Tricarboxylic acid cycle activity in perfused rat lungs after O2 exposure
| Autor: | D. J. P. Bassett, S. S. Reichenbaugh |
|---|---|
| Rok vydání: | 1992 |
| Předmět: |
Pulmonary and Respiratory Medicine
Male medicine.medical_specialty Pulmonary Circulation Physiology Coenzyme A Citric Acid Cycle Guanosine Monophosphate Palmitic Acid Oxidative phosphorylation Palmitic Acids Biology Guanosine Diphosphate Palmitic acid chemistry.chemical_compound Physiology (medical) Internal medicine Pyruvic Acid medicine Animals Pyruvates Lung Catabolism Adenine Nucleotides Rats Inbred Strains Cell Biology Metabolism Rats Citric acid cycle Oxygen Endocrinology Isocitrate dehydrogenase Biochemistry chemistry Ketoglutaric Acids Pyruvic acid Guanosine Triphosphate |
| Zdroj: | The American journal of physiology. 262(4 Pt 1) |
| ISSN: | 0002-9513 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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