Kim H, Kim K H
Department of Pharmacology and Institute of Gastroenterology, Yonsei University College of Medicine, Seoul, Korea.
Pharmacology. 1998 Dec;57(6):323-30. doi: 10.1159/000028258.
The present study aims at investigating the effects of nitric oxide (NO) on hydrogen peroxide (H2O2)-induced damage in isolated rabbit gastric glands. NO synthesis modulators such as L-arginine and NG-nitro-L-arginine methyl ester (L-NAME) and an NO donor, sodium nitroprusside, were added to isolated rabbit gastric glands exposed to H2O2, generated by glucose oxidase acting on beta-D-glucose. As a result, glucose/glucose oxidase caused an increase in lipid peroxide production and decreases in reduced glutathione (GSH) content, GSH peroxidase activity, nitrite release, and mucus secretion in gastric glands. The alterations in lipid peroxide production, GSH content, and mucus secretion were prevented by pretreatment with L-arginine, a substrate for NO synthase and sodium nitroprusside, but not by L-NAME. In conclusion, NO protects gastric glands from H2O2 by inhibiting lipid peroxidation and maintaining cellular GSH content and mucus secretion.
