Involvement of long-chain acyl CoA in the antagonistic effects of halothane and L-carnitine on mitochondrial energy-linked processes

• Published in: Biochemical and biophysical research communications Vol. 139; no. 1; pp. 303 - 307
• Main Authors: Branca, D., Toninello, A., Scutari, G., Florian, M., Siliprandi, N., Vincenti, E., Giron, G.P.
• Format: Journal Article
• Language: English
• Published: San Diego, CA Elsevier Inc 29.08.1986; Elsevier
• Subjects: Acyl Coenzyme A - analysis; Acyl Coenzyme A - physiology; Adenosine Diphosphate - pharmacology; Animals; Applied sciences; Carnitine - pharmacology; Energy Metabolism - drug effects; Exact sciences and technology; Halothane - pharmacology; In Vitro Techniques; Membrane Potentials; Mitochondria - drug effects; Mitochondria - metabolism; Other techniques and industries; Oxidative Phosphorylation - drug effects; Rats; Rats, Inbred Strains; Δ μ ~ H; Δ ψ; LCACoA; HPLC; Hepes
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/S0006-291X(86)80113-9

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.