Brief antecedent anoxia preserves mitochondrial function after sustained undersupply: A subcellular correlate to ischemic preconditioning?
| Autor: | Felix T. Wieland, Achim M. Vogt, Hugo A. Katus, Sven Y. Vetter, Albrecht Elsässer, Wolfgang Kübler, Anja Pott, Cordula Ackermann, Wolfgang Schoels, Constanze Reinhard, Sabrina C Lang, Osman Tutdibi |
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| Rok vydání: | 2006 |
| Předmět: |
Male
Potassium Channels Cell Respiration Clinical Biochemistry Cell Intracellular Space Pharmacology Mitochondrion Mitochondria Heart Mice Adenosine Triphosphate ATP hydrolysis Respiration Diazoxide medicine Animals Rats Wistar Hypoxia Creatine Kinase Molecular Biology Aspartate Aminotransferase Mitochondrial biology Myocardium Cell Biology General Medicine Adaptation Physiological Potassium channel Rats medicine.anatomical_structure Biochemistry Ischemic Preconditioning Myocardial biology.protein Ischemic preconditioning Creatine kinase Aspartate Aminotransferase Cytoplasmic medicine.drug |
| Zdroj: | Molecular and Cellular Biochemistry. 285:191-196 |
| ISSN: | 1573-4919 0300-8177 |
| DOI: | 10.1007/s11010-005-9071-9 |
| Popis: | Background: There is increasing evidence that mitochondria – owning a high degree of autonomy within the cell – might represent the target organelles of the myocardial protection afforded by ischemic preconditioning. It was the aim of the study to investigate a possible subcellular correlate to ischemic preconditioning at the mitochondrial level. In addition, we tested whether this protection depends on mitochondrial ATP-dependent potassium channels (KATP) and an might involve an attenuation of mitochondrial ATP hydrolysis during sustained anoxia.Methods and Results: Sustained anoxia (A, 14 min) and reoxygenation (R) completely inhibited state 3 and state 4 respiration of isolated ventricular mitochondria from Wistar rats. An antecedent brief anoxic incubation (4 min) followed by reoxygenation (2 min) prevented this loss of mitochondrial function. The protection afforded by anoxic preconditioning could be mimicked by the KATP opener diazoxide (30 μmol/l) and was completely inhibited by the KATP blocker 5-hydroxydecanoic acid (300 μmol/l). Structural mitochondrial integrity, as estimated from externalization of the mitochondrial enzymes creatine kinase and glutamateoxalacetate transaminase, remained unchanged between the groups, as did mitochondrial ATP loss during anoxia.Conclusion: For the first time, we provide direct evidence for a subcellular preconditioning-like functional mitochondrial adaptation to sustained anoxia. This effect apparently depends on opening of KATP but is independent of ATP preservation. |
| Databáze: | OpenAIRE |
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