摘要：Damage to gastric mucosa caused by restraint stress has been attributed to impaired blood flow that resulted in ischemia followed by reperfusion, a process that generates free radical s. Therefore oxygen radicals may mediate the lesions produced in restraint stress. To test this hypothesis, we studied the effect of free radical scavengers on restraint-induced lesions in rats. Forty rats were divided in to four groups of 10 rats. Two control groups was fed with a normal rat diet and two treatment groups fed with a vitamin E deficient diet with either tocopherol or tocotrienol, which serves as free radical scavengers. The two forms of vitamin E were administered orally at 60mg/kg body weight for 28 days. After 28 days, rats from one control group and the two treated groups were subjected to restraint stress 2 hours daily for 4 consecutive days. The rats were killed after the fourth exposure, their stomach isolated and examined for lesions, and gastric malondialdehyde (MOA) content and the gastric reduced glutathione level were measured as an index to reflect the scavenging abilities of tocopherol and tocotrienol. Both the regimes significantly attenuated the total lesion area in the stomach compared to the control. The MOA content was also significantly lower in the rats given tocopherol and tocotrienol supplementation compared to the control and the reduced glutathione levels were preserved in rats supplemented with both tocopherol and tocotrienol. We conclude that it is indeed probable that oxygen radical is involved in the pathogenesis of restraint stress-induced lesions thus supplementation with antioxidant such as vitamin E may be able to reduce or inhibit the formation of these lesions.
