Laurence M. Corwin

Studies on peroxidation in vitamin E-deficient rat liver homogenates

Abstract Peroxidation in liver homogenates from rats on vitamin E-deficient diets, as measured by the thiobarbituric acid assay, is greatly increased by the addition of DPN-linked substrates, but not succinate. This increase is prevented by respiratory inhibitors. Tocopherol can be added in vitro in quantities sufficient to prevent the decline in α-ketoglutarate oxidation, but not enough to prevent peroxide formation. Higher quantities of tocopherol, but not dietary selenite, will prevent this enzymic peroxide formation. Some evidence is presented which indicates that damage to cell fractions may result in endogenous peroxide formation rather than only the reverse.

Relation of tocopherol to enzyme sulfhydryl sites

Tocopherol affects neither cytochrome oxidase nor antimycin A sensitivity of α-tocopherol-deficient rat liver homogenates. The decline of α-ketoglutarate oxidation by these homogenates can be prevented by glutathione and BAL. A concomitant decline of free sulfhydryl groups in the homogenate with time can be prevented by all the reagents which protect against oxidative decline. Tocopherol lowers the sensitivity to arsenite and cadmium ions of α-ketoglutarate oxidation in cell fractions. Similarly, tocopherol can largely prevent inhibition of glutamate and β-hydroxybutyrate oxidation by p-hydroxymercuribenzoate. Protecting agents are required at the beginning of the incubation period, but the presence of DPN with the homogenate extends the critical period for the addition of these agents. It is concluded that tocopherol acts in some way to maintain the proper functioning of enzyme sulfhydryl groups.