Role of oxygen radicals in the pathogenesis of gastric mucosal lesions induced by water-immersion restraint stress and burn stress in rats.

Abstract

The formation of gastric mucosal lesions and the increase in thiobarbituric acid (TBA)-reactive substances induced by water-immersion restraint stress or burn stress in rats were significantly inhibited by the treatment with superoxide dismutase (SOD) and/or catalase. Allopurinol inhibited the formation of gastric mucosal injury induced by burn stress, but not the increase in TBA reactants. A drop in the polymorphonuclear leukocyte (PMN) count induced by an injection of anti-rat PMN antibody did not inhibit the aggravation of gastric mucosal lesions or the increase in TBA reactants in either of the stress models. These results suggest that active oxygen species and lipid peroxidation may play a role in the formation of gastric mucosal damage induced by stress. Reduced microcirculation of the gastric mucosa induced by water-immersion restraint or burn stress did not change following treatment with SOD and/or catalase, suggesting that the effectiveness of SOD and catalase on the gastric mucosal lesions induced by stress may occur via the scavenging of oxygen radicals, and not through an effect on gastric mucosal microcirculation.