Abstract
Among various arachidonic acid metabolites examined, only 15(S)-hydroperoxy-5,8,11,13-eicosatetraenoic acid (15-HPETE), a lipoxygenase product, caused a time- and dose-dependent injury to bovine endothelial cells in culture. There also occurred a significant inhibition of endothelial prostacyclin (PGI 2) production due to 15-HPETE. But there were obvious dissociations in time course and dose dependence between 15-HPETE-induced cellular injury and 15-HPETE-induced inhibition of PGI 2 synthesis. In addition, the cytotoxicity of 15-HPETE was not aggravated even when the endothelial monolayers were pretreated with several inhibitors of PGI 2 synthesis. Also, some stable analogues of PGI 2 had no protective effect on the injury. These results suggest that the reduced production of PGI 2 caused by 15-HPETE is not directly associated with the onset of cellular injury, and that PGI 2 does not play any cytoprotective role in endothelial cell injury induced by at least such lipid peroxides as 15-HPETE.
Published Version
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