Lipid peroxidation in the vitamin E deficient rat liver.

Abstract

The rate of lipid peroxidation, estimated by thiobarbituric acid (TBA) method, was 4.5 fold higher in liver homogenates of the vitamin E dificient rat than in those of the normal rat. But the peroxidation even in normal homogenates was elevated, when linolenate was added to the incubation medium. The increase of peroxidation was promptly reflected the linolenate addition and the rate of oxidation was almost proportionally increased with the incubation time. The optimal pH was sharply shown at 5.9, ATP and GSH increased the rate of the peroxidation, and NADPH accelerated the reaction than NADH. Cell fractionation revealed higher rate of peroxidation in every subcellular fraction.The mechanism of lipid peroxidation in liver homogenates of E-deficient rat seems to be different from that of the normal animal. Since in the E-deficient system the elevation of peroxidation did not appear promptly but an induction period was observed in an early stage of the incubation. The optimal pH was broad from 5.8 to 6.2, ATP and GSH inhibited the peroxidation, and the reaction was more accerelated with NADH than with NADPH. Cell fractionation procedure decreased the rate of peroxidation in every subcellular fraction, and recombination of these fractions recovered the high rate of the lipid peroxidation.