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ToxSci Advance Access published online on January 12, 2005
Toxicological Sciences, doi:10.1093/toxsci/kfi084
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Toxicological Sciences © Society of Toxicology 2005; all rights reserved.
Received September 28, 2004
Accepted January 10, 2005

Environmental Toxicology

Activation of Mitogen Activated Protein Kinases by PCB126 (3,3',4,4',5-pentachlorobiphenyl) in HepG2 Cells

Min Ok Song 1 and Jonathan H. Freedman 1*

1 Nicholas School of the Environment and Earth Sciences, Duke University, Durham, NC 27708-0328, USA

* To whom correspondence should be addressed.
Jonathan H. Freedman, E-mail: jonf{at}duke.edu


  Abstract

Polychlorinated biphenyls (PCBs) are persistent organic pollutants. Exposure to PCB126 (3,3', 4,4', 5-pentachlorobiphenyl), a non-ortho-chlorinated, coplanar congener has been correlated with the production of reactive oxygen species in vivo. In this report, we show that treatment of HepG2 cells with PCB126 significantly increases oxidative stress responsive transcription. In addition, PCB126-induced transcription is enhanced in cells depleted of glutathione. Exposure to PCB126 induces a cellular stress response in HepG2 cells that results in a significant increase in the activity of the mitogen activated protein kinases: extracellular signal regulated kinases 1/2 and p38. PCB126 exposure also causes an increase in c-Jun phosphorylation. These results suggest a model for PCB126 toxicity in which PCB126 exposure induces oxidative stress that causes an increase in MAPK activities, and a subsequence increase in c-Jun phosphorylation. Activation of c-Jun results in enhanced AP-1 activity, which leads to elevated expression of ARE/AP-1-dependent genes.

Keywords: PCB126; MAPK; ARE; HepG2; oxidative stress; signal transduction.
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