The ga-tocopherol and phospholipid fatty acid content of rat liver subcellular membranes in vitamin E and selenium deficiency

Abstract

(1) Rats were given a diet deficient in vitamin E and selenium, or diets supplemented with either or both of these nutrients. The livers were subfractionated by standard procedures, and the purity of the fractions was assessed by marker enzyme techniques. α-Tocopherol was measured and profiles of phospholipid fatty acids were determined. (2) All the organelles studied were severely depleted of α-tocopherol in the rats deprived of vitamin E: no organelle was particularly severely depleted. There was a large rise in the α-tocopherol content in organelles of rats deprived of selenium but given adequate amounts of vitamin E, suggesting an increased uptake or mobilization of tocopherol to compensate for the detrimental effects of selenium deficiency. (3) The following general conclusions were reached from the results of the phospholipid fatty acid analyses, (i) vitamin E deficiency caused a consistent fall in the polyunsaturated fatty acid (PUFA) content (13–66% of the control level); (ii) selenium deficiency alone caused no consistent effect on phospholipid PUFA in the fractions studied; (iii) double deficiency of vitamin E and selenium caused a consistent rise in the proportion of PUFA in the fractions studied, ranging from 11 to 311%. (4) The result given in 3(i) is consistent with peroxidative destruction of membrane phospholipid PUFA during vitamin E deficiency. The result in 3(iii) is paradoxical: a possible explanation is that during severe disruption of antioxidant defences, there is an overshoot in the increased incorporation of unsaturated fatty acids into the membrane phospholipids, or in the chain-elongation and desaturation process required for the formation of PUFA, which may require vitamin E and/or selenium for its regulation.