Disruption of gastric mucosal antioxidant defense system and its relation to the development of gastric mucosal lesions in rats with repeated treatment of compound 48/80, a mast cell degranulator

Abstract

Abstract The disruption of gastric mucosal antioxidant defense system and its relation to the development of gastric mucosal lesions was examined in Donryu rats treated once daily with compound 48/80 (0.75 mg/kg body weight), a mast cell degranulator, over a four day period. Mucosal lesions appeared after the 1st treatment and developed as the treatment was repeated. Mucosal lipid peroxide levels increased with an increase in the treatment period. Xanthine oxidase activity increased with a decrease in xanthine dehydrogenase activity in the mucosal tissue during the treatment, although the sum of both activities did not change during the treatment. Mucosal myeloperoxidase activity increased with an increase in the treatment period. Mucosal superoxide dismutase activity decreased after the 2nd treatment and a further decrease in activity occurred until the end of the treatment. Mucosal catalase and Se-dependent glutathione peroxidase activities decreased with an increase in the treatment period. A relatively constant decrease in mucosal glutathione reductase activity occurred after the 2nd, 3rd, and 4th treatment. Neither mucosal glucose-6-phosphate dehydrogenase activity nor nonprotein SH content changed during the treatment. A relatively constant decrease in mucosal vitamin E content occurred during the treatment. Mucosal hexosamine content decreased after the 1st treatment. But, mucosal hexosamine content in the compound 48/80-treated rats was equal to the control level after the 2nd treatment and was over the control level after the 3rd and 4th treatment. These results suggest that in rats with repeated compound 48/80-treatment, the disruption of gastric mucosal antioxidant defense system could be related to the development of gastric mucosal lesions.