Maintenance of α-Ketoglutarate and Succinate Oxidation in E-Deficient Liver Homogenates by α-Tocopherol, a Tocopherol Metabolite, Menadione and Diphenylphenylenediamine

Abstract

RATS on a Torula yeast diet deficient in vitamin E and factor 3 show a metabolic disturbance in liver slices, termed respiratory decline, 1–2 weeks prior to succumbing to necrotic liver degeneration¹. Dietary supplementation of vitamin E as well as intraportal injection of the vitamin prevents the disturbance, whereas dietary factor 3 (and also selenite) alleviates the decline without, however, preventing it fully. The effects following dietary, intraportal, and in vitro application of a number of antioxidants have been analysed. A tocopherol metabolite² as well as diphenylphenylenediamine³ are effective, in vitro, in preventing the respiratory failure of liver slices. While mitochondria of the deficient livers show an accelerated diminution of succinate oxidation in the presence of dinitropyridine nucleotide⁴, homogenates of such livers, in previous work, did not show decline with glucose as substrate and optimal supplements of adenosine triphosphate and dinitropyridine nucleotide¹. In this communication, a different homogenate system is described which shows respiratory decline with α-ketoglutarate or succinate as substrates. The preventive effects, ^{in vitro}, of tocopherol, the tocopherol metabolite (kindly supplied by Dr. Eric J. Simon of New York University College), menadione and diphenylphenylenediamine are demonstrated.