IMR Press / FBE / Volume 2 / Issue 4 / DOI: 10.2741/E194

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


Effects of acetaldehyde inhalation in mitochondrial aldehyde dehydrogenase deficient mice (Aldh2-/-)

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1 Departments of Environmental Health, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Fukuoka, 807-8555, Japan
2 Research Center for Environmental Quality Management, Kyoto University, Otsu, Shiga, 520-0811, Japan
3 Osaka Prefectural Institute of Public Health, Osaka, 537-0025, Japan
4 Section of Postgraduate Guidance, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Fukuoka, 807-8555, Japan
5 Global COE, Nagoya University School of Medicine, Nagoya, Aichi, 466-8550, Japan
6 Division of Digestive Endoscopy/Gastrointestinal Oncology, National Cancer Center Hospital East, Kashiwa, Chiba, 277-8577, Japan
Front. Biosci. (Elite Ed) 2010, 2(4), 1344–1354;
Published: 1 June 2010

Human body might be exposed to acetaldehyde from smoking or occupational environment, which is known to be associated with cancer through the formation of DNA adducts, in particular, N2-ethylidene-2'-deoxyguanosine (N2-ethylidene-dG). Aldehyde dehydrogenase 2 (ALDH2) is the major enzyme that contribute to the detoxification of acetaldehyde in human body. In this study, wild type (Aldh2+/+) and Aldh2KO (Aldh2-/-) mice were exposed to the air containing 0, 125, 500 ppm acetaldehyde for 2 weeks. After inhalation, levels of N2-ethylidene-dG in the chromosomal DNA were analyzed by liquid chromatography tandem mass spectrometry (LC/MS/MS). N2-ethylidene-dG levels in livers of Aldh2-/- mice were always lower than those of Aldh2+/+ mice, suggesting that Aldh2 deficiency might cause the induction of acetaldehyde metabolizing enzymes in the liver such as P450s. The differences between Aldh2-/- and Aldh2+/+ mice were greater in the order of nasal epithelium > lung > dorsal skin, suggesting that nasal epithelium and lung are the major target sites for acetaldehyde. Acetaldehyde inhalation may cause a high risk in nasal epithelium and lung cancers for individuals with inactive ALDH2.

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