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Vitamin E is a lipid-soluble and is present in biological membranes. It contains a hydroxyl group that reacts with unpaired electrons and can reduce to form peroxyl radicals. We investigated the effects of vitamin E against neuronal death associated with cerebral ischemia-reperfusion, particularly apoptosis, in Wistar Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). In both WKY and SHRSP, hypoxia alone did not produce a marked increase in neuronal death. However, hypoxic stimuli followed by oxygen reperfusion induced neuronal damage in both WKY and SHRSP. The percentage of neuronal apoptosis occurring during hypoxia-reperfusion was markedly higher in the neurons of SHRSP than in those of WKY. The addition of vitamin E almost completely inhibited neuronal death in both strains. In the hippocampus of SHRSP, the formation of hydroxyl radicals and the cerebral blood flow-independent formation of nitric oxide (NO) increased after reperfusion. The expression of the neuronal thioredoxin and Bcl-2 genes decreased significantly more in SHRSP than in WKY. From these results, we conclude that vitamin E exerts a marked inhibitory effect against neuronal damage by being incorporated into biological membranes, particularly mitochondrial membranes, and capturing the reactive oxygen and free radicals formed. We also speculate that the susceptibility of neurons to apoptosis in SHRSP is partly due to an insufficiency of mitochondrial thioredoxin and apoptosis-inhibitory protein.