Gene Expression profile by 2,3,7,8-Tetrachlorodibenzo-p-Dioxin in the Liver of Wild-Type (AhR+/+) and Aryl Hydrocarbon Receptor-Deficient (AhR-/-) Mice

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  • YOON Chang Yong
    Department of Toxicology, National Institute of Toxicological Research
  • PARK Misun
    Department of Toxicology, National Institute of Toxicological Research
  • KIM Bang Hyun
    Department of Toxicology, National Institute of Toxicological Research
  • PARK Ji Yeon
    Department of Toxicology, National Institute of Toxicological Research
  • PARK Mun Suk
    Department of Toxicology, National Institute of Toxicological Research
  • JEONG Youn Kyoung
    Department of Toxicology, National Institute of Toxicological Research
  • KWON Hyugsung
    Department of Toxicology, National Institute of Toxicological Research
  • JUNG Hai Kwan
    Department of Toxicology, National Institute of Toxicological Research
  • KANG HoIl
    Department of Toxicology, National Institute of Toxicological Research
  • LEE Yong Soon
    Department of Veterinary Public Health, College of Veterinary Medicine, Seoul National University
  • LEE Beom Jun
    Department of Veterinary Public Health, Research Institute of Veterinary Medicine and College of Veterinary Medicine, Chungbuk National University

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2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is one of the most toxic environmental pollutants that cause various biological effects on mammals. The purpose of our study was to identify the genes involved in hepatotoxicity and hepatocarcinogenesis caused by TCDD. C57BL/6 (AhR+/+, wild type) and B6.129-AhR<tm1Bra>/J (AhR-/-, knock out) mice were injected i.p. with a single treatment of TCDD at the dose of 100 μg/kg body weight. Relative liver weight was significantly increased at 72 hr after TCDD treatment without an apparent histopathological change in AhR+/+ mice (p<0.05). TCDD treatment also significantly increased activity of serum alanine aminotransferase in AhR-/- mice (p<0.05). The liver was analyzed for gene expression profiles 72 hr later. As compared with AhR-/- mice, the expression of 51 genes (>3-fold) was changed in AhR+/+ mice; 28 genes were induced, while 23 genes were repressed. Most of the genes were associated with chemotaxis, inflammation, carcinogenesis, acute-phase response, immune responses, cell metabolism, cell proliferation, signal transduction, and tumor suppression. This study suggests that the microarray analysis of genes in the liver of AhR+/+ and AhR-/- mice may help to clarify the mechanism of AhR-mediated hepatotoxicity and hepatocarcinogenesis by TCDD.<br>

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