Vitamin E Deficiency in the Rat

Weanling male rats were fed for approximately 3 weeks either a vitamin E-deficient or a vitamin E-supplemented diet. Liver homogenates were prepared and separated into mitochondrial, microsomal, and supernatant fractions, and the contributions of the microsomal and supernatant fractions to the maintenance or inhibition of mitochondrial oxidation of β-hydroxybutyrate were studied. When microsomes were added to mitochondria such that approximately equal amounts of protein from each fraction were present, oxidation was inhibited in a manner similar to that of vitamin E-deficient homogenates, regardless of whether the mitochondria or microsomes were derived from either vitamin E-deficient or vitamin E-supplemented rats. The further addition of the supernatant fraction from either type of liver resulted in maintenance of oxygen consumption when vitamin E-supplemented microsomes were present. The microsomal inhibitor was inactivated by boiling, but remained bound to the microsomal membranes after both sonic disruption followed by dialysis and sonic disruption followed by centrifugation. Dialysis of the supernatant fraction removed the factor, or factors, which overcame the inhibition due to the vitamin E-supplemented microsomes. Inhibition of oxygen consumption was not correlated with either peroxidation or lysosomal enzyme activity. It is suggested that the microsomal inhibitor is protein in nature.