IR@PKUHSC  > 北京大学公共卫生学院
学科主题公共卫生
Metallothionein (I/II) suppresses genotoxicity caused by dimethylarsinic acid
Jia, G; Sone, H; Nishimura, N; Satoh, M; Tohyama, C
关键词dimethylarsinic acid metallothionein oxidative DNA damage apoptosis oxidative stress
刊名INTERNATIONAL JOURNAL OF ONCOLOGY
2004-08-01
25期:2页:325-333
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology
研究领域[WOS]Oncology
关键词[WOS]OXIDATIVE STRESS ; DNA-DAMAGE ; NULL MICE ; GENE-EXPRESSION ; INORGANIC ARSENICS ; PROTECTIVE ROLE ; INDUCED CYTOTOXICITY ; HEME OXYGENASE ; FREE-RADICALS ; CARCINOGENESIS
英文摘要

Arsenic is an environmental chemical of considerable concern due to its association with an increased risk of human cancer. Dimethylarsinic acid (DMAA) is one of the major methylated metabolites of ingested arsenicals in most mammals. To better clarify the role of metallothionein (MT) in modifying DMAA genotoxicity, MT-I/II null mice, and the corresponding wild-type mice, were exposed to DMAA (0, 188, 375 or 750 mg/kg body weight) via a single oral dose. Twenty-four hours after the DMAA injection, there was increased formation of 8-hydroxy-2′-deoxyguanosine (8-OHdG) in serum and urine and a higher number of DNA strand breaks in peripheral blood cells. These increased levels were concomitant with increasing dose concentrations of DMAA in both strains of mice and they were significantly higher in MT-I/II null mice than in wild-type mice. Furthermore, the induction of apoptotic cells in the urinary bladder epithelium of MT-I/II null mice was significantly higher than in dose-matched wild-type mice exposed to DMAA. On the other hand, in both liver and in the alveolar and bronchial areas of the lung, the extent of DMAA-induced apoptosis was not different between wild-type and MT-I/II null mice and was increased in both strains. In addition, the concentration of hepatic MT in wild-type mice increased in a DMAA dose-dependent manner but was undetectable in MT-I/II null mice and could not subsequently be induced by DMAA. In conclusion, DMAA exposure causes oxidative stress, DNA damage and specific induction of apoptosis in target organs of arsenic carcinogenesis, which may be attributable to the mechanism(s) of arsenic-induced carcinogenesis in rodents. MT exhibited some protective roles during DNA damage presumably by acting as an antioxidant.

语种英语
WOS记录号WOS:000222730200010
引用统计
被引频次:14[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/64596
专题北京大学公共卫生学院
作者单位1.Gifu Pharmaceut Univ, Dept Hyg, Gifu 5028585, Japan
2.Natl Inst Environm Studies, Hlth Effects Res Team, Tsukuba, Ibaraki 3058506, Japan
3.Natl Inst Environm Studies, Environm Hlth Sci Div, Tsukuba, Ibaraki 3058506, Japan
4.Peking Univ, Sch Publ Hlth, Dept Occupat & Environm Hlth Sci, Beijing 100083, Peoples R China
推荐引用方式
GB/T 7714
Jia, G,Sone, H,Nishimura, N,et al. Metallothionein (I/II) suppresses genotoxicity caused by dimethylarsinic acid[J]. INTERNATIONAL JOURNAL OF ONCOLOGY,2004,25(2):325-333.
APA Jia, G,Sone, H,Nishimura, N,Satoh, M,&Tohyama, C.(2004).Metallothionein (I/II) suppresses genotoxicity caused by dimethylarsinic acid.INTERNATIONAL JOURNAL OF ONCOLOGY,25(2),325-333.
MLA Jia, G,et al."Metallothionein (I/II) suppresses genotoxicity caused by dimethylarsinic acid".INTERNATIONAL JOURNAL OF ONCOLOGY 25.2(2004):325-333.
条目包含的文件
条目无相关文件。
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Jia, G]的文章
[Sone, H]的文章
[Nishimura, N]的文章
百度学术
百度学术中相似的文章
[Jia, G]的文章
[Sone, H]的文章
[Nishimura, N]的文章
必应学术
必应学术中相似的文章
[Jia, G]的文章
[Sone, H]的文章
[Nishimura, N]的文章
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。