Ramasamy S, Boissonneault G A, Decker E A, Hennig B
Department of Nutrition, University of Kentucky, Lexington 40506.
J Biochem Toxicol. 1991 Spring;6(1):29-35. doi: 10.1002/jbt.2570060105.
High plasma levels of linoleic acid (18:2) may injure endothelial cells, resulting in decreased barrier function of the vascular endothelium. The effects of linoleic acid on endothelial barrier function (transendothelial movement of albumin), membrane-bound enzyme activities, and possible autooxidation of linoleic acid under experimental conditions were studied. The exposure of endothelial monolayers to 18:2 for 24 hr at 60, 90, and 120 microM fatty acid concentrations caused a significant increase in transendothelial movement of albumin, with maximum albumin transfer at 90 microM. Fatty acid treatment resulted in the increased appearance of cytosolic lipid droplets. Activities of the membrane-bound enzymes, angiotensin-converting enzyme (ACE), and Ca(2+)-ATPase increased steadily with increasing time of cell exposure to 90 microM 18:2, reaching significance at 24 hr. Treatment of endothelial cultures with up to 120 microM 18:2 did not cause cytotoxicity, as evidenced by a nonsignificant change in cellular release of [3H]-adenine. Incubation of 18:2-supplemented serum-containing culture media with 1000 microM 18:2 at 37 degrees C for up to 48 hr did not result in formation of autooxidation products. These results suggest that 18:2 itself, and not its oxidation products, plays a major role in disrupting endothelial barrier function.
血浆中高浓度的亚油酸（18:2）可能会损伤内皮细胞，导致血管内皮屏障功能下降。研究了亚油酸在实验条件下对内皮屏障功能（白蛋白的跨内皮移动）、膜结合酶活性以及亚油酸可能的自动氧化的影响。在内皮细胞单层中，在脂肪酸浓度为60、90和120微摩尔时，将其暴露于18:2中24小时，导致白蛋白的跨内皮移动显著增加，在90微摩尔时白蛋白转移达到最大值。脂肪酸处理导致胞质脂质滴的出现增加。膜结合酶血管紧张素转换酶（ACE）和钙ATP酶的活性随着细胞暴露于90微摩尔18:2的时间增加而稳步增加，在24小时时达到显著水平。用高达120微摩尔的18:2处理内皮细胞培养物未引起细胞毒性，这通过[3H]腺嘌呤的细胞释放无显著变化得到证明。在37℃下，将含18:2的血清培养基与1000微摩尔的18:2孵育长达48小时，未导致自动氧化产物的形成。这些结果表明，18:2本身而非其氧化产物在破坏内皮屏障功能中起主要作用。
