A function for the vitamin E metabolite α‐tocopherol quinone as an essential enzyme cofactor for the mitochondrial fatty acid desaturases

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Abstract
A critical analysis of the changes in fatty acid patterns and their metabolism elicited by vitamin E deficiency leads to the proposal that a major role of dietary RRR-α-tocopherol (α-TOC) is as an enzymatic precursor of α-tocopherolquinone (α-TQ) whose semiquinone radical functions as an essential enzyme cofactor for the fatty acid desaturases of the recently elucidated carnitine-dependent, channeled, mitochondrial desaturation-elongation pathway; a detailed mechanism for its function is proposed. Pathophysiological states produced by vitamin E deficiency and α-TOC transfer protein defects, such as ataxia, myopathy, retinopathy, and sterility are proposed to develop from the effects of impaired α-TQ-dependent desaturases and the resulting deficiency of their polyenoic fatty acid products.