Effect of hypoxia on steady-state arachidonic acid metabolism in bovine aortic endothelial cells

George M. Patton, Hiroko Kadowaki, Hassan Albadawi, Hiram M. Soler, Michael T. Watkins

Research output: Contribution to journalArticlepeer-review


At the onset of acute hypoxia, eicosanoid synthesis by bovine aortic endothelial cells (BAEC) markedly decreases, reflecting a decreased release of arachidonic acid from endogenous stores. To determine the cause of decreased arachidonic acid release, we pulse-labeled BAEC with [14C] arachidonic acid for 5 min under normoxic conditions and chased cells for l h under normoxic or hypoxic conditions. The 14C incorporation and specific activity (disintegrations per minute per nanomole) of three major arachidonyl molecular species (16:0-20:4, 18:120:4, and 18:0-20:4) of each phospholipid class were determined in cells chased under either of the two conditions. There was no relevant difference between normoxic and hypoxic cells in the metabolism of any of the arachidonyl molecular species of diacyl lipids. 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 BAEC is alkenylacyl phosphatidylethanolamine and that the limiting enzyme activity determining the rate of eicosanoid synthesis is a plasmalogen-specific phospholipase A2.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number3
StatePublished - Dec 1 1997
Externally publishedYes


  • Alkenylacyl phosphatidylethanolamine
  • Phospholipase A2
  • Phospholipid molecular species

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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