Abstract
The aerobic incubation of brain afer a period of ischemia induced lipid peroxidation. The effect was greatest in vitamin E—deficient rats, intermediate in vitamin E—normal rats, and least in animals supplemented with vitamin E. In contrast, nitrogen incubation following ischemia produced a small effect only in the vitamin E—deficient animals. It appears that reoxygenation is required for lipid peroxides to accumulate in the brain. However, a trace of oxygen remaining during extreme ischemic hypoxia may be sufficient to cause slow propagation of free radical reactions when the vitamin E level is low.
