THE FUNCTION OF ATP-ADP TRANSLOCATOR IN THE REGULATION OF MITOCHONDRIAL RESPIRATION DURING DEVELOPMENT OF HEART ISCHEMIC-INJURY

Inhibitor titration studies were carried out in order to quantify the amount of control exerted by ATP/ADP translocator on the rate of succinate, palmitoylcamitine + malate and pyruvate + malate oxidation in ischemia-damaged heart mitochondria. It was shown that after 30 min of total ischemia in vitro the maximal value of the control coefficient of the translocator was as high as in the control: 0.5-0.72 (succinate), 0.8-0.87 (palmitoylcarnitine + malate), 0.83-0.95 (pyruvate + malate). However, the translocator-controlled range of respiratory rates of ischemic mitochondria was narrower than that of normal mitochondria. The control coefficient of the translocator close to State 3 and State 4 was equal to 0-0.15. After 45 min ischemia the maximal value of the translocator control coefficient decreased by 25-30% in comparison with normal mitochondria with all substrates investigated. This value was preserved within a wide range of mitochondrial respiratory rates including the maximal rate in State 3. It was found that the amount of ATP/ADP translocator in mitochondria decreased by 20% after only 45 min ischemia. Our data show that the ATP/ADP translocator is one of the most important steps in regulation of oxidative phosphorylation in isolated mitochondria during development of heart ischemic injury.