The effect of vitamin E on the lipid environment of rat hepatocyte membranes

Abstract

Tocopherol is one of the known beneficial natural antioxidants ensuring the optimal level of functioning of mammalian organisms. Numerous in vitro and in vivo experiments have shown that the biological role of vitamin E is to prevent the development of pathologies caused by oxidative stress. In particular, the role of enzymatic factors of lipid peroxidation and related inflammation as a result of eicosanoid synthesis was clearly shown. We studied changes in the structural and functional state of hepatocyte membranes in the classical model of E-hypovitaminosis caused by long-term (70 days) insufficient intake of vitamin E in the diet of rats. The test components were determined spectrophotometrically after appropriate chromatographic procedures. The amount of total and individual leukotrienes was determined by ELISA. Prolonged tocopherol deficiency in rats caused a 49.4% decrease in tocopherol, more than 27.0% – in cholesterol. Of the 8 individual phospholipids studied, 6 showed significant changes: a decrease in cardiolipin and phosphatidylserine, and an increase in phosphatidylethanolamine by 3.24 times, an increse in lysophosphatidylcholine by 86.9%, in phospha­tidylcholine by 52.8%, and in sphingomyelin by 30.6%, relative to control. There were changes in the levels of unsaturated fatty acids playing a significant role in the development of functional disorders in cells and affecting the metabolism of ecosanoids derived from arachidonic acid by the 5-lipoxygenase oxidation pathway. Changes in the levels of total and individual cysteinyl leukotrienes in the state of E-hypovitaminosis were revealed. Restoration of vitamin E intake returns most of the studied indicators such as tocopherol, cholesterol, polyunsaturated fatty acids to the control levels and activates the processes of sequential conversion of leukotrienes in the body of rats. The obtained results indicate the potentiating effect of vitamin E on metabolic processes in the body as a whole and in hepatocytes and eicosanoid metabolism. The degree of tocopherol intake allows one to influence the course of inflammatory processes associated with eicosanoids, not only through the impact on precursors, but also on the utilization of metabolites, including leukotrienes.