Effect of hypoxia on steady state arachidonic acid metabolism in
bovine aortic endothelial cells.
Patton, George M., Hiroko Kadowaki, Hassan Albadawi, Hiram M. Soler,
and Michael T. Watkins.
Departments of Surgery and Pathology, Medicine, Boston University
School of Medicine, Boston, Massachusetts 02118, and Boston Veterans
Affairs Medical Center, Boston, Massachusetts 02130
APStracts 3:0483H, 1996.
At the onset of acute hypoxia, eicosanoid synthesis by bovine aortic
endothelial cells markedly decreases reflecting a decreased release
of arachidonic acid from endogenous stores. To determine the cause of
decreased arachidonic acid release, bovine aortic endothelial cells
were pulse-labeled with [14C]arachidonic acid for 5 min under
normoxic conditions, and chased for one hour under normoxic or
hypoxic conditions. The amount and 14C specific activity (dpm/nmol)
of three major arachidonyl molecular species (16:0-20:4, 18:1-20:4,
and 18:0-20:4) of each phospholipid class were determined from cells
chased under the two conditions. There were no relevant differences
in the metabolism of any of the arachidonyl molecular species of
diacyl lipids between the cells chased under two conditions. However,
there was a marked decrease (40%) in the turnover of arachidonyl
alkenylacyl phosphatidylethanolamine in the hypoxic cells. From these
results, it appears that the source of arachidonic acid supporting
constitutive eicosanoid synthesis in bovine aortic endothelial cells
is alkenylacyl phosphatidylethanolamine and the limiting enzyme
activity determining the rate of eicosanoid synthesis is a
plasmalogen specific phospholipase A2.
Received 23 July 1996; accepted in final form 15 October 1996.
APS Manuscript Number H659-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996