Vitamin E in gastric mucosal injury induced by ischemia-reperfusion

Am J Clin Nutr. 1991 Jan;53(1 Suppl):210S-214S. doi: 10.1093/ajcn/53.1.210S.


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 alpha-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 alpha-tocopherol-cholesterol ratio and gastric mucosal alpha-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.

MeSH terms

  • Animals
  • Cholesterol / blood
  • Gastric Mucosa / blood supply
  • Gastric Mucosa / chemistry
  • Gastric Mucosa / metabolism*
  • Gastric Mucosa / pathology
  • Ischemia
  • Lipid Peroxidation
  • Male
  • Rats
  • Rats, Inbred Strains
  • Reperfusion Injury / metabolism*
  • Reperfusion Injury / pathology
  • Vitamin E / analysis
  • Vitamin E / blood
  • Vitamin E / metabolism*
  • Vitamin E Deficiency / metabolism*
  • Vitamin E Deficiency / pathology


  • Vitamin E
  • Cholesterol