Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.


The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Your Environment. Your Health.

Publication Detail

Title: Acrolein induced DNA damage, mutagenicity and effect on DNA repair.

Authors: Tang, Moon-shong; Wang, Hsiang-tsui; Hu, Yu; Chen, Wei-Sheng; Akao, Makoto; Feng, Zhaohui; Hu, Wenwei

Published In Mol Nutr Food Res, (2011 Sep)

Abstract: 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.

PubMed ID: 21714128 Exiting the NIEHS site

MeSH Terms: Acrolein/chemistry; Acrolein/metabolism*; Acrolein/toxicity*; Animals; Carcinogenicity Tests; Carcinogens/metabolism; DNA Adducts/chemistry; DNA Damage*; DNA Repair*; Humans; Lipid Peroxidation; Lung Neoplasms/genetics; Mutagenicity Tests; Mutation; Rats; Tumor Suppressor Protein p53/genetics; Urinary Bladder Neoplasms/etiology

to Top