The protective effect of cyclosporine A, carnitine, and Mg(2+) with ADP during calcium(2+)-dependent permeabilization of mitochondria by fatty acids and activation of NADH oxidation by an external pathway

The ability of cyclosporin A, Mg2+ plus ADP and L-carnitine to enhance energy recoupling in liver mitochondria and to inhibit the induction of the external pathway of NADH oxidation during Ca(2+)-dependent oxidative phosphorylation uncoupling by palmitate has been studied. Cyclosporin A, Mg2+ plus A...

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Published inBiokhimiia (Moscow, Russia) Vol. 58; no. 8; p. 1266
Main Authors Starkov, A A, Markova, O V, Mokhova, E N, Arrigoni-Martelli, E, Battelli, D, Bobyleva, V A
Format Journal Article
LanguageRussian
Published Russia (Federation) 01.08.1993
Subjects
Adenosine Diphosphate - pharmacology
Animals
Calcium - metabolism
Carnitine - pharmacology
Cyclosporine - pharmacology
Energy Metabolism
Fatty Acids - pharmacology
Magnesium - pharmacology
Mitochondria, Liver - drug effects
Mitochondria, Liver - metabolism
NAD - metabolism
Oxidation-Reduction
Rats
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Summary:The ability of cyclosporin A, Mg2+ plus ADP and L-carnitine to enhance energy recoupling in liver mitochondria and to inhibit the induction of the external pathway of NADH oxidation during Ca(2+)-dependent oxidative phosphorylation uncoupling by palmitate has been studied. Cyclosporin A, Mg2+ plus ADP and L-carnitine plus ATP prevent with an equal efficiency the induction of the external pathway of NADH oxidation by palmitate and Ca2+ in mitochondria but differ drastically by their ability to increase the coupling in permeabilized mitochondria. The recoupling effect of cyclosporin is manifested after addition of Mg2+ plus ADP. The protective action of Mg2+ plus ADP is prevented by preincubation with carboxyatractylate. Oxidation of NADH via an external pathway results in delta psi generation, however, only in the presence of the recoupling factors. The role of the cyclosporin-sensitive pore in Ca(2+)-dependent damage of mitochondria as well as in the induction of the external pathway of NADH oxidation is discussed.
ISSN:0320-9725