Adenine Nucleotide Metabolism by Isolated Kidney Tubules during Oxygen Deprivation

Degradation of cell nucleotides during ischemic tissue injury is well documented and has been characterized in some detail for several tissues (l-l 1). This process may contribute to cell injury by limiting the availability of nucleotide precursors during recovery (7-9) and as a result of deleterious effects of reactive oxygen metabolites generated during metabolism of hypoxanthine and xanthine by xanthine oxidase (12,13). Published data for the kidney have been collected during in viva models of renal ischemia (l-6). Zn viva studies, however, do not allow assessment of the individual contributions of the various different cell types within the kidney to the observed changes and generally sample from a rather heterogenous pattern of injury. The recent development of models of oxygen deprivation injury to isolated rabbit proximal tubules (14,15) has provided the opportunity to assess tubule purine nucleotide metabolism during oxygen deprivation in a particularly well-controlled setting which allows direct measurements in tubule cells during both reversible and irreversible forms of cell injury. This manuscript details the patterns of purine degradation produced by oxygen deprivation injury to th