[Lipid peroxidation in the rat liver in mild forms of vitamin A deficiency].

The content of malonic dialdehyde (MDA) and diene conjugates (DC) in homogenates and microsomes of the liver, as well as the rate of spontaneous NADPH- and ascorbate-dependent lipid peroxidation (LPO) were studied in hepatic microsomes of rats with nonsevere types of experimental vitamin A deficiency: a) rapid and synchronously induced vitamin A deficiency developing in the animals with a pre-exhausted hepatic retinol reserve, which received retinoic acid, after the retinoic acid administration was stopped; b) subnormal provision with retinol by the injection to rats of minimal vitamin doses (7 IU/day). Both experimental models were characterized by a drastic exhaustion of vitamin A reserve in the liver, manifest disorders in the growth and appetite of the animals being absent. In both models the DC content and NADPH-dependent LPO rate in the liver of rats with vitamin A deficiency proved to be decreased as compared to the control, while the rate of ascorbate-dependent LPO was little changed. The study of the fatty-acid composition of microsomal lipids in synchronous vitamin A deficiency revealed decreased arachidonic acid and increased palmitic acid levels as compared to the controls. A conclusion has been made that the results obtained confirm the earlier data on the lowering of LPO intensity in severe types of retinol deficiency, and evidence specificity of shifts associated with deficiency of retinol proper, but not with secondary metabolic disorders due to the changes in nutrition and growth of animals.