An effect of vitamin E on the regulation of succinate oxidation in rat liver mitochondria.

The relation of vitamin E deficiency diseases to the possible function of tocopherol as a catalyst in enzyme systems is at present unknown. A characteristic metabolic disturbance, respiratory decline, has been described in liver slices from rats on vitamin E-deficient diets which produce necrotic liver degeneration (l-3). The deficiency disease, which is produced conveniently by diets containing Torula yeast as the sole source of protein, is the result of the simultaneous lack of two main factors, vitamin E and Factor 3. The latter has been recognized as a selenium-containing compound (4). Respiratory decline is found during the latent phase of the deficiency, approximately IO days before the onset of necrosis. It consists of an inability of liver slices to maintain osygen uptake for extended periods of incubation. Animals whose diets have been supplemented with vitamin E show no such decline. Supplementation with Factor 3 will prevent the decline somewhat, but not completely. This paper deals with an investigation of the oxidative properties of mitochondria of livers from deficient and supplemented rats, and the effect of vitamin E in regulating the succinoxidase system, with the aim of explaining respiratory decline in terms of concrete enzymatic mechanisms. Recently a catalytic role for vitamin E in the DPNH-cytochrome c reductase system has been described by Nason et al. (5, 6). The lack of correlation of their results with the effect of vitamin E on this system will also be discussed.