Abstract
The interaction of phosphoenolypyruvate with isolated rat liver mitochondria has been further investigated. The uptake of P-enolpyruvate is accompanied by the stoichiometric release of intramitochondrial adenine nucleotides resulting in the inhibition of mitochondrial protein synthesis. Addition of specific inhibitors of either the adenine nucleotide carrier or the tricarboylic acid carrier blocks the P-enolpyruvate-stimulated loss of adenine nucleotides and thereby prevents the resultant inhibition of mitochondrial protein synthesis. These data suggest that there is a specific interaction between the mitochondrial adenine nucleotide translocase and the tricarboxylic acid carrier resulting in the control of intramitochondrial adenine nucleotide levels of phosphoenolpyruvate.
Highlights
The interaction of phosphoenolypyruvate with isolated rat liver mitochondria has been further investigated
We showed that P-enolpyruvate inhibition could be overcome by either increasing the concentration of externally added ADP or by the addition of atractyloside, an inhibitor of the adenine nucleotide translocase system, and that addition of P-enolpyruvate caused the loss of radioactivity from mitochondria that had been prelabeled with [YZ]ADP
These values are in excellent agreement with those reported by others for the interaction of atractyloside with whole mitochondria [2, 29], isolated inner mitochondrial membranes [30], and reconstituted vesicles
Summary
The interaction of phosphoenolypyruvate with isolated rat liver mitochondria has been further investigated. Seven anion carriers have been ascribed to the inner mitochondrial membrane These include transport systems for the adenine nucleotides (l-3), inorganic phosphate [4,5,6], dicarboxylic acids (7-IO), a-ketoglutarate [7], tricarboxylic acids (ll-13), aspartate [14], and glutamate [14, 15]. Harris has shown that phosphoenolpyruvate, long thought to be a nonpermeating species because of its hydrophilic nature, can influence the net accumulation of citrate within the mitochondrial matrix [18] This observation is consistent with the earlier observation by Gamble and Mazur [19] that citrate facilitated the release of endogenous P-enolpyruvate from rabbit liver mitochondria.
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