Selenium Modulates 1- O -Alkyl-2-Acetyl- sn -Glycero-3-Phosphocholine (PAF) Biosynthesis in Bovine Aortic Endothelial Cells

Abstract

Selenium (Se) deficiency has been reported to increase platelet-activating factor (PAF) production in human endothelial cells; however, the mechanism is unclear. This study demonstrated that tumor necrosis factor-α (TNF-α) stimulated Se-deficient bovine aortic endothelial cells (BAEC) produced significantly more PAF than Se-supplemented cells. Moreover, the increase in the level of PAF was associated with enhanced activity of two anabolic enzymes in the remodeling pathway: phospholipase A₂ and Lyso-PAF:acetyl-coenzyme A acetyltransferase (Lyso-PAF-AcT). In contrast, the activity of the PAF catabolic enzyme, PAF-acetylhydrolase, was not affected by Se status. Interestingly, prostacyclin, a potent vasodilator and inhibitor of platelet aggregation, inhibited the activity of Lyso-PAF-AcT and reduced the PAF production in TNF-α-stimulated BAEC. Therefore, we conclude that Se deficiency alters PAF production in TNF-α-stimulated BAEC by altering the activity of anabolic enzymes involved in the remodeling pathway partially through the inhibition of prostacyclin production.