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首页> 外文期刊>Urologic oncology >Commentary on 'Tissue-specific mutagenesis by N-butyl-N-(4-hydroxybutyl) nitrosamine as the basis for urothelial cell carcinogenesis.' He Z, Kosinska W, Zhao ZL, Wu XR, Guttenplan JB, Department of Basic Science, New York University Dental College, NY, USA. Mutat Res 2012;742(1-2):92-5 [Epub 2011 Dec 4].
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Commentary on 'Tissue-specific mutagenesis by N-butyl-N-(4-hydroxybutyl) nitrosamine as the basis for urothelial cell carcinogenesis.' He Z, Kosinska W, Zhao ZL, Wu XR, Guttenplan JB, Department of Basic Science, New York University Dental College, NY, USA. Mutat Res 2012;742(1-2):92-5 [Epub 2011 Dec 4].

机译：关于“ N-丁基-N-（4-羟丁基）亚硝胺作为尿路上皮细胞致癌基础的组织特异性诱变”的评论。美国纽约大学牙科学院基础科学系何Z，科辛斯卡W，赵ZL，吴XR，Guttenplan JB。 Mutat Res 2012; 742（1-2）：92-5 [Epub 2011 Dec 4]。

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Bladder cancer is one of the few cancers that have been linked to carcinogens in the environment and tobacco smoke. Of the carcinogens tested in mouse chemical carcinogenesis models, N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) is one that reproducibly causes high-grade, invasive cancers in the urinary bladder, but not in any other tissues. However, the basis for such a high-level tissue-specificity has not been explored. Using mutagenesis in lacI (Big Blue?) mice, we show here that BBN is a potent mutagen and it causes high-level of mutagenesis specifically in the epithelial cells (urothelial) of the urinary bladder. After a 2-6-week treatment of 0.05% BBN in the drinking water, mutagenesis in urothelial cells of male and female mice was about two orders of magnitude greater than the spontaneous mutation background. In contrast, mutagenesis in smooth muscle cells of the urinary bladder was about five times lower than in urothelial tissue. No appreciable increase in mutagenesis was observed in kidney, ureter, liver or forestomach. In lacI (Big Blue?) rats, BBN mutagenesis was also elevated in urothelial cells, albeit not nearly as profoundly as in mice. This provides a potential explanation as to why rats are less prone than mice to the formation of aggressive form of bladder cancer induced by BBN. Our results suggest that the propensity to BBN-triggered mutagenesis of urothelial cells underlies its heightened susceptibility to this carcinogen and that mutagenesis induced by BBN represents a novel model for initiation of bladder carcinogenesis.
机译：膀胱癌是与环境中的致癌物和烟草烟雾相关的少数癌症之一。在小鼠化学致癌模型中测试的致癌物中，N-丁基-N-（4-羟丁基）亚硝胺（BBN）是一种可重现性地在膀胱中而非其他组织中引起高度浸润性癌症的药物。然而，尚未探索这种高水平组织特异性的基础。使用lacI（蓝色巨人）小鼠的诱变，我们在这里显示BBN是有效的诱变剂，它会引起高水平的诱变，特别是在膀胱上皮细胞（尿道上皮）中。经过2至6周的饮用水中0.05％BBN处理后，雄性和雌性小鼠尿道上皮细胞的诱变比自发突变本底大约两个数量级。相反，膀胱平滑肌细胞的诱变作用比尿路上皮组织低约五倍。在肾脏，输尿管，肝脏或前胃未发现诱变明显增加。在lacI（蓝色巨人）大鼠中，尿路上皮细胞中BBN诱变也升高，尽管远没有小鼠明显。这为为什么大鼠不如小鼠更容易形成BBN引起的侵袭性膀胱癌提供了可能的解释。我们的结果表明，尿道上皮细胞对BBN触发诱变的倾向是其对这种致癌物的敏感性增强，并且由BBN诱变代表了膀胱癌发生的新模型。

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