Effects of antiperoxidants on FeCl2-induced lipid peroxidation and focal edema in rat brain.
Head trauma with contusion or cortical laceration and hemorrhage causes focal edema with encephalomalacia and gliosis. Because cerebral hemorrhage ultimately results in deposition of heme compounds and iron into the neuropil, we injected an aqueous solution of iron salts to simulate the decompartmentalization of iron after trauma. We pretreated animals with saline or with 600 mg/kg alpha-tocopherol plus 5 ppm selenium added to the drinking water. Formation of lipid peroxidation products was significantly inhibited within the iron injection site in the antiperoxidant-pretreated rats at 30, 60, and 120 min after injection of iron into the isocortex. The antiperoxidants failed to prevent formation of focal brain edema at the injection site between 1 and 8 h after injection; however, significantly less edema was present in the alpha-tocopherol + selenium-pretreated animals 24 and 48 h after injection. The efficacy of antiperoxidants in preventing lipid peroxidation, and enhancing the resolution of ferrous-induced focal brain edema suggest that tocopherol + selenium administration caused free radical quenching and termination of lipid peroxidation, and increased membrane stabilization, an effect similar to the action of glucocorticoids.
D000818:Animals; D001929:Brain Edema / Q000188:drug therapy / Q000378:metabolism*; D001930:Brain Injuries / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism*; D002712:Chlorides; D005290:Ferric Compounds; D007501:Iron / Q000378:metabolism; D008054:Lipid Peroxides / Q000378:metabolism*; D008315:Malondialdehyde / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012643:Selenium / Q000494:pharmacology; D014810:Vitamin E / Q000494:pharmacology
D002712:Chlorides; D005290:Ferric Compounds; D008054:Lipid Peroxides; D014810:Vitamin E; D008315:Malondialdehyde; D007501:Iron; D012643:Selenium; C024555:ferric chloride