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J. Biol. Chem., Vol. 268, Issue 2, 938-947, Jan, 1993
DA Cox and MA Matlib
The role of the Na(+)-Ca2+ exchanger of heart mitochondria in cellular
functioning is not yet clear. The objectives of this study were to
investigate the effects of stimulation and inhibition of the Na(+)-Ca2+
exchanger on the matrix free Ca2+ concentration in isolated heart
mitochondria and to determine the consequences of these changes on the rate
of NADH production via Krebs cycle turnover and the oxidative
phosphorylation rate (OPR) supported by alpha-ketoglutarate dehydrogenase,
a Ca(2+)-regulated matrix enzyme. Activation of Na(+)- Ca2+ exchange by
increasing extramitochondrial Na+ concentration was found to decrease the
matrix free [Ca2+] in a concentration-dependent manner. Inhibitors of
mitochondrial Na(+)-Ca2+ exchange activity inhibited the decrease in matrix
free [Ca2+] mediated by Na+. Increasing concentrations of Na+ were also
found to inhibit both the rate of NADH production and OPR. Inhibitors of
mitochondrial Na(+)-Ca2+ exchange also blocked the effects of Na+ on the
rate of NADH production and OPR in a similar concentration range. The
results indicate that alterations in matrix free [Ca2+] induced by changes
in mitochondrial Na(+)-Ca2+ exchange activity are translated into changes
in the rate of NADH production and the overall rate of oxidative
phosphorylation.
A role for the mitochondrial Na(+)-Ca2+ exchanger in the regulation of oxidative phosphorylation in isolated heart mitochondria
Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Ohio 45267-0575.
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