Vitamin E in gastric mucosal injury induced by ischemia-reperfusion

• Published in: The American journal of clinical nutrition Vol. 53; no. 1; pp. 210S - 214S
• Main Authors: Yoshikawa, T, Yasuda, M, Ueda, S, Naito, Y, Tanigawa, T, Oyamada, H, Kondo, M
• Format: Journal Article Conference Proceeding
• Language: English
• Published: Bethesda, MD Elsevier Inc 01.01.1991; American Society for Clinical Nutrition
• Subjects: Animals; Biological and medical sciences; Cholesterol - blood; Gastric Mucosa - blood supply; Gastric Mucosa - chemistry; Gastric Mucosa - metabolism; Gastric Mucosa - pathology; gastric mucosal injury; Ischemia; ischemia-reperfusion; Lipid Peroxidation; Male; Medical sciences; oxygen radicals; Rats; Rats, Inbred Strains; Reperfusion Injury - metabolism; Reperfusion Injury - pathology; Traumas. Diseases due to physical agents; Vitamin E; Vitamin E - analysis; Vitamin E - blood; Vitamin E - metabolism; Vitamin E Deficiency - metabolism; Vitamin E Deficiency - pathology; gastric mucosal injury; ischemia-reperfusion; oxygen radicals; Vitamin E; lipid peroxidation; Stomach; Reperfusion; Ischemia; Animal; Mucosa; Exploration; Lipids; Tocopherol; Trauma; Peroxidation
• ISSN: 0002-9165; 1938-3207
• 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 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.