Effect of Vitamin E Deficiency on Ubiquinone Levels in Rat and Rabbit Liver

Abstract

IN a series of publications by Green and others^1–9 it wag reported that the concentration of ubiquinone in animal tissues is depressed in tocopherol deficiency and that this vitamin (or a structurally related form) is specifically required for its maintenance or restoration. Investigations by Draper and others^10–13 indicated that all the well-characterized lesions observed in vitamin E deficiency are amenable to treatment with certain structurally unrelated synthetic antioxidants, notably N,N′-diphenyl-p-phenylenediamine (DPPD). These latter experiments led to the conclusion that functional displacement of tocopherol by DPPD occurs in metabolism and that the biological role of the vitamin is entirely attributable to its antioxidant properties. However, Green et al. reported that neither DPPD nor ‘Santoquin’ (1,2-dihydro-6-ethoxy-2,2,4-trimethylquinoline, another antioxidant which is active as a dietary substitute for tocopherols) was effective in maintaining ubiquinone levels^1,6,7 and they concluded that vitamin E plays a specific non-antioxidant part in the metabolism of this quinone. In view of these reports we have investigated the effect of vitamin E deficiency and DPPD administration on ubiquinone concentrations in rat and rabbit liver. Liver was chosen because it can be extensively, if not entirely, depleted of tocopherols and might, therefore, be expected to show maximal changes in ubiquinone content.