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

Authors
Kim, Hyun-SookPark, So-YoungYoo, Ki-YeolLee, Seung KwanJung, Woon-Won
Issue Date
12월-2012
Publisher
KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
Keywords
2,3,7,8-Tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD); Antioxidant enzymes; Gene expression; Heat shock proteins; Real-time PCR
Citation
KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY, v.16, no.6, pp.469 - 476
Indexed
SCIE
SCOPUS
KCI
Journal Title
KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
Volume
16
Number
6
Start Page
469
End Page
476
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/106894
DOI
10.4196/kjpp.2012.16.6.469
ISSN
1226-4512
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.
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