The Inhibition of Ascorbic Acid Synthesis by the Process of Lipid Peroxidation in Vitamin E Deficiency

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Abstract
The mechanism of inhibition of gulonolactone oxidase in liver homogenates from vitamin E deficient rats and rabbits appears to involve the reaction of either an intermediate formed in the enzymic conversion of gulonolactone to ascorbic acid or ascorbic acid itself with a lipid component in the system to produce an inhibitor. The inhibitor or a by-product of its production eventually degradates to yield detectable amounts of malonaldehyde. The action of tocopherol in this sequence would be to prevent the interaction of the postulated intermediate and some component of the tissue lipids. Although gulonolactone oxidase is inhibited in liver homogenates from vitamin E deficient rats and rabbits, and the inhibition is attributed to lipid peroxidation in the enzyme system, there is, as yet, no direct evidence that a similar phenomenon takes place in vivo. The data show that the usual method for detecting lipid peroxidation in vivo (as defined in this report) would probably give negative results even if such was occurring.