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ToxSci Advance Access originally published online on January 12, 2005
Toxicological Sciences 2005 84(2):308-318; doi:10.1093/toxsci/kfi084
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Toxicological Sciences vol. 84 no. 2 © The Author 2005. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

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

Min Ok Song and Jonathan H. Freedman1

Nicholas School of the Environment and Earth Sciences, Duke University, Durham, North Carolina 27708–0328

Received September 28, 2004; accepted January 10, 2005

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 mitogen-activated protein kinase (MAPK) activities and a subsequent increase in c-Jun phosphorylation. Activation of c-Jun results in enhanced activating protein-1 (AP-1) activity, which leads to elevated expression of antioxidant responsive element (ARE)/AP-1-dependent genes.

Key Words: PCB126; MAPK; ARE; HepG2; oxidative stress; signal transduction.


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