This study investigated the response of bovine pulmonary artery endothelial cells to incubation in hyperoxia (95% O2-5% CO2). Changes in cell number and morphology, release of lactate dehydrogenase, and production of arachidonic acid metabolites were assessed during continuous exposure of confluent endothelial monolayers to air (air-5% CO2, 'controls') or O2 (95% O2-5% CO2, 'O2-exposed') for periods of 12-72 h. Control monolayer cell numbers remained constant (~2,000,000 cells/flask), whereas the number of cells in O2-exposed monolayers decreased progressively to 30% of controls (P < 0.01) by 72 h. As assessed by radioimmunoassay, both control and O2-exposed cells produced the prostacyclin metabolite, 6-ketoprostaglandin F(1α) (6-keto-PGF(1α)), and prostaglandin F(2α) (PGF(2α)), but no thomboxane metabolite (TxB2) was detected. The O2-exposed cells released significantly more 6-keto-PGF(1α) and PGF(2α) than control cells when apparent net production rates over the entire 72-h period were compared. In addition, both control and O2-exposed (48 h) endothelial monolayers released immunoreactive leukotriene B4 (LTB4) on stimulation with calcium ionophore (10 μM A23187). As with the cyclooxygenase products, O2-exposed cells released more immunoreactive LTB4 than did controls. Both cyclooxygenase and lipoxygenase metabolites of arachidonic acid are released by cultured endothelial cells during the development of O2 toxicity.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of applied physiology|
|State||Published - Jan 1 1986|
ASJC Scopus subject areas
- Physiology (medical)