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Induction of Heat Shock Proteins and Antioxidant Enzymes in 2,3,7,8-TCDD-Induced Hepatotoxicity in Rats

  • Kim, Hyun-Sook (Department of Biomedical Science, College of Health Science, Korea University) ;
  • Park, So-Young (Laboratory of Pharmacognosy, College of Pharmacy, Dankook University) ;
  • Yoo, Ki-Yeol (Department of Life Sciences, College of Advanced Science, Dankook University) ;
  • Lee, Seung Kwan (Department of Biomedical Science, College of Health Science, Korea University) ;
  • Jung, Woon-Won (Research Institute of Heath Science, College of Health Science, Korea University)
  • Received : 2012.07.20
  • Accepted : 2012.10.16
  • Published : 2012.12.31

Abstract

2,3,7,8-Tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) is an environmental toxicant with a polyhalogenated aromatic hydrocarbon structure and is one of the most toxic man-made chemicals. Exposure to 2,3,7,8-TCDD induces reproductive toxicity, immunotoxicity, and hepatotoxicity. In this study, we evaluated how 2,3,7,8-TCDD-induced hepatotoxicity affect the expression of heat shock proteins and antioxidant enzymes using the real-time polymerase chain reaction (PCR) in rat. 2,3,7,8-TCDD increased heat shock protein (Hsp27, ${\alpha}$-B-crystallin, Mortalin, Hsp105, and Hsp90s) and antioxidant enzymes (SOD-3, GST and catalase) expression after a 1 day exposure in livers of rats, whereas heat shock protein (${\alpha}$-B-crystallin, Hsp90, and GRP78) and antioxidant enzymes (SOD-1, SOD-3, catalase, GST, and GPXs) expression decreased on day 2 and then slowly recovered back to control levels on day 8. These results suggest that heat shock proteins and antioxidant enzymes were induced as protective mechanisms against 2,3,7,8-TCDD induced hepatotoxicity, and that prolonged exposure depressed their levels, which recovered to control levels due to reduced 2,3,7,8-TCDD induced hepatotoxicity.

Keywords

References

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