Involvement of long-chain acyl CoA in the antagonistic effects of halothane and L-carnitine on mitochondrial energy-linked processes.
Incubation of rat liver mitochondria in the presence of halothane induced a consistent impairment of mitochondrial oxidative phosphorylation without significantly affecting the steady-state of transmembrane electrical potential. These alterations of mitochondrial energy-linked processes were associated with a consistent accumulation of long-chain acyl CoA. Addition of L-carnitine partially prevented the effects of halothane on oxidative phosphorylation and completely abolished the halothane-induced long-chain acyl CoA accumulation. The possibility is discussed that the damaging action of halothane on mitochondrial functions might be partially ascribed to the noxious action of the excess of long-chain acyl CoA induced the anesthetic.
D000214:Acyl Coenzyme A / Q000032:analysis / Q000502:physiology*; D000244:Adenosine Diphosphate / Q000494:pharmacology; D000818:Animals; D002331:Carnitine / Q000494:pharmacology*; D004734:Energy Metabolism / Q000187:drug effects*; D006221:Halothane / Q000494:pharmacology*; D066298:In Vitro Techniques; D008564:Membrane Potentials; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D010085:Oxidative Phosphorylation / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains
D000214:Acyl Coenzyme A; D000244:Adenosine Diphosphate; D002331:Carnitine; D006221:Halothane