Quantitative fatty acid analyses in cultured porcine pulmonary artery endothelial cells: The combined effects of fatty acid supplementation and oxidant exposure

1992 ◽  
Vol 153 (1) ◽  
pp. 76-87 ◽  
Author(s):  
C. Michael Hart ◽  
J. Keith Tolson ◽  
Edward R. Block
1992 ◽  
Vol 262 (5) ◽  
pp. L606-L613 ◽  
Author(s):  
G. B. Bhat ◽  
E. R. Block

The effect of exposure of porcine pulmonary artery endothelial cells to hypoxic (0% O2) and normoxic (20% O2) conditions for 24 and 48 h on phospholipid metabolism was studied. Sonicates prepared from endothelial cells that were exposed to 24 h of hypoxia showed significant increases in phospholipase A1 (91%), phospholipase C (75%), and diacylglycerol lipase (57%) activities. Hypoxic exposure of cells for 48 h caused an increase in diacylglycerol lipase activity (54%) only. Hypoxia also caused significant decreases in ATP levels and ATP-dependent arachidonyl coenzyme A (CoA) synthetase activity. Phospholipase A2, lysophosphatidylcholine acyltransferase, and diacylglycerol acyltransferase activities were not influenced by 24 or 48 h of hypoxia. When endothelial cells were prelabeled with [3H]arachidonic acid and then exposed to hypoxia, increased counts were recovered from the free fatty acid fraction of medium and from the cell fatty acid esters, lysophospholipids, diacylglycerols, and triacylglycerols. There was a concomitant decreased recovery of counts from cell phospholipids. These results indicate that hypoxic exposure of endothelial cells altered phospholipid metabolism by activating deacylation pathways and inhibiting reacylation via ATP-dependent arachidonyl CoA synthetase.


1993 ◽  
Vol 156 (1) ◽  
pp. 24-34 ◽  
Author(s):  
C. Michael Hart ◽  
Sharon P. Andreoli ◽  
Carolyn E. Patterson ◽  
Joe G. N. Garcia

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