AIM To determine the effect of glutathione (GSH) on stress gastric mucosal lesion.METHODS The stress gastric mucosal lesion as produced by restraint water-immersion in rats and gastricmucosal lesion, gastric mucosal GSH content, gastric acid secretion and gastric barrier mucus secretion wereexamined. We also observed the effect of GSH on gastric mucosal lesion and the effect of N-ethylmaleimine(NEM) and indomethacin on GSH protection. Comparisons between two groups were made using the Students t test.RESULTS GSH (100 and 200 mg/kg) intraperitoneally protected against stress gastric mucosal lesion(P<0.001 and P<0.001). Restraint water-immersion stress significantly reduced gastric mucosal GSHcontent (P < 0.001), but pretreatment with GSH (100 mg/kg) had no effect on gastric mucosal GSH content(P>0.05). The preinjection of NEM (10 mg/kg, sc.), a sulfhydryl-blocking reagent, or indomethacin(5 mg/kg, im.), a cyclooxygenase inhibitor, had no effect on protection of GSH (P>0.05). GSH(100mg/kg) significantly increased secretion of gastric barrier mucus (P<0.05), but had no effect onsecretion of gastric acid in restraint water-immersed rats (P >0.05).CONCLUSION GSH can inhibit the formation of gastric mucosal lesions induced by restraint water-immersion. The protective effect of GSH was due, in part, to promoting the secretion of gastric barriermucus, but not to suppress the gastric acid secretion. The protection effect of GSH has no relation withgastric mucosal GSH and PGs.

Free radicals induced by traumatic brain injury have deleterious effects on the function and antioxidant vitamin levels of several organ systems including the brain. Melatonin possesses antioxidant effect on the brain by maintaining antioxidant enzyme and vitamin levels. We in-vestigated the effects of melatonin on antioxidant ability in the cerebral cortex and blood of traumatic brain injury rats. Results showed that the cerebral cortex β-carotene, vitamin C, vita-min E, reduced glutathione, and erythrocyte reduced glutathione levels, and plasma vitamin C level were decreased by traumatic brain injury whereas they were increased following melatonin treatment. In conclusion, melatonin seems to have protective effects on traumatic brain inju-ry-induced cerebral cortex and blood toxicity by inhibiting free radical formation and supporting antioxidant vitamin redox system.