日本語フィールド
著者：Nagayoshi H, Matsumoto A, Nishi R, Kawamoto T, Ichiba M, Matsuda T.題名：Increased formation of gastric N(2)-ethylidene-2'-deoxyguanosine DNA adducts in aldehyde dehydrogenase-2 knockout mice treated with ethanol.発表情報：Mutat Res. 巻: 673 号: 1 ページ: 74-77キーワード：Aldh2 knock-out mouse, acetaldehyde, stomach, LC/MS/MS,
N2-ethylidene-2’-deoxyguanosine, N2-ethyl-2’-deoxyguanosine概要：抄録：We analyzed an acetaldehyde-derived DNA adduct, N2-ethylidene-2’-deoxyguanosine (N2-Eti-dG) in stomach DNA of aldehyde dehydrogenase (Aldh)-2-knockout mice that were fed with alcohol to determine effects of alcohol consumption and Aldh2 genotype on the level of DNA damage in stomach. Aldh2-active(+/+), heterozygote(+/-) and knockout(-/-) mice were fed 20% ethanol for 5 weeks, then the level of N2-Eti-dG in stomach was etermined by liquid chromatography tandem mass spectrometry. The average N2-Eti-dG level in DNA from untreated mice was not significantly different among Aldh2 genotypes (2.0 - 3.1adducts/107 bases), however, the average N2-Eti-dG level in DNA from ethanol-treated mice was 4.8±2.6 adducts/ 107 bases in Aldh2+/+ mice, 7.9±1.1 adducts/ 107 bases in Aldh2+/- mice, and 48.6±12.0 adducts/ 107 bases in Aldh2-/- mice, respectively. Our data clearly showed that alcohol drinking caused DNA damage in stomach, which was Aldh2 genotype dependent in this experimental animal model. This result suggests that heavy-alcohol drinking and Aldh2 deficiency might be risk factors of stomach cancer.英語フィールド
Author：Nagayoshi H, Matsumoto A, Nishi R, Kawamoto T, Ichiba M, Matsuda T.Title：Increased formation of gastric N(2)-ethylidene-2'-deoxyguanosine DNA adducts in aldehyde dehydrogenase-2 knockout mice treated with ethanol.Announcement information:Mutat Res. Vol: 673 Issue: 1 Page: 74-77Keyword：Aldh2 knock-out mouse, acetaldehyde, stomach, LC/MS/MS,
N2-ethylidene-2’-deoxyguanosine, N2-ethyl-2’-deoxyguanosineAn abstract：We analyzed an acetaldehyde-derived DNA adduct, N2-ethylidene-2’-deoxyguanosine (N2-Eti-dG) in stomach DNA of aldehyde dehydrogenase (Aldh)-2-knockout mice that were fed with alcohol to determine effects of alcohol consumption and Aldh2 genotype on the level of DNA damage in stomach. Aldh2-active(+/+), heterozygote(+/-) and knockout(-/-) mice were fed 20% ethanol for 5 weeks, then the level of N2-Eti-dG in stomach was etermined by liquid chromatography tandem mass spectrometry. The average N2-Eti-dG level in DNA from untreated mice was not significantly different among Aldh2 genotypes (2.0 - 3.1adducts/107 bases), however, the average N2-Eti-dG level in DNA from ethanol-treated mice was 4.8±2.6 adducts/ 107 bases in Aldh2+/+ mice, 7.9±1.1 adducts/ 107 bases in Aldh2+/- mice, and 48.6±12.0 adducts/ 107 bases in Aldh2-/- mice, respectively. Our data clearly showed that alcohol drinking caused DNA damage in stomach, which was Aldh2 genotype dependent in this experimental animal model. This result suggests that heavy-alcohol drinking and Aldh2 deficiency might be risk factors of stomach cancer.