THE MITOCHONDRIAL PHOSPHOGLYCEROYL-ATP-CONTAINING POLYMER, PURINOGEN,IS UNCHANGED BY CARDIAC ISCHEMIA AND REPERFUSION BUT MAY FUNCTION IN THE REGULATION OF FREE INTRACELLULAR INORGANIC-PHOSPHATE CONCENTRATIONS

Previous work in our laboratory demonstrating large unexplained system atic 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 whi ch we characterised as spho-glyceroyl-gamma-triphospho(5')adenosine(3' )], abbreviated to (PG-ATP)(n). More recently, we provided evidence th at these oligomers appear to be the end chains of a complex polymer lo cated in the mitochondrial intermembrane space of a number of rat tiss ues. We called this polymer purinogen and devised a means of assaying it quantitively [Patel, B., Sarcina, M. & Mowbray, J. (1994) Eur. J. B iochem. 220, 663-669]. Here we report measurements of purinogen in per fused hearts subjected to moderate and severe global ischaemia and rep erfusion. Measurements of tissue and perfusate nucleotides, nucleoside s and purine degradation products demonstrate that ischaemia led to th e augmentation of the free nucleotide content by up to 30% and its re- sequestration on reperfusion in reversible but not in irreversible isc haemia. The purinogen content was unchanged by ischaemia or reperfusio n implying the existence of some other unidentified storage pool. By c ontrast, glucose addition to glycolytically deprived hearts or removal of Pi from perfusion medium, conditions which might be expected to al ter demand for intracellular Pi, led to the quantitative transfer of n ucleotides between phosphate-rich purinogen and free nucleotides. The possibility that purinogen may act as a rapidly accessible reservoir o f intracellular inorganic phosphate is discussed.