Gene Expression Analysis of the Bromobenzene Treated Liver with Non-hepatotoxic Doses in Mice

  • Lim, Jung-Sun (Korea Institute of Toxicology, Korea Research Institute of Chemical Technology) ;
  • Jeong, Sun-Young (Korea Institute of Toxicology, Korea Research Institute of Chemical Technology) ;
  • Hwang, Ji-Yoon (Korea Institute of Toxicology, Korea Research Institute of Chemical Technology) ;
  • Park, Han-Jin (Korea Institute of Toxicology, Korea Research Institute of Chemical Technology) ;
  • Cho, Jae-Woo (Korea Institute of Toxicology, Korea Research Institute of Chemical Technology) ;
  • Song, Chang-Woo (Korea Institute of Toxicology, Korea Research Institute of Chemical Technology) ;
  • Kim, Yang-Seok (Bioinformatics Division, ISTECH Inc.) ;
  • Lee, Wan-Seon (Bioinformatics Division, ISTECH Inc.) ;
  • Moon, Jin-Hee (Bioinformatics Division, ISTECH Inc.) ;
  • Han, Sang-Seop (Korea Institute of Toxicology, Korea Research Institute of Chemical Technology) ;
  • Yoon, Seok-Joo (Korea Institute of Toxicology, Korea Research Institute of Chemical Technology)
  • Published : 2005.12.30

Abstract

Bromobenzene (BB) is well known hepatotoxicant. Also, BB is an industrial solvent that arouses toxicity predominantly in the liver where it causes centrilobular necrosis. BB is subjected to Cytochrome P450 mediated epoxidation followed by either conjugation with glutathione, enzymatic hydrolysis or further oxidation. In this study, we focused on BB-induced gene expression at non-hepatotoxic dose. Mice were exposed to two levels of BB, sampled at 24 h, and hepatic gene expression levels were determined to evaluate dose dependent changes. When examining the toxic dose of BB treated group in other previous studies, genes related to heat shock protein, oxidative stress, and drug metabolism are expressed. Compared to these results, our study, in which non-toxic dose of BB was administrated, showed similar patterns as the toxic conditions above. The purpose of the study was to select genes that showed changes in relation to the differing dose through confirmation of the difference within transcriptomic boundaries, but those that are not detected by the existing classic toxicology tools in non-hepatotoxic dose.

Keywords

References

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