Ohki K, Takamura T, Nozawa Y
J Nutr Sci Vitaminol (Tokyo). 1984 Jun;30(3):221-34. doi: 10.3177/jnsv.30.221.
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 even at the lowest content of alpha-tocopherol dealt with in this experiment, 0.2 molar fraction, while addition of alpha-tocopherol after peroxidation resulted in a slight inhibition of peroxide production and small alteration in fatty acid composition. By an ESR measurement using 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. The experiment using 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. On the other hand, the mobility of the fatty acyl chain was not affected by spermine at concentrations which could inhibit lipid peroxidation. These results suggest that the inhibitory effect of alpha-tocopherol on lipid peroxidation is due to antioxidant activity rather than the indirect effect of membrane stabilization.
以NADPH为底物，研究了α-生育酚对维生素E（α-生育酚）缺乏大鼠肝脏微粒体脂质过氧化和膜流动性的影响。通过在乙醇溶液中与不同浓度的α-生育酚孵育，制备了含有不同α-生育酚含量的微粒体。NADPH依赖性脂质过氧化降低了多不饱和脂肪酸、花生四烯酸和4,7,10,13,16,19-二十二碳六烯酸的含量。在过氧化之前用α-生育酚处理，即使在本实验中处理的最低α-生育酚含量（0.2摩尔分数）下，也能减少脂质过氧化物的产生和脂肪酸组成的变化，而在过氧化之后添加α-生育酚则导致过氧化物产生的轻微抑制和脂肪酸组成的微小改变。通过使用硬脂酸自旋探针的电子自旋共振测量，掺入微粒体中的α-生育酚在0.2摩尔分数以下不会改变酰基链的流动性，但在0.2摩尔分数以上会降低其流动性。脂质过氧化显著降低了酰基链的流动性。在过氧化之前用α-生育酚处理的微粒体中，膜流动性的降低受到抑制，但在过氧化之后处理的微粒体中则没有受到抑制。使用蛋黄磷脂酰胆碱和大鼠肝脏磷脂酰胆碱人工膜的实验表明，α-生育酚对膜流动性的影响取决于磷脂的脂肪酸组成，尤其是花生四烯酸的含量。另一方面，在能够抑制脂质过氧化的浓度下，精胺不会影响脂肪酰链的流动性。这些结果表明，α-生育酚对脂质过氧化的抑制作用是由于抗氧化活性，而不是膜稳定的间接作用。
