Title: Linoleic acid-induced endothelial cell injury: role of membrane-bound enzyme activities and lipid oxidation.

Authors: Ramasamy, S; Boissonneault, G A; Decker, E A; Hennig, B

Published In J Biochem Toxicol, (1991)

Abstract: 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.

PubMed ID: 1831858

MeSH Terms: Animals; Calcium-Transporting ATPases/metabolism; Cell Membrane Permeability/drug effects; Cells, Cultured; Deoxyribose/metabolism; Endothelium, Vascular/drug effects*; Endothelium, Vascular/metabolism; Endothelium, Vascular/physiology; Linoleic Acid; Linoleic Acids/toxicity*; Lipid Metabolism; Oxidation-Reduction; Peroxides/metabolism; Serum Albumin, Bovine/metabolism; Swine; Thiobarbiturates/metabolism; Time Factors