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Title: Stability of acetaldehyde-derived DNA adduct in vitro.
Authors: Hori, Kimiko
Miyamoto, Shin'ichi  kyouindb  KAKEN_id
Yukawa, Yoshiyuki
Muto, Manabu  kyouindb  KAKEN_id
Chiba, Tsutomu  kyouindb  KAKEN_id
Matsuda, Tomonari  kyouindb  KAKEN_id
Author's alias: 武藤, 学
Keywords: Alcohol
Acetaldehyde
DNA adduct
N(2)-ethylidene-2′-deoxyguanosine
Esophageal cancer
Carcinogenesis
Issue Date: 13-Jul-2012
Publisher: Elsevier Inc.
Journal title: Biochemical and biophysical research communications
Volume: 423
Issue: 4
Start page: 642
End page: 646
Abstract: Acetaldehyde (AA) derived from alcoholic beverages is a confirmed carcinogen for esophageal and head and neck cancers. AA forms various DNA adducts and is thought to play a crucial role in carcinogenesis. Transient DNA adducts are usually repaired, but the stability of AA-derived DNA adducts has not been elucidated. We investigated the stability of N(2)-ethylidene-2'-deoxyguanosine (N(2)-ethylidene-dG), a major AA-derived DNA adduct, in cultured cells. First, to determine the optimal concentration of AA for detecting N(2)-ethylidene-dG in cell culture, a dose-response study was performed using HL60 cells of the human promyelocytic leukemia cell line. An AA concentration ≥ 0.01% (1.8 mM) was required to detect N(2)-ethylidene-dG in vitro. We next examined the stability of N(2)-ethylidene-dG. After a 1 or 2h exposure to 0.01% of AA in a tightly sealed bottle, N(2)-ethylidene-dG content was measured by sensitive liquid chromatography tandem mass spectrometry immediately, 24h, and 48 h after exposure. After the 1h exposure, the mean (± SD) N(2)-ethylidene-dG contents were 12.1 ± 1.28, 8.20 ± 0.64, and 6.70 ± 0.52 adducts per 10(7) bases at each postexposure time. After the 2h exposure, N(2)-ethylidene-dG content increased to 21.4 ± 7.50, 10.5 ± 3.61, and 9.83 ± 3.90 adducts per 10(7) bases at each postexposure time. The half-life of this adduct was calculated as ∼35 h in independent experiments. These results indicate that AA exposure from daily alcohol consumption may cause DNA damage and may increase the risk of alcohol-related carcinogenesis.
Rights: © 2012 Elsevier Inc.
この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。This is not the published version. Please cite only the published version.
URI: http://hdl.handle.net/2433/160034
DOI(Published Version): 10.1016/j.bbrc.2012.05.158
PubMed ID: 22683642
Appears in Collections:Journal Articles

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