SummaryThe role of lipid peroxidation in the pathogenesis of gastric ulcer was investigated in a rat model produced by water-immersion restraint stress. After the immersion of rats in 23°C water with restraint, blood flow of the gastric wall was significantly decreased and hemorrhagic erosions were seen in the body of the stomach. Thiobarbituric acid-reactive substances, an index of lipid peroxidation, in the gastric mucosa were significantly increased after the stress. These results suggest that lipid peroxidation may play a role in the pathogenesis of gastric mucosal lesions induced by stress.

The role of lipid peroxidation in the pathogenesis of gastric ulcer was investigated in a rat model produced by burn shock. After the immersion of rats in 80•Ž water for 10 min, blood pressure was significantly decreased, and serum levels of lysosomal enzymes, such as acid phosphatase and ƒÀ-glucuronidase were significantly increased. These findings

SummaryThe formation of gastric mucosal lesions and the increase in thiobarbituric acid (TBA)-reactive substances induced by waterimmersion 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 waterimmersion 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.

SummaryWe measured serum superoxide dismutase activity by electron spin resonance, using 100 m1vl 5, 5-dimethyl-l -pyrroline-N-oxide (DMPO) as a trap. The addition of superoxide dismutase decreased the height of the DMPO-OOH signal produced by the hypoxanthine-xanthine oxidase system. Serum superoxide dismutase activity was determined from a quantitative line for superoxide dismutase. When bovine Cu,Znsuperoxide dismutase (50,000 U/kg) was injected intravenously into rats, the superoxide dismutase activity decreased almost linearly with a half life of about 6 min. This method allowed direct detection of superoxide radicals and new measurement of superoxide dismutase activity.

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