The role of trivalent dimethylated arsenic in dimethylarsinic acid-promoted skin and lung tumorigenesis in mice: Tumor-promoting action through the induction of oxidative stress
The role of trivalent dimethylated arsenic in dimethylarsinic acid-promoted skin and lung tumorigenesis in mice: Tumor-promoting action through the induction of oxidative stress
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DOI：
10.1016/j.toxlet.2005.03.009
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发表时间：
2005-08-14
影响因子：
3.5
通讯作者：
Yamanaka, K
中科院分区：
文献类型：
--
作者：
Mizoi, M;Takabayashi, F;Yamanaka, K
我们研究了二甲基砷酸(DMA(V))对小鼠肺和皮肤肿瘤的促进作用与氧化应激之间的关系。与(-)表没食子儿茶素没食子酸酯(EGCG)联用，可抑制由肺肿瘤起始剂(4NQO)、二甲基亚胺(V)和8-氧-2‘-脱氧鸟苷(8-oxodG)诱导的小鼠肺肿瘤的发生。用三价二甲基化砷(DMA(V)的进一步还原代谢物DMA(Ill))局部治疗小鼠时，不仅观察到皮肤肿瘤的增加，而且观察到表皮中8-oxodG的升高。这些结果表明，DMA(V)的促癌作用是由DMA(III)通过诱导氧化应激介导的。(C)2005爱思唯尔爱尔兰有限公司。保留所有权利。
We investigated the relationship between lung- and skin-tumor promotion and oxidative stress caused by administration of dimethylarsinic acid (DMA(V)) in mice. The incidence of lung tumors induced by lung tumor initiator (4NQO) and DMA(V) were, as well as 8-oxo-2'-deoxyguanosine (8-oxodG), suppressed by cotreatment with (-)epigallocatechin gallate (EGCG). When mice were topically treated with trivalent dimethylated arsenic (DMA(Ill)), a further reductive metabolite of DMA(V), not only an increase in skin tumors but also an elevation of 8-oxodG in epidermis were observed. These results suggest that tumor promotion due to DMA(V) administration is mediated by DMA(III) through the induction of oxidative stress. (c) 2005 Elsevier Ireland Ltd. All rights reserved.