Saad Sherif Y, Al-Rikabi Ammar C
Department of Clinical Pharmacy, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.
Chemotherapy. 2002 Mar;48(1):42-8. doi: 10.1159/000048587.
Taurine, which is the major intracellular free beta-amino acid, is known to be an antioxidant and a membrane-stabilizing agent. This study was designed to investigate the protective role of taurine supplementation against cisplatin-induced nephrotoxicity.
Male Wistar rats were divided into six groups and treated as follows: (1) saline-treated control drinking tap water, (2) saline-treated plus taurine-supplemented (1.5% taurine in the drinking water), (3) saline-treated plus taurine-depleted (3% beta-alanine in the drinking water), (4) cisplatin-treated, CDDP 6 mg/kg intraperitoneally, (5) taurine-supplemented plus CDDP-treated and (6) taurine-depleted plus CDDP-treated. Rats were sacrificed 7 days after CDDP treatment, and serum as well as kidneys were isolated and analyzed.
CDDP-treated rats showed increased kidney weight as a percentage of total body weight, serum creatinine and BUN levels and decreased serum albumin and calcium levels. Also, CDDP treatment resulted in a depletion of kidney GSH content, a reduction in the kidney glutathione peroxidase (GSH-Px) activity and increased kidney MDA production level. Taurine supplementation attenuated CDDP-induced nephrotoxicity which was manifested by jeopardizing the elevation in serum creatinine and BUN levels and the reduction in serum albumin and calcium levels. Moreover, taurine supplementation restored kidney GSH content and GSH-Px activity and reduced platinum accumulation and MDA production levels in the kidney tissue following CDDP treatment. Histopathological examination of the kidney of CDDP-treated rats revealed tubular atrophy, tubular necrosis and desquamation of renal tubular cells. However, taurine supplementation protected against CDDP-induced histopathological changes.
The data suggest that taurine supplementation effectively attenuates the accumulation of platinum within kidney tissue and counteracts the deleterious effect of CDDP on the renal tubular function.
牛磺酸是细胞内主要的游离β-氨基酸，已知具有抗氧化和膜稳定作用。本研究旨在探讨补充牛磺酸对顺铂诱导的肾毒性的保护作用。
将雄性Wistar大鼠分为六组，处理如下：（1）饮用自来水的生理盐水处理对照组；（2）饮用添加牛磺酸（饮用水中含1.5%牛磺酸）的生理盐水处理组；（3）饮用耗尽牛磺酸（饮用水中含3%β-丙氨酸）的生理盐水处理组；（4）腹腔注射顺铂（CDDP）6 mg/kg的顺铂处理组；（5）补充牛磺酸加顺铂处理组；（6）耗尽牛磺酸加顺铂处理组。顺铂处理7天后处死大鼠，分离血清和肾脏并进行分析。
顺铂处理的大鼠肾脏重量占总体重的百分比、血清肌酐和尿素氮水平升高，血清白蛋白和钙水平降低。此外，顺铂处理导致肾脏谷胱甘肽（GSH）含量减少、肾脏谷胱甘肽过氧化物酶（GSH-Px）活性降低以及肾脏丙二醛（MDA）生成水平升高。补充牛磺酸减轻了顺铂诱导的肾毒性，表现为血清肌酐和尿素氮水平升高以及血清白蛋白和钙水平降低的情况得到缓解。此外，补充牛磺酸可恢复顺铂处理后肾脏组织中的GSH含量和GSH-Px活性，并减少铂的蓄积以及MDA生成水平。对顺铂处理大鼠的肾脏进行组织病理学检查发现肾小管萎缩、肾小管坏死和肾小管细胞脱落。然而，补充牛磺酸可预防顺铂诱导的组织病理学变化。
数据表明，补充牛磺酸可有效减轻铂在肾脏组织中的蓄积，并抵消顺铂对肾小管功能的有害影响。
