Linoleic acid-induced endothelial cell injury: Role of membrane-bound enzyme activities and lipid oxidation
✍ Scribed by Ramasamy, Santhini ;Boissonneault, Gilbert A. ;Decker, Eric A. ;Hennig, Bernhard
- Publisher
- John Wiley and Sons
- Year
- 1991
- Tongue
- English
- Weight
- 839 KB
- Volume
- 6
- Category
- Article
- ISSN
- 0887-2082
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✦ Synopsis
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 pM fatty acid concentrations caused a significant increase in transendothelial movement of albumin, with maximum albumin transfer at 90 pM. Fatty acid treatment resulted in the increased appearance of cytosolic lipid droplets. Activities of the membrane-bound enzymes, angiotensin-converting enzyme (ACE), and Ca2+-ATPase increased steadily with increasing time of cell exposure to 90 pM 18:2, reaching significance at 24 hr. Treatment of endothelial cultures with up to 120 pM 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 pM 1 8 9 at 37°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.