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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >The effect of N-acetylcysteine on the antitumor activity of ifosfamide.
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The effect of N-acetylcysteine on the antitumor activity of ifosfamide.

机译：N-乙酰半胱氨酸对异环磷酰胺的抗肿瘤活性的影响。

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摘要

Ifosfamide-induced nephrotoxicity is a serious adverse effect in children undergoing chemotherapy. Our previous cell and rodent models have shown that the antioxidant N-acetylcysteine (NAC), used extensively as an antidote for acetaminophen poisoning, protects renal tubular cells from ifosfamide-induced nephrotoxicity at a clinically relevant concentration. For the use of NAC to be clinically relevant in preventing ifosfamide nephrotoxicity, we must ensure there is no effect of NAC on the antitumor activity of ifosfamide. Common pediatric tumors that are sensitive to ifosfamide, human neuroblastoma SK-N-BE(2) and rhabdomyosarcoma RD114-B cells, received either no pretreatment or pretreatment with 400 micromol/L of NAC, followed by concurrent treatment with NAC and either ifosfamide or the active agent ifosfamide mustard. Ifosfamide mustard significantly decreased the growth of both cancer cell lines in a dose-dependent manner (p < 0.001). The different combined treatments of NAC alone, sodium 2-mercaptoethanesulfonate alone, or NAC plus sodium 2-mercaptoethanesulfonate did not significantly interfere with the tumor cytotoxic effect of ifosfamide mustard. These observations suggest that NAC may improve the risk/benefit ratio of ifosfamide by decreasing ifosfamide-induced nephrotoxicity without interfering with its antitumor effect in cancer cells clinically treated with ifosfamide.
机译：异环磷酰胺诱导的肾毒性是接受化疗的儿童的严重不良反应。我们以前的细胞和啮齿动物模型表明，抗氧化剂N-乙酰半胱氨酸（NAC）被广泛用作对乙酰氨基酚中毒的解毒剂，在临床相关浓度下可保护肾小管细胞免受异环磷酰胺诱导的肾毒性。为了使NAC在预防异环磷酰胺肾毒性方面具有临床意义，我们必须确保NAC对异环磷酰胺的抗肿瘤活性没有影响。对异环磷酰胺，人神经母细胞瘤SK-N-BE（2）和横纹肌肉瘤RD114-B细胞敏感的常见儿科肿瘤，未接受预处理或用400 micromol / L NAC进行预处理，然后同时接受NAC和异环磷酰胺或异环磷酰胺或活性成分异环磷酰胺芥末。异环磷酰胺芥末以剂量依赖的方式显着降低了两种癌细胞的生长（p <0.001）。单独使用NAC，单独使用2-巯基乙磺酸钠或单独使用NAC加2-巯基乙磺酸钠的不同联合治疗方法均不会显着干扰异环磷酰胺芥子的肿瘤细胞毒性作用。这些观察结果表明，NAC可通过降低异环磷酰胺诱导的肾毒性来改善异环磷酰胺的风险/获益比，而不会干扰其在经异环磷酰胺临床治疗的癌细胞中的抗肿瘤作用。

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