期刊论文详细信息
Journal of Veterinary Medical Science
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
Bang Hyun KIM3  Mun Suk PARK3  Chang Yong YOON3  Yong Soon LEE1  Ji Yeon PARK3  Beom Jun LEE2  HoIl KANG3  Hyugsung KWON3  Misun PARK3  Youn Kyoung JEONG3  Hai Kwan JUNG3 
[1] Department of Veterinary Public Health, College of Veterinary Medicine, Seoul National University;Department of Veterinary Public Health, Research Institute of Veterinary Medicine and College of Veterinary Medicine, Chungbuk National University;Department of Toxicology, National Institute of Toxicological Research
关键词: gene expression;    liver;    microarray;    TCDD;   
DOI  :  10.1292/jvms.68.663
学科分类:兽医学
来源: Japanese Society of Veterinary Science
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【 摘 要 】

References(43)Cited-By(6)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/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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