Global ischaemia induces a biphasic response of the mitochondrial respiratory chain. Anoxic pre-perfusion protects against ischaemic damage
| Autor: | H. Pouleur, D. Caucheteux, A. Hombroeckx, Louis Hue, K. Veitch |
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| Přispěvatelé: | UCL - MD/BICL - Département de biochimie et de biologie cellulaire |
| Rok vydání: | 1992 |
| Předmět: |
Male
medicine.medical_specialty Time Factors Malates Ischemia Respiratory chain Glutamic Acid Coronary Disease Myocardial Reperfusion Injury Oxidative phosphorylation Buffers Mitochondrion Biochemistry Mitochondria Heart Electron Transport Complex IV Electron Transport Complex III Oxygen Consumption Glutamates Multienzyme Complexes Internal medicine NAD(P)H Dehydrogenase (Quinone) medicine Animals NADH NADPH Oxidoreductases Molecular Biology biology Electron Transport Complex II NADH dehydrogenase NADH Dehydrogenase Rats Inbred Strains Cell Biology NAD medicine.disease Rats Oxygen Succinate Dehydrogenase Kinetics Endocrinology Mitochondrial respiratory chain Coenzyme Q – cytochrome c reductase biology.protein Oxidoreductases Oxidation-Reduction Perfusion Research Article |
| Zdroj: | The Biochemical journal, Vol. 281 ( Pt 3), p. 709-15 (1992) |
| ISSN: | 1470-8728 0264-6021 |
| DOI: | 10.1042/bj2810709 |
| Popis: | Studies of Langendorff-perfused rat hearts have revealed a biphasic response of the mitochondrial respiratory chain to global ischaemia. The initial effect is a 30-40% increase in the rate of glutamate/malate oxidation after 10 min of ischaemia, owing to an increase in the capacity for NADH oxidation. This effect is followed by a progressive decrease in these oxidative activities as the ischaemia is prolonged, apparently owing to damage to Complex I at a site subsequent to the NADH dehydrogenase component. This damage is exacerbated by reperfusion, which causes a further decrease in Complex I activity and also decreases the activities of the other complexes, most notably of Complex III. Perfusion for up to 1 h with anoxic buffer produced only the increase in NADH oxidase activity, and neither anoxia alone, nor anoxia and reperfusion, caused loss of Complex I activity. Perfusing for 3-10 min with anoxic buffer before 1 h of global ischaemia had a significant protective effect against the ischaemia-induced damage to Complex I. |
| Databáze: | OpenAIRE |
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