Effects of high oxygen exposure on bioenergetics in isolated type II pneumocytes.
O2-mediated alterations in cell energy metabolism may play a role in structural and functional abnormalities described in type II pneumocytes (T-II-P) following in vivo hyperoxia. Bioenergetic alterations produced by hyperoxia (95% O2) were therefore examined in a culture-maintained cell line derived from T-II-P. Exposure of cell monolayers to 95% O2 for 96 h results in a significant decrease in O2 consumption (from 0.52 +/- 0.07 to 0.30 +/- 0.08, P less than 0.01), suggesting impaired mitochondrial energy provision. In addition, there are increased rates of aerobic lactate production (from 2.89 +/- 0.52 to 3.84 +/-0.80, P less than 0.05) with loss of Pasteur effect, indicating a shift to glycolytic metabolism at relatively high PO2's. These metabolic changes are not accompanied by altered activities of critical mitochondrial (cytochrome oxidase) or glycolytic (pyruvate kinase, phosphofructokinase) enzymes. Altered cell bioenergetics following hyperoxia may this represent an important secondary mechanism leading to functional abnormalities in T-II-P.
D000332:Aerobiosis; D000818:Animals; D002999:Clone Cells; D003576:Electron Transport Complex IV / Q000378:metabolism; D004734:Energy Metabolism; D006019:Glycolysis; D007773:Lactates / Q000096:biosynthesis; D010100:Oxygen; D010101:Oxygen Consumption; D010732:Phosphofructokinase-1 / Q000378:metabolism; D011650:Pulmonary Alveoli / Q000166:cytology* / Q000378:metabolism; D011770:Pyruvate Kinase / Q000378:metabolism; D051381:Rats
D007773:Lactates; D003576:Electron Transport Complex IV; D010732:Phosphofructokinase-1; D011770:Pyruvate Kinase; D010100:Oxygen