Vitamin E in gastric mucosal injury induced by ischemia-reperfusion

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Abstract
To clarify the relationship among vitamin E, oxygen radicals, and lipid peroxidation in ischemia-reperfusion, we produced an experimental model of gastric mucosal injury in rats by ischemia-reperfusion with clamping of the celiac artery and measurements of the area of gastric erosion, thiobarbituric acid (TBA)-reactive substances, and α-tocopherol in serum and gastric mucosa during ischemia-reperfusion. The area of gastric erosions and TBA-reactive substances in gastric mucosa were significantly increased after 30 and 60 min of reperfusion. The serum α-tocopherol-cholesterol ratio and gastric mucosal α-tocopherol were significantly decreased after 30 and 60 min of reperfusion. On the other hand, in vitamin E–deficient rats, gastric mucosal injury induced by ischemia-reperfusion was more severe than that in vitamin E–nondeficient rats. These results indicate that vitamin E is consumed in the process of lipid peroxidation induced by oxygen radicals in ischemia-reperfusion to prevent the development of tissue damage.