Effect of .ALPHA.-tocopherol on lipid peroxidation and acyl chain mobility of liver microsomes from vitamin E-difficient rat.

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Abstract
Effects of .alpha.-tocopherol on lipid peroxidation and membrane fluidity were studied in liver microsomes from vitamin E (.alpha.-tocopherol)-deficient rats using NADPH as a substrate. Microsomes containing various contents of .alpha.-tocopherol were prepared by incubation with various concentrations of .alpha.-tocopherol in ethanol solution. NADPH-dependent lipid peroxidation decreased the content of polyunsaturated fatty acids, arachidonic acid and 4, 7, 10,13, 16, 19-docosahexaenoic acid. The treatment with .alpha.-tocopherol before peroxidation reduced the production of lipid peroxides and the change in fatty acid composition at the lowest content of .alpha.-tocopherol (0.2 molar fraction). Addition of .alpha.-tocopherol after peroxidation slightly inhibited peroxide production and small alteration in fatty acid composition. By stearate spin probe, the .alpha.-tocopherol incorporated into microsomes did not alter the acyl chain mobility up to 0.2 molar fraction but reduced the mobility above 0.2 molar fraction. The acyl chain mobility was markedly decreased by lipid peroxidation. The decrease of membrane fluidity was repressed in microsomes treated with .alpha.-tocopherol before peroxidation, but was not repressed in microsomes treated after peroxidation. Use of artificial membranes of egg yolk phosphatidylcholine and rat liver phosphatidylcholine revealed that the effect of .alpha.-tocopherol on membrane fluidity depends on the fatty acid composition of phospholipid, especially the content of arachidonic acid. The mobility of the fatty acyl chain was not affected by spermine at concentrations which could inhibit lipid peroxidation. The inhibitory effect of .alpha.-tocopherol on lipid peroxidation may be due to antioxidant activity rather than the indirect effect of membrane stabilization.