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[The mechanism of action of a synthetic derivative of 1,4-naphthoquinone on the respiratory chain of liver and heart mitochondria].

It was found that the 1.4-naphthoquinone derivative AK-135 (2-methyl-3-piperidine-methyl-1.4-naphthoquinone hydrochloride) possesses a marked acceptor capacity during succinate and glutamate oxidation by rat liver and rabbit heart mitochondria. AK-135 fully restores the rate of glutamate (but not succinate) oxidation by liver and heart mitochondria catalyzed by rotenone, antimycin A and cyanide. In non-phosphorylating preparations of liver and heart mitochondria, AK-135 eliminates the inhibition of respiration on exogenous NADH induced by the same electron transport inhibitors. In liver mitochondria, the stimulation of succinate oxidation is due to a reverse electron transfer, whereas in the heart it proceeds via the rotenone-insensitive pathway. The experimental results suggest that in the liver and heart AK-135 accepts electrons from NADH-dehydrogenase oxidizing endogenous NADH. Besides, in the liver this compound is also capable of accepting electrons from NADH-cytochrome b5 reductase.