卡铂致大鼠肾毒性的剂量效应。

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Husai K, Jagannathan R, Hasan Z, Trammell GL, Rybak LP, Hazelrigg SR, Somani SM

卡铂致大鼠肾毒性的剂量效应。

中华毒物学杂志，2002;31(2):83-9。

PubMed ID

12420797 (PubMed视图

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摘要

摘要:卡铂是第二代含铂的抗癌药物，目前被用于治疗多种癌症。大剂量卡铂化疗可引起肿瘤患者肾小管损伤。然而，卡铂致肾损伤的生化机制尚未得到很好的研究。本研究探讨了卡铂诱导大鼠肾脏内源性抗氧化剂、脂质过氧化和铂含量变化的剂量效应。雄性Wistar大鼠(250 ~ 300 g)分为5组:(1)对照组(生理盐水，腹腔注射);(2)卡铂(64mg /kg，腹腔注射);(3)卡铂(128 mg/kg，腹腔注射);(4)卡铂(192 mg/kg，腹腔注射);(5)卡铂(256 mg/kg，腹腔注射)。这些动物在治疗四天后被处死。 The blood and kidneys were isolated and analyzed. Plasma creatinine and blood urea nitrogen levels were increased significantly in response to carboplatin in a dose-dependent manner. Renal superoxide dismutase and catalase activities were decreased significantly due to carboplatin at dosages of 128 mg/kg and above. The protein expressions of renal copper/zinc-superoxide dismutase and manganese-superoxide dismutase significantly depleted after carboplatin. Carboplatin (192 and 256 mg/kg) significantly increased lipid peroxidation (malondialdehyde concentration) in rat kidneys. Carboplatin dose-dependently increased the renal platinum concentration, with significance at dosages of 128 mg/kg and above. Carboplatin (256 mg/kg) significantly increased renal xanthine oxidase activity, while ratio of reduced to oxidized glutathione depleted significantly. The data suggested that carboplatin caused dose-dependent oxidative renal injury, as evidenced by renal antioxidant depletion, enhanced lipid peroxidation, platinum content, plasma creatinine and blood urea nitrogen levels in rats.

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药物酶

药物	酶	种类	生物	药理作用	行动
卡铂	黄嘌呤脱氢酶和氧化酶	蛋白质	人类	未知的	诱导物	细节