Weinberg J M
Department of Internal Medicine, Veterans Administration Medical Center, Ann Arbor, Michigan.
Biochem Med Metab Biol. 1988 Jun;39(3):319-29. doi: 10.1016/0885-4505(88)90092-8.
Suspensions enriched in isolated rabbit proximal tubules were subjected to varying degrees of oxygen deprivation-induced injury by incubating them under hypoxic conditions at pH 7.4 or pH 6.6 or under high density pelleted conditions and adenine nucleotide degradation was characterized. The major metabolite was hypoxanthine. Its levels increased with the extent of irreversible injury. It was not further degraded or salvaged. Recovery of cell ATP during reoxygenation was predominantly from the remaining cell nucleotides. Allopurinol did not alter the pattern of purine metabolism or the extent of cell injury. These observations provide information on the intrinsic purine metabolic capacity of renal tubule cells during oxygen deprivation which is relevant to understanding both the salvage mechanisms available in these cells as well as the contribution of purine metabolism to the pathogenesis of oxygen deprivation-induced tubule cell injury.
将富含分离兔近端肾小管的悬浮液在pH 7.4或pH 6.6的缺氧条件下孵育，或在高密度沉淀条件下孵育，使其遭受不同程度的缺氧诱导损伤，并对腺嘌呤核苷酸降解进行表征。主要代谢产物是次黄嘌呤。其水平随不可逆损伤程度的增加而升高。它不会进一步降解或补救。复氧过程中细胞ATP的恢复主要来自剩余的细胞核苷酸。别嘌呤醇不会改变嘌呤代谢模式或细胞损伤程度。这些观察结果提供了关于缺氧期间肾小管细胞内在嘌呤代谢能力的信息，这与理解这些细胞中可用的补救机制以及嘌呤代谢对缺氧诱导的肾小管细胞损伤发病机制的贡献有关。
