The role of long‐chain acyl‐CoA in the damage of oxidative phosphorylation in heart mitochondria

Abstract

The aim of this investigation was to study the effect of intramitochondrial acyl-CoA on the respiration of rabbit heart mitochondria over the whole range of stationary respiratory rates between States 4 and 3. The creatine phosphokinase system was used for stabilization of extramitoehondrial adenine nueleotide concentration. It was shown that acyl-CoA depressed respiration more effectively in the intermediate range of respiration between States 4 and 3. The effect of acylCoA was negligible near State 4 and in State 3. These data are in line with our previous results concerning the dependence of the adenine nucleotide transloeator control coefficient on the rate of mitochondrial respiration. Thus, our data suggest that long-chain acyl-CoA may regulate oxidative phosphorylation in heart mitochondria in vivo.Adenine nucleotide translocator; Long-chain acyl-CoA; Oxidative phosphorylation; (Heart mitochondria)