Abstract

1. A Q 10 of about 3 for palmitoyl-CoA synthetase (EC 6.2.1.3) in rat heart and liver mitochondria is found. 2. In heart mitochondria Nagarse (EC 3.4.4.16) destroys the ability to activate palmitate. When, however, heart mitochondria are oxidizing palmitate, they are protected from the inactivating action of Nagarse. 3. Although treatment of liver mitochondria with Nagarse causes the loss of about 95 % of the palmitoyl-CoA synthetase activity, no influence is observed on palmitate oxidation. 4. Adenosine inhibits palmitoyl-CoA synthetase in liver and heart mitochondria. Adenosine is a competitive inhibitor with respect to ATP with an apparent K i of 0.1 mM. The residual palmitoyl-CoA synthetase in Nagarse-treated liver mitochondria is much less sensitive to adenosine. 5. 2 mM adenosine or 2 mM adenosinesulfate inhibit palmitate oxidation (in the presence of 2.5 mM ATP) in heart mitochondria 60–90 %. 6. The data obtained are consistent with the concept of a palmitoyl-CoA synthetase localized on the outside of the outer membrane of rat heart and liver mitochondria, with an additional locus of (ATP-dependent) palmitoyl-CoA synthesis in the inner membrane matrix compartment of liver mitochondria.

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