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首页> 外文期刊>Life sciences >Dimethylarsine likely acts as a mouse-pulmonary tumor initiator via the production of dimethylarsine radical and/or its peroxy radical.
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Dimethylarsine likely acts as a mouse-pulmonary tumor initiator via the production of dimethylarsine radical and/or its peroxy radical.

机译：二甲基ar可能通过产生二甲基ar自由基和/或其过氧自由基而充当小鼠-肺肿瘤引发剂。

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AIMS: Recent animal experiments have indicated that dimethylarsinic acid (DMA), a main metabolite of inorganic arsenic, is a complete carcinogen in the lung of mice and the urinary bladder of rats, nevertheless, no ultimate-active metabolite from DMA has been identified thus far. We have proposed that dimethylarsine ((CH(3))(2)AsH), an ultimate reductive metabolite of DMA, is excreted in the expired air of mice administered DMA, and furthermore, was easily converted into dimethylarsine radical ((CH(3))(2)As*) and dimethylarsine peroxy radical ((CH(3))(2)AsOO*) by its reaction with O(2). The aim of the present study was to elucidate the possible mode of the tumorigenic action by dimethylated arsenic. MAIN METHODS: In vitro experiments using GSH reductase as a two-electron donor of dimethylarsenic-glutathione conjugate ((CH(3))(2)As-SG) and DNA adduct assay via a photochemical approach were performed. A lung tumorigenicity assay of (CH(3))(2)AsH suspended in argon-atmospheric olive oil for 5 days was also conducted in mice. KEY FINDINGS: The results indicated that (CH(3))(2)AsH was easily produced enzymatically from (CH(3))(2)As-SG and showed tumor-initiating action in mouse lung via the production of (CH(3))(2)As* and (CH(3))(2)AsOO* by its reaction with O(2), and that these radicals have the ability to form DNA adducts. SIGNIFICANCE: The carcinogenicity of DMA, at least in mouse lung, could be explained based on the proposal that oral administration of DMA induces pulmonary tumors in mice, and arises from the arsine radicals produced through (CH(3))(2)AsH, which was enzymatically reduced from (CH(3))(2)As-SG.
机译：目的：最近的动物实验表明，无机砷的主要代谢产物二甲基ar酸（DMA）是小鼠肺和大鼠膀胱中的完全致癌物，但是，至今尚未鉴定出来自DMA的最终活性代谢物。远。我们已经提出，二甲基ar（（CH（3））（2）AsH），一种DMA的最终还原性代谢物，在施用DMA的小鼠呼出的空气中排泄，而且很容易转化为二甲基ar基（（CH（3 ））（2）As *）和二甲基ar过氧自由基（（CH（3））（2）AsOO *）与O（2）反应。本研究的目的是阐明二甲基化砷致癌作用的可能模式。主要方法：使用GSH还原酶作为二甲基砷-谷胱甘肽共轭物（（CH（3））（2）As-SG）的双电子供体的体外实验和通过光化学方法进行的DNA加合物测定。还在小鼠中进行了悬浮于氩气橄榄油中5天的（CH（3））（2）AsH的肺致瘤性分析。主要发现：结果表明（CH（3））（2）AsH易于从（CH（3））（2）As-SG酶促产生，并通过（CH（3 3））（2）As *和（CH（3））（2）AsOO *与O（2）反应，并且这些自由基具有形成DNA加合物的能力。意义：至少在小鼠肺中，DMA的致癌性可以基于以下建议来解释：口服DMA会诱发小鼠肺部肿瘤，并且是由（CH（3））（2）AsH产生的rs基产生的，从（CH（3））（2）As-SG酶法还原而得。

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