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Am J Physiol Lung Cell Mol Physiol 262: L495-L501, 1992;
1040-0605/92 $5.00
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AJP - Lung Cellular and Molecular Physiology, Vol 262, Issue 4 495-L501, Copyright © 1992 by American Physiological Society

ARTICLES

Tricarboxylic acid cycle activity in perfused rat lungs after O2 exposure

D. J. Bassett and S. S. Reichenbaugh
Division of Physiology, Johns Hopkins University School of Hygiene and Public Health, Baltimore, Maryland 21205.

O2-induced impairment of mitochondrial energy generation was examined in intact lungs isolated from rats after 18-30 h exposure to either air or 100% O2 in vivo. Mitochondrial metabolic rates were determined by separate measurements of 14CO2 production from [1-14C]pyruvate and [U-14C]palmitate, perfused under normal and stimulated metabolic conditions brought about by perfusion with the uncoupler of oxidative phosphorylation, 2,4-dinitrophenol (DNP). In the absence of DNP, O2 exposure did not significantly alter 14CO2 productions from either substrate. DNP increased lung pyruvate and palmitate catabolism to CO2 twofold in air-exposed lungs but did not alter 14CO2 production in lungs isolated from O2-exposed rats. These data demonstrated an O2-induced impairment of maximal mitochondrial metabolism of both pyruvate and palmitate that could not be explained by alterations in tissue free coenzyme A or by loss of pyridine nucleotides. However, comparisons of the steady-state levels of tricarboxylic acid cycle intermediates between O2- and air-exposed lungs did identify isocitrate dehydrogenase as a possible site of O2-induced enzyme inactivation.


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