Abstract
It has been known that a major role of vitamin E is to inhibit lipid peroxidation by scavenging a lipid peroxyl radical by donating an electron and hydrogen from the phenol group on the chroman ring. The radical scavenging activity of tocopherols in solution is dependent on the methyl substituents on the chroman ring but not on the side chain at the C-2 position. Therefore, tocopherol (Toc) and tocotrienol (Toc3) show almost the same efficacy in the inhibition of lipid peroxidation in solution. However, the action of vitamin E in the cell is more complicated and is dependent on the efficacy of its incorporation, retention, and mobility, which in turn are affected by the nature of the side chains. Toc3 shows an advantage in the inhibition of oxidative-stress-involved alteration of a cell's function due to its higher uptake by the cell. The critical effect of the side chain of vitamin E has been implicated in the inhibition of cell death, depending on what causes the cell death. For example, the cell death induced by 24S-hydroxycholesterol was inhibited by Toc but not by Toc3. In this chapter, the efficacy of vitamin E homologues in the inhibition of lipid peroxidation under different conditions and against cell death caused by different stimuli is described.
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