The mitochondrial phosphoglyceroyl‐ATP‐containing polymer, purinogen, is unchanged by cardiac ischaemia and reperfusion but may function in the regulation of free intracellular inorganic phosphate concentrations

Previous work in our laboratory demonstrating large unexplained systematic variations in the heart contents of free adenine nucleotides led us to propose the existence of some unrecognised sequestered form and thence to the purification of very labile acid‐insoluble oligomers which we characterised as oligo[3‐phospho‐glyceroyl‐γ‐triphospho(5′)adenosine(3′)], abbreviated to (PG‐ATP) n . More recently, we provided evidence that these oligomers appear to be the end chains of a complex polymer located in the mitochondrial intermembrane space of a number of rat tissues. We called this polymer purinogen and devised a means of assaying it quantitively [Patel, B., Sarcina, M. & Mowbray, J. (1994) Eur. J. Biochem. 220 , 663−669]. Here we report measurements of purinogen in perfused hearts subjected to moderate and severe global ischaemia and reperfusion. Measurements of tissue and perfusate nucleotides, nucleosides and purine degradation products demonstrate that ischaemia led to the augmentation of the free nucleotide content by up to 30 % and its re‐sequestration on reperfusion in reversible but not in irreversible ischaemia. The purinogen content was unchanged by ischaemia or reperfusion implying the existence of some other unidentified storage pool. By contrast, glucose addition to glycolytically deprived hearts or removal of P i from perfusion medium, conditions which might be expected to alter demand for intracellular P i , led to the quantitative transfer of nucleotides between phosphate‐rich purinogen and free nucleotides. The possibility that purinogen may act as a rapidly accessible reservoir of intracellular inorganic phosphate is discussed.