Patel J M, Edwards D A
Department of Medicine, University of Florida College of Medicine, Gainesville 32610.
Toxicol Appl Pharmacol. 1988 Oct;96(1):101-14. doi: 10.1016/0041-008x(88)90252-9.
Vitamin E, a dietary antioxidant, is known to inhibit peroxidation of membrane lipids and to protect the lungs of vitamin E-deficient animals and to a lesser extent vitamin E-sufficient animals from oxidant injury. Since the protective interaction between vitamin E and biological membranes may be related to alterations in composition and physical state of membrane lipids, we evaluated the effect of vitamin E deficiency on lung microsomal lipids and membrane fluidity. Both intact microsomes and lipid vesicles prepared from the total lipid extracts of these microsomes were used. The percentage incorporation of vitamin E and cholesterol, membrane fluidity, and lipid peroxidation were measured in microsomes as well as their lipid vesicles. Fluidity was measured by monitoring changes in fluorescence anisotropy for 1,6-diphenyl-1,3,5-hexatriene (DPH). Lipid peroxidation was measured by thiobarbituric acid reaction. There were significant increases in the phospholipid (p less than 0.01), the total cholesterol (p less than 0.05), and the total saturated fatty acids (p less than 0.05) and decreases in total polyunsaturated fatty acid (p less than 0.01) content of vitamin E-deficient microsomes. There were no detectable peroxidative products in freshly isolated microsomes from either vitamin E-sufficient or -deficient lungs. However, lipids from vitamin E-deficient microsomal membranes were more susceptible to free radical initiated peroxidation than lipids from vitamin E-sufficient microsomes. Fluidity in vitamin E-deficient microsomes or in their lipid vesicles was significantly (p less than 0.05) decreased compared to the respective controls. In vitamin E-deficient microsomes or their lipid vesicles, the incorporation rate of vitamin E was two- to three-fold greater than in vesicles of vitamin E-sufficient microsomes or their lipid vesicles. However, the percentage incorporation of cholesterol was identical in both vitamin E-deficient and vitamin E-sufficient microsomes or in their respective lipid vesicles. As a result of vitamin E incorporation, fluidity was significantly decreased (p less than 0.05) in vitamin E-sufficient vesicles and was further decreased (p less than 0.001) in vitamin E-deficient vesicles. Incorporation of cholesterol also decreased fluidity in both vitamin E-deficient and vitamin E-sufficient vesicles but to the same extent (p less than 0.001). Lipid peroxide formation was two-fold greater in the vitamin E-deficient than in the vitamin E-sufficient vesicles.(ABSTRACT TRUNCATED AT 400 WORDS)
维生素E是一种膳食抗氧化剂，已知它能抑制膜脂质的过氧化反应，并保护维生素E缺乏的动物的肺部，在一定程度上也能保护维生素E充足的动物的肺部免受氧化损伤。由于维生素E与生物膜之间的保护作用可能与膜脂质的组成和物理状态的改变有关，我们评估了维生素E缺乏对肺微粒体脂质和膜流动性的影响。我们使用了完整的微粒体以及由这些微粒体的总脂质提取物制备的脂质囊泡。在微粒体及其脂质囊泡中测量了维生素E和胆固醇的掺入百分比、膜流动性和脂质过氧化反应。通过监测1,6-二苯基-1,3,5-己三烯（DPH）的荧光偏振变化来测量流动性。通过硫代巴比妥酸反应测量脂质过氧化反应。维生素E缺乏的微粒体中磷脂（p<0.01）、总胆固醇（p<0.05）和总饱和脂肪酸（p<0.05）含量显著增加，而总多不饱和脂肪酸含量（p<0.01）降低。从维生素E充足或缺乏的肺部新鲜分离的微粒体中均未检测到过氧化产物。然而，维生素E缺乏的微粒体膜中的脂质比维生素E充足的微粒体中的脂质更容易受到自由基引发的过氧化反应的影响。与各自的对照相比，维生素E缺乏的微粒体或其脂质囊泡中的流动性显著降低（p<0.05）。在维生素E缺乏的微粒体或其脂质囊泡中，维生素E的掺入率比维生素E充足的微粒体或其脂质囊泡中的掺入率高两到三倍。然而，维生素E缺乏和维生素E充足的微粒体或其各自的脂质囊泡中胆固醇的掺入百分比是相同的。由于维生素E的掺入，维生素E充足的囊泡中的流动性显著降低（p<0.05），而在维生素E缺乏的囊泡中进一步降低（p<0.001）。胆固醇的掺入也降低了维生素E缺乏和维生素E充足的囊泡中的流动性，但程度相同（p<0.001）。维生素E缺乏的囊泡中脂质过氧化物的形成比维生素E充足的囊泡中高两倍。（摘要截短至400字）
