Sekharam K M, Patel J M, Block E R
Division of Pulmonary Medicine, University of Florida College of Medicine, Gainesville.
J Cell Physiol. 1990 Dec;145(3):555-63. doi: 10.1002/jcp.1041450324.
Vitamin E, a dietary antioxidant, is presumed to be incorporated into the lipid bilayer of biological membranes to an extent proportional to the amount of polyunsaturated fatty acids or phospholipids in the membrane. In the present study we evaluated the distribution of incorporated polyunsaturated fatty acids (PUFA) and phosphatidylethanolamine (PE) in various membranes of pulmonary artery endothelial cells. We also studied whether incorporation of PUFA or PE is responsible for increased incorporation of [3H]-vitamin E into the membranes of these cells. Following a 24-hr incubation with linoleic acid (18:2), 18:2 was increased by 6.9-, 9.2-, and 13.2-fold in plasma, mitochondrial, and microsomal membranes, respectively. Incorporation of 18:2 caused significant increases in the unsaturation indexes of mitochondrial and microsomal polyunsaturated fatty acyl chains (P less than .01 versus control in both membranes). Incubation with arachidonic acid (20:4) for 24 hr resulted in 1.5-, 2.3-, and 2.4-fold increases in 20:4 in plasma, mitochondrial, and microsomal membranes, respectively. The unsaturation indexes of polyunsaturated fatty acyl chains of mitochondrial and microsomal membranes also increased (P less than .01 versus control in both membranes). Although incubations with 18:2 or 20:4 resulted in several-fold increases in membrane 18:2 or 20:4 fatty acids, incorporation of [3H]-vitamin E into these membranes was similar to that in controls. Following a 24-hr incubation with PE, membrane PE content was significantly increased, and [3H]-vitamin E incorporation was also increased to a comparable degree, i.e., plasma membrane greater than mitochondria greater than microsomes. Endogenous vitamin E content of the cells was not altered because of increased incorporation of PE and [3H]-vitamin E. When [3H]-vitamin E was incorporated into lipid vesicles prepared from the total lipid extracts of endothelial cells and varying amounts of exogenous PE, vitamin E content was directly related to PE content. These results demonstrate that PUFA and PE distribute in all pulmonary artery endothelial cell membranes. However, only increases in PE were associated with increased incorporation of [3H]-vitamin E in membranes of these cells.
维生素E是一种膳食抗氧化剂，据推测它会按与膜中多不饱和脂肪酸或磷脂含量成比例的程度掺入生物膜的脂质双层中。在本研究中，我们评估了掺入的多不饱和脂肪酸（PUFA）和磷脂酰乙醇胺（PE）在肺动脉内皮细胞各种膜中的分布情况。我们还研究了PUFA或PE的掺入是否导致[3H] - 维生素E更多地掺入这些细胞的膜中。在用亚油酸（18:2）孵育24小时后，血浆膜、线粒体膜和微粒体膜中的18:2分别增加了6.9倍、9.2倍和13.2倍。18:2的掺入导致线粒体和微粒体多不饱和脂肪酰链的不饱和度指数显著增加（两种膜中与对照相比P均小于0.01）。用花生四烯酸（20:4）孵育24小时导致血浆膜、线粒体膜和微粒体膜中的20:4分别增加了1.5倍、2.3倍和2.4倍。线粒体和微粒体膜的多不饱和脂肪酰链的不饱和度指数也增加了（两种膜中与对照相比P均小于0.01）。尽管用18:2或20:4孵育导致膜中18:2或20:4脂肪酸增加了几倍，但[3H] - 维生素E掺入这些膜中的情况与对照相似。在用PE孵育24小时后，膜PE含量显著增加，并且[3H] - 维生素E的掺入也增加到相当程度，即质膜大于线粒体大于微粒体。细胞内源性维生素E含量并未因PE和[3H] - 维生素E掺入增加而改变。当[3H] - 维生素E掺入由内皮细胞总脂质提取物和不同量的外源性PE制备的脂质体中时，维生素E含量与PE含量直接相关。这些结果表明，PUFA和PE分布于所有肺动脉内皮细胞膜中。然而，只有PE的增加与这些细胞的膜中[3H] - 维生素E掺入增加有关。
