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

FEBS Letters

Mildaz̆ien≐, V.¹  Kholodenko, B.²  Toleikis, A.¹  Borutait≐, V.¹  Ivanovien≐, L.¹  Pras̆kevic̆ius, A.¹ 

[1] Central Research Laboratory, Kaunas Medical Institute, Z. Januškevičius Str. 4, 233007 Kaunas USSR;Research Institute for Technology and Safety of Drugs, Kirov Str. 23, Kupavna, 142450 Moscow Region, USSR

关键词: Adenine nucleotide translocator;    Long-chain acyl-CoA;    Oxidative phosphorylation;    (Heart mitochondria);    ANT;    adenine nucleotide translocator;   

DOI  :  10.1016/0014-5793(89)80141-3

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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 extramitochondrial adenine nucleotide 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 acyl-CoA 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 translocator 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.

【 授权许可】

Unknown