Takeda M, Jung K Y, Sekine T, Endou H, Koide H
Department of Pharmacology and Toxicology, Kyorin University School of Medicine, Tokyo, Japan.
Toxicol Lett. 1995 Nov 15;81(2-3):85-9. doi: 10.1016/0378-4274(95)03411-0.
Since guanidinoacetic acid (GAA), a precursor of creatine, is synthesized mainly in the proximal tubule of the kidney where gentamicin (GM) nephrotoxicity often occurs, GM-induced renal cell damage was investigated using GAA synthesis in tubular suspension as an indicator. Results obtained were as follows: (1) GAA synthesis was significantly suppressed with 1 mM GM; (2) GM-induced decrease in GAA synthesis was recognized during incubation longer than 15 min; (3) furosemide significantly enhanced the suppression of GAA synthesis by GM. The results obtained parallel with those in the whole animal thus making GAA synthesis in tubular suspension a valid system for evaluating the GM-induced proximal tubular damage.
由于肌酸的前体胍基乙酸（GAA）主要在肾脏近端小管合成，而庆大霉素（GM）肾毒性常在此发生，因此以肾小管悬液中的GAA合成作为指标，研究了GM诱导的肾细胞损伤。结果如下：（1）1 mM GM可显著抑制GAA合成；（2）孵育超过15分钟时，可观察到GM诱导的GAA合成减少；（3）呋塞米可显著增强GM对GAA合成的抑制作用。这些结果与在整体动物中的结果一致，从而使肾小管悬液中的GAA合成成为评估GM诱导的近端肾小管损伤的有效系统。
