Block E R, Patel J M, Edwards D
Research Service, Veterans Administration Medical Center, Gainesville, Florida.
Am J Physiol. 1989 Aug;257(2 Pt 1):C223-31. doi: 10.1152/ajpcell.1989.257.2.C223.
We exposed monolayer cultures of pulmonary artery endothelial cells or plasma membranes derived from these cells to hypoxic (0 and 5% O2) and normoxic (20% O2; control) conditions and measured cellular contents of malondialdehyde and conjugated dienes, plasma membrane fluidity and lipid composition, and plasma membrane-dependent transport of 5-hydroxytryptamine (5-HT). Hypoxia caused significant increases in malondialdehyde and conjugated dienes, in fluidity, and in 5-HT transport. Hypoxia also caused a significant decrease in plasma membrane total phospholipids and a marked increase in plasma membrane free fatty acids that appeared to be due to release of fatty acids from the plasma membrane phospholipids. The increases in fluidity and 5-HT transport and the alterations in fatty acids were reversible after return to control conditions. These results indicate that hypoxia alters the physical state, lipid composition, and function of endothelial cell plasma membranes by a combination of stimulation of membrane lipid peroxidation and accelerated degradation of membrane phospholipids, the latter probably secondary to activation of membrane phospholipases.
我们将肺动脉内皮细胞单层培养物或源自这些细胞的质膜暴露于低氧（0%和5%氧气）和常氧（20%氧气；对照）条件下，并测量丙二醛和共轭二烯的细胞含量、质膜流动性和脂质组成，以及5-羟色胺（5-HT）的质膜依赖性转运。低氧导致丙二醛和共轭二烯、流动性以及5-HT转运显著增加。低氧还导致质膜总磷脂显著减少，质膜游离脂肪酸显著增加，这似乎是由于脂肪酸从质膜磷脂中释放所致。恢复到对照条件后，流动性和5-HT转运的增加以及脂肪酸的改变是可逆的。这些结果表明，低氧通过刺激膜脂质过氧化和加速膜磷脂降解（后者可能继发于膜磷脂酶的激活）的组合，改变内皮细胞质膜的物理状态、脂质组成和功能。
