Dehpour A R, Ghafourifar P, Ahangari N
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Iran.
Toxicology. 1996 Jun 17;110(1-3):9-15. doi: 10.1016/0300-483x(96)03317-3.
N-acetyl-beta-D-glucosaminidase (NAG) is one of the sensitive hydrolytic lysosomal enzymes which is released after renal tubular damages. We studied gentamicin-induced nephrotoxicity by determining the NAG release in perfused rat kidney. 100 micrograms/ml of gentamicin caused a time-dependent increase in enzymuria, peaking at 90 min. At this time the released NAG is about sixfold more than the control. The effect of concurrent perfusion with 100 micrograms/ml gentamicin and with 0.5 mmol/l lithium chloride or 0.5 mmol/l rubidium chloride in the perfusion fluid was also studied by measuring NAG activity in the perfusate. Both cations decrease the gentamicin-induced NAG release. However, the inhibitory effect of lithium chloride may be due to interference of this ion with the polyphosphoinositide cycle in renal tubular lysosomal membranes. There is no obvious evidence for an inhibitory effect of rubidium chloride.
N - 乙酰 - β - D - 氨基葡萄糖苷酶（NAG）是一种敏感的溶酶体水解酶，在肾小管损伤后会释放出来。我们通过测定灌注大鼠肾脏中的NAG释放量来研究庆大霉素诱导的肾毒性。100微克/毫升的庆大霉素导致酶尿呈时间依赖性增加，在90分钟时达到峰值。此时释放的NAG约为对照组的六倍。通过测量灌注液中的NAG活性，还研究了在灌注液中同时灌注100微克/毫升庆大霉素与0.5毫摩尔/升氯化锂或0.5毫摩尔/升氯化铷的效果。两种阳离子均降低庆大霉素诱导的NAG释放。然而，氯化锂的抑制作用可能是由于该离子干扰了肾小管溶酶体膜中的多磷酸肌醇循环。没有明显证据表明氯化铷有抑制作用。
