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A function for the vitamin E metabolite α‐tocopherol quinone as an essential enzyme cofactor for the mitochondrial fatty acid desaturases
Author(s) -
Infante Juan P.
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)00170-2
Subject(s) - cofactor , biochemistry , quinone , tocopherol , metabolite , enzyme , chemistry , vitamin e , function (biology) , biology , antioxidant , microbiology and biotechnology
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.