Biomedical Science Letters (대한의생명과학회지)

The Korean Society for Biomedical Laboratory Sciences (대한의생명과학회)
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Malondialdehyde Level by Ethanol Exposure in Mouse According to the ALDH2 Enzyme Activity

  • Lee, Chung-Jong (Department of Preventive Medicine and Medical Research Institute, College of Medicine, Chungbuk National University) ;
  • Kim, Yong-Dae (Department of Preventive Medicine and Medical Research Institute, College of Medicine, Chungbuk National University) ;
  • Kim, Sung-Hoon (Department of Preventive Medicine and Medical Research Institute, College of Medicine, Chungbuk National University) ;
  • Eom, Sang-Yong (Department of Preventive Medicine and Medical Research Institute, College of Medicine, Chungbuk National University) ;
  • Zhang, Yan Wei (Department of Preventive Medicine and Medical Research Institute, College of Medicine, Chungbuk National University) ;
  • Kim, Heon (Department of Preventive Medicine and Medical Research Institute, College of Medicine, Chungbuk National University)
  • ;
  • 김용대 (충북대학교 의과대학 예방의학교실) ;
  • ;
  • ;
  • ;
  • Published : 2008.03.31
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Abstract

Excessive alcohol consumption is associated with increased risks of many diseases including cancer. Individuals who regularly consume excessive quantities of alcohol have a greater risk of developing head and neck cancers such as esophageal, pharyngeal and oral cavity cancers if they are deficient in ALDH2 expression compared to normal populations. We evaluated lipid peroxidation in Aldh2 +/+ and Aldh2 -/- mice after they had been subjected to acute ethanol exposure. Malondialdehyde(MDA) level in liver tissue was evaluated as a biomarker of oxidative lipid peroxidation. Although the ethanol treatment did not increase the hepatic MDA level both in Aldh2 +/+ mice and in Aldh2 -/- mice, the MDA level was significant higher in the Aldh2 -/- mice than in the Aldh2 +/+ group. The MDA level was also significantly correlated with olive tail moment in blood and the level of 8-OHdG in liver tissue. This is a strong evidence to support our hypothesis that oxidative stress is more intense in Aldh2 -/- mice than in Aldh2 +/+ mice. Our results suggest that ALDH2-deficient individuals may be more susceptible than wild-type ALDH2 individuals to ethanol-mediated liver disease, including cancer.

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