Abstract
In order to gain insight into the mechanism by which AZT affects mitochondrial metabolism in heart, leading to the ATP deficiency syndrome, the capability of AZT to affect certain mitochondrial translocators was checked in coupled mitochondria isolated from rat heart. AZT was found to strongly inhibit the ADP/ATP antiport, in a competitive manner (Ki 7 microM), as photometrically measured. Contrarily, the rate of the succinate/malate exchange via the dicarboxylate carrier, of the oxaloacetate uptake via the oxodicarboxylate carrier and of cis-aconitate uptake via the tricarboxylate carrier was found to be unchanged in the presence of AZT.
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