The effect of ethanol on the formation of N2-ethylidene-dG adducts in mice: implications for alcohol-related carcinogenicity of the oral cavity and esophagus

被引:14
|
作者
Yu, Hsu-Sheng
Oyama, Tsunehiro
Matsuda, Tomonari [2 ]
Isse, Toyohi [3 ]
Yamaguchi, Tetsunosuke
Tanaka, Masayuki
Tsuji, Mayumi
Kawamoto, Toshihiro [1 ]
机构
[1] Univ Occupat & Environm Hlth, Sch Med, Dept Environm Hlth, Yahatanishi Ku, Kitakyushu, Fukuoka 8078555, Japan
[2] Kyoto Univ, Res Ctr Environm Qual Management, Otsu, Shiga, Japan
[3] Univ Occupat & Environm Hlth, Sch Med, Sect Postgrad Guidance, Yahatanishi Ku, Kitakyushu, Fukuoka 8078555, Japan
关键词
Acetaldehyde; ALDH2; carcinogenesis; DNA adduct; ethanol; N-2-ethyl-dG; DNA-ADDUCTS; ALDEHYDE DEHYDROGENASE; GENETIC POLYMORPHISMS; KNOCKOUT MICE; ACETALDEHYDE; CANCER; RISK; N-2-ETHYLDEOXYGUANOSINE; IDENTIFICATION; CONSUMPTION;
D O I
10.3109/1354750X.2012.666675
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
The present study aimed to experimentally confirm that long-term alcohol drinking causes a high risk of oral and esophageal cancer in aldehyde dehydrogenase 2 (ALDH2)-deficient individuals. Aldh2 knockout mice, an animal model of ALDH2-deficiency, were treated with 8% ethanol for 14 months. Levels of acetaldehyde-derived DNA adducts were increased in esophagus, tongue and submandibular gland. Our finding that a lack of Aldh2 leads to more DNA damage after chronic ethanol treatment in mice supports epidemiological findings on the carcinogenicity of alcohol in ALDH2-deficient individuals who drink chronically.
引用
收藏
页码:269 / 274
页数:6
相关论文
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