686 INTESTINAL LIPID PEROXIDATION: INFLUENCE OF ISCHEMIA AND VITAMIN E DEFICIENCY

Abstract

Free radical mechanisms are important mediators of ischemic injury in many tissues. Unscavenged free radicals can react with cellular fatty acids leading to fatty acid peroxidation (FAP) and loss of membrane function and integrity. Vitamin E (vit E) is an important defense against free radical injury. We have developed a model to explore the susceptibility of small intestinal mucosa to FAP in response to ischemia and vit E deficiency. Vit E deficient and replete Sprague-Dawley rats were subjected to mesenteric artery occlusion of 45 min followed by a 15 min reperfusion period. Nonoccluded control animals, vit E deficient and replete, were subjected to sham, time matched laparotomy and exposure. Following ischemia and reperfusion or sham operation, intestinal mucosal scrapings from separate portions of the gut (duodenum, jejunum, and ileum) were homogenized and assayed for in vitro FAP based on thiobarbituric acid assay of malondialdehyde. With n=4 for each of the four groups (vit E deficient and replete, with and without arterial occlusion) the following observations have been made: 1) there is no difference in FAP between control and vit E deficient rats in the duodenum and no changes in FAP are observed in this proximal gut segment with ischemia; 2) significantly greater (p<0.05) FAP occurs in the jejunum and ileum of nonoccluded vit E deficient compared to replete animals; 3) ischemia causes no change in FAP in any gut segment of replete animals, but causes a significant (p<0.05) further increase in FAP in the ileum of vit E deficient animals.