Exposure of pulmonary artery endothelial cells to nitrogen dioxide activates phospholipase A1.
Phospholipase A1, A2, and C and diacylglycerol lipase activities were measured in cell sonicates after exposing confluent monolayers of porcine pulmonary artery endothelial cells to 5 ppm NO2, a toxic constituent of environmental pollution, for 24 and 48 hr. There was a significant increase (2.25-fold) in phospholipase A1 activity in 24 and 48 hr NO2-exposed cells, whereas activities of phospholipases A2 and C and diacylglycerol lipase were comparable to control cells at both time points. When endothelial cells were prelabeled with [3H]-arachidonic acid and then exposed to NO2 for 48 hr, increased counts were recovered from cell lysophospholipids with concomitant decreased recovery of counts from cell phosphatidylcholine and phosphatidylethanolamine. These results demonstrate that NO2 exposure results in specific activation of phospholipase A1.
Division of Pulmonary Medicine, University of Florida College of Medicine, Gainesville 32602.
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Bhat
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Patel
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Block
D000818:Animals; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects* / Q000201:enzymology; D004789:Enzyme Activation / Q000187:drug effects; D009585:Nitrogen Dioxide / Q000494:pharmacology*; D010740:Phospholipases / Q000378:metabolism*; D010741:Phospholipases A / Q000378:metabolism*; D054466:Phospholipases A1; D011651:Pulmonary Artery / Q000187:drug effects / Q000201:enzymology; D013552:Swine
D010740:Phospholipases; D010741:Phospholipases A; D054466:Phospholipases A1; D009585:Nitrogen Dioxide