Journal of Veterinary Medical Science
Online ISSN : 1347-7439
Print ISSN : 0916-7250
ISSN-L : 0916-7250
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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
Chang Yong YOONMisun PARKBang Hyun KIMJi Yeon PARKMun Suk PARKYoun Kyoung JEONGHyugsung KWONHai Kwan JUNGHoIl KANGYong Soon LEEBeom Jun LEE
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2006 Volume 68 Issue 7 Pages 663-668

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Abstract

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.

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© 2006 by the Japanese Society of Veterinary Science

この記事はクリエイティブ・コモンズ [表示 - 非営利 - 改変禁止 4.0 国際]ライセンスの下に提供されています。
https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
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