[The effect of magnesium pool isotopy on reactivation of mitochondrial ATP synthesis suppressed by 1-methyl-nicotine amide].
The ATP-generating activity of both rat myocardial mitochondria and intramitochondrial creatine phosphokinase (CPK) was examined as a function of the incubation medium magnesium pool isotopy. The in vitro systems tested were prepared from the hearts of animals treated with single injection of 1-methyl-nicotine amide (MNA) suppressing the NAD(P)-dependent reactions in vivo. The presense of the 25Mg paramagnetic cations leads to essential compensation of intramitochondrial ATP deficiency caused by the MNA induced blockade of oxidative phosphorylation. This effect is merely unreachable in those systems where the magnesium pool consists of isotopes with a zero nuclear spin (24Mg, 26Mg). The reactivation of mitochondrial ATP synthesis described here involves CPK activity which does not depends on MNA. In this case, a high efficiency of this reactivation seems to be a spin selective phenomenon which requires, predominantly, 25Mg2+ cations.
Kuznetsov
D A
DA
Aliautdin
R N
RN
Markarian
A A
AA
Berdieva
A G
AG
Khasigov
P Z
PZ
Gatagonova
T M
TM
Ktsoeva
S A
SA
Orlova
M A
MA
D000244:Adenosine Diphosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000096:biosynthesis*; D000818:Animals; D002413:Cations, Divalent; D003402:Creatine Kinase / Q000037:antagonists & inhibitors; D007554:Isotopes; D007700:Kinetics; D008274:Magnesium / Q000378:metabolism*; D008297:Male; D008929:Mitochondria, Heart / Q000201:enzymology / Q000378:metabolism*; D009536:Niacinamide / Q000031:analogs & derivatives* / Q000494:pharmacology; D010084:Oxidation-Reduction; D010085:Oxidative Phosphorylation; D051381:Rats; D011918:Rats, Inbred SHR
D002413:Cations, Divalent; D007554:Isotopes; D009536:Niacinamide; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D003402:Creatine Kinase; D008274:Magnesium; C024058:N(1)-methylnicotinamide