Biological Effects of Smoking-induced Environmental Toxicity

  • Sohn, Sung-Hwa (Department of Biochemistry & Molecular Biology, College of Medicine, Korea University) ;
  • Kim, In-Kyoung (Department of Biochemistry & Molecular Biology, College of Medicine, Korea University) ;
  • Kim, Ki-Nam (Department of Biochemistry & Molecular Biology, College of Medicine, Korea University) ;
  • Kim, Hye-Won (Department of Biochemistry & Molecular Biology, College of Medicine, Korea University) ;
  • Seo, Sang-Hui (Department of Biochemistry & Molecular Biology, College of Medicine, Korea University) ;
  • Lee, Seung-Ho (Department of Biochemistry & Molecular Biology, College of Medicine, Korea University) ;
  • Kim, Yu-Ri (Department of Biochemistry & Molecular Biology, College of Medicine, Korea University) ;
  • Lee, Eun-Il (Department of Preventive, College of Medicine, Korea University) ;
  • Kim, Meyoung-Kon (Department of Biochemistry & Molecular Biology, College of Medicine, Korea University)
  • Published : 2006.09.30

Abstract

Our objective is to identify molecular factors which contribute to the increased risk of smoke in human. About 677 workers who had control and experimental groups according to their urinary Naphthol levels were enrolled in our study. In the present study, we investigated the effects of smoking on gene expression profiles in human. We determined differential gene expression patterns in smoker versus non-smoker using cDNA microarray. Specific genes were up-or down-regulated according to smoking and age. Inflammatory related genes such as cytokine, interleukin, and tumor necrosis factor were up-regulated, DNA repair related genes such as high-mobility group (nonhistone chromosomal) protein 1, and protein 2 were down-regulated, apoptosis related genes such as myeloperoxidase and Bcl-2-associated athanogene were down-regulated, and cell cycle related genes were down-regulated. In our epidemiological study, notably, inflammatory, DNA repair, apoptosis, signal transduction, metabolism, cell cycle, cell proliferation, transcription related genes were regulated.

Keywords

References

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