G)-nitro-L-arginine were treated to the cells with glucose/glucose oxidase. Lipid peroxidation and nitrite release and cellular content of glutathione were determined. As a result, dose-dependent increase in lipid peroxide production as well as dose-dependent decrease in nitrite release and cellular glutathione content were observed in glucose/glucose oxidase-treated cells. Pretreatment of L-arginine, a substrate for nitric oxide synthase, prevented the increase of lipid peroxide production and the reduction of nitrite release as well as glutathione content. Inhibitors of nitric oxide synthase such as N(G)-nitro-L-arginine methyl ester and N(G)-nitro-L-arginine did not protect hydrogen peroxide-induced cell damage. In conclusion, nitric oxide protects gastric cells from hydrogen peroxide possibly by inhibiting lipid peroxidation and by preserving cellular glutathione stores.
|Number of pages||9|
|Journal||Korean Journal of Pharmacology|
|Publication status||Published - 1996|
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