Ozone exposure of human tracheal epithelial cells inactivates cyclooxygenase and increases 15-hete production. Alpert, Stephen E., Ronald W. Walenga. Pediatric Pulmonary Division, Case Western Reserve University, Cleveland, Ohio
APStracts 2:0126L, 1995.
We assessed the immediate and prolonged effects of ozone on arachidonic acid (AA) metabolism by primary cultured human tracheal epithelial (TE) cells. TE monolayers were exposed at a gas-fluid interface to air or 0.1, 0.25 or 0.5 ppm ozone (15 minutes air, then 45 minutes air / ozone) and serially collected effluents analyzed by thin layer and/or high pressure liquid chromatography (TLC/HPLC). Release of prostaglandin E2 (PGE2) and AA, but not 15 -hydroxyeicosatetraenoic acid (15-HETE) or its metabolites, were detected from cultures prelabeled with 14C-AA. PGE2 production, measured by immunoassay, was nearly constant during air exposure. In contrast, PGE2 increased 2-3 fold during the first 15 minutes exposure to all concentrations of ozone, but then progressively declined to 78 +/- 17%, 57 +/- 12% (P
Received 12 April 1995; accepted in final form 13 July 1995.
APS Manuscript Number L114-5.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 10 August 1995.