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Acrolein induced DNA damage, mutagenicity and effect on DNA repair
Author(s) -
Tang Moonshong,
Wang Hsiangtsui,
Hu Yu,
Chen WeiSheng,
Akao Makoto,
Feng Zhaohui,
Hu Wenwei
Publication year - 2011
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201100148
Subject(s) - dna damage , dna , dna repair , carcinogen , nucleic acid , chemistry , acrolein , adduct , dna methylation , dna adduct , biochemistry , microbiology and biotechnology , cpg site , cancer research , gene , biology , gene expression , catalysis , organic chemistry
Acrolein (Acr) is a ubiquitous environmental contaminant; it also can be generated endogenously by lipid peroxidation. Acr contains a carbonyl group and an olefinic double bond; it can react with many cellular molecules including amino acids, proteins and nucleic acids. In this review article we focus on updating information regarding: (i) Acr‐induced DNA damage and methods of detection, (ii) repair of Acr–DNA damage, (iii) mutagenicity of Acr–DNA adducts, (iv) sequence specificity and methylation effect on Acr–DNA adduct formation and (v) the role of Acr in human cancer. We have found that Acr can inhibit DNA repair and induces mutagenic Acr–dG adducts and that the binding spectrum of Acr in the p53 gene in normal human bronchial epithelial cells is similar to the p53 mutational spectrum in lung cancer. Since Acr–DNA adduct has been identified in human lung tissue and Acr causes bladder cancer in human and rat models, we conclude that Acr is a major lung and bladder carcinogen, and its carcinogenicity arises via induction of DNA damage and inhibition of DNA repair.