Involvement of Aspartate/Glutamate Antiporter in Uncoupling Effect of Fatty Acids in Heart Mitochondria

V. N. Samartsev¹, I. P. Zeldi², and E. N. Mokhova^1*

¹Belozerskii Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, 119899 Russia; fax: (095) 939-3181

²Mari State University, Yoshkar-Ola, Russia

^* To whom correspondence should be addressed.

Received September 26, 1997; Revision received November 12, 1997

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Earlier it was shown that fatty acid-induced uncoupling in liver mitochondria is suppressed by the substrates of the aspartate/glutamate antiporter (V. N. Samartsev, A. V. Smirnov, I. P. Zeldi, O. V. Markova, E. N. Mokhova, and V. P. Skulachev (1997) Biochim. Biophys. Acta, 1319, 251-257). In this study it is shown that in heart mitochondria aspartate, glutamate, and diethyl pyrocarbonate do not affect oxygen consumption and membrane potential in the presence of laurate at pH 7.4. These compounds have a weak (versus carboxyatractylate) coupling effect at pH 7.0. This effect is manifested only in the presence of carboxyatractylate, magnesium, and phosphate in the incubation medium. It is suggested that these tissue-specific effects are due not only to the specific characteristics of aspartate/glutamate antiporter, but also to the differences in the content of endogenous metabolites in heart mitochondria.

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KEY WORDS: uncoupling, fatty acids, ADP/ATP-antiporter, aspartate/glutamate antiporter, carboxyatractylate, glutamate, aspartate, heart mitochondria

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