Inhibition of 2,4-Dinitrophenol-Induced Potassium Efflux by Adenine Nucleotides in Mitochondria

O. V. Baranova, Yu. Yu. Skarga, A. E. Negoda, and G. D. Mironova^*

Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, pr. Nauki 3, Pushchino, Moscow Region, 142292 Russia; fax: 7 (0967) 79-0553; E-mail: mironova@venus.iteb.serpukhov.su

^* To whom correspondence should be addressed.

Received April 24, 1999; Revision received August 5, 1999

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The influence of nucleotides on 2,4-dinitrophenol (DNP)-induced K⁺ efflux from intact rat liver mitochondria has been studied. ATP and ADP at micromolar concentrations were found to inhibit mitochondrial potassium transport, whereas GTP, GDP, CTP, and UTP did not show tha same effect. The values of half-maximal inhibition (IC₅₀) were ~20 µM for ATP and ~60 µM for ADP. It is suggested that adenine nucleotides exert their inhibitory action at the matrix side of the inner mitochondrial membrane since the inhibitor of adenine nucleotide translocase atractyloside at concentration of 1 µM completely removed the inhibitory effect of ATP and ADP. The mitochondrial ATPase inhibitor oligomycin (2 µg/ml) was found to reduce slightly the rate of DNP-induced K⁺ efflux and had no effect on inhibition by adenine nucleotides; the latter was insensitive to Mg²⁺ and the changes in pH. It seems likely that the regulation of potassium transport is not due to phosphorylation of the channel-forming protein but to binding of the nucleotides in specific regulatory sites. The possibility of potassium efflux from mitochondria in the presence of uncoupler via the ATP-dependent potassium channel is discussed.

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KEY WORDS: mitochondria, potassium transport, adenine nucleotides, uncoupler, regulation

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