Hayashi H, Kanisawa M, Yamanaka K, Ito T, Udaka N, Ohji H, Okudela K, Okada S, Kitamura H
Department of Pathology, Yokohama City University School of Medicine, Yokohama, Japan.
Cancer Lett. 1998 Mar 13;125(1-2):83-8. doi: 10.1016/s0304-3835(97)00484-9.
The pulmonary tumorigenicity of dimethylarsinic acid (DMAA), a main metabolite of inorganic arsenics, was examined in A/J mice fed with drinking water containing DMAA for 25 and 50 weeks. Mice fed with 400 ppm DMAA for 50 weeks produced more pulmonary tumors than untreated mice (mean number per animal 1.36 versus 0.50; P < 0.05). Histological examination revealed that the number of mice which bore adenocarcinomas or papillary adenomas correlated with the concentration of DMAA given (untreated versus 400 ppm; P = 0.002), suggesting that DMAA could promote tumorigenic processes. These results are consistent with the epidemiological studies on the pulmonary carcinogenesis of arsenics and suggest that DMAA alone can act as a carcinogen in mice.
在通过饮用含二甲基胂酸（DMAA）的水喂养25周和50周的A/J小鼠中，检测了无机砷的主要代谢产物二甲基胂酸（DMAA）的肺致瘤性。用400 ppm DMAA喂养50周的小鼠比未处理的小鼠产生更多的肺肿瘤（每只动物的平均数为1.36对0.50；P < 0.05）。组织学检查显示，患有腺癌或乳头状腺瘤的小鼠数量与给予的DMAA浓度相关（未处理组与400 ppm组；P = 0.002），表明DMAA可促进致瘤过程。这些结果与关于砷肺致癌作用的流行病学研究一致，并表明单独的DMAA可在小鼠中作为致癌物起作用。
