Stable isotopes of Mg2+ as activators of the suppressed ATP-generating function of mitochondria

The ATP-generating activity of rat myocardial mitochondria and intramitochondrial creatine kinase was examined as a function of the isotopy of the incubation medium magnesium pool. The study was performed using in vitro systems prepared from the hearts of animals injected with 1-methylnicotine amide...

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Bibliographic Details
Published in:	Biofizika Vol. 50; no. 1; p. 80
Main Authors:	Kuznetsov, D A, Arkhantel'skiĭ, S E, Berdieva, A G, Markarian, A A, Khasigov, P Z, Gatagonova, T M, Ktsova, S A, Orlova, M A
Format:	Journal Article
Language:	Russian
Published:	Russia (Federation) 01-01-2005
Subjects:	Adenosine Triphosphate - biosynthesis Animals Creatine Kinase - metabolism Magnesium - pharmacology Male Mitochondria, Heart - drug effects Mitochondria, Heart - enzymology Mitochondria, Heart - metabolism NAD - metabolism Rats Rats, Inbred SHR
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Summary:	The ATP-generating activity of rat myocardial mitochondria and intramitochondrial creatine kinase was examined as a function of the isotopy of the incubation medium magnesium pool. The study was performed using in vitro systems prepared from the hearts of animals injected with 1-methylnicotine amide, which suppresses the NAD (NADP)-dependent reactions in vivo. It was shown that the presence of the 25Mg paramagnetic cations essential by compensates for the intramitochondrial ATP deficiency caused by the 1-methyl-nicotine amide-induced blockade of oxidative phosphorylation. This effect is hardey achievable in systems where the magnesium pool consists of isotopes with a zero nuclear spin (24Mg, 26Mg). The restoration of mitochondrial ATP synthesis involves the participation of creatine kinase since the activity of the latter does not depend on 1-methyl-nicotine amide. In this case, the high efficiency of this restaration seems to be a spin-selective phenomenon which requires predominantly 25Mg2+ cations. A possible meaning of the data for further studies on the mechanisms of enzymatic catalysis regulation is discussed.
ISSN:	0006-3029