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National Institute of Environmental Health Sciences

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Your Environment. Your Health.

Publication Detail

Title: Activation of mitogen activated protein kinases by PCB126 (3,3',4,4',5-pentachlorobiphenyl) in HepG2 cells.

Authors: Song, Min Ok; Freedman, Jonathan H

Published In Toxicol Sci, (2005 Apr)

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 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.

PubMed ID: 15647597 Exiting the NIEHS site

MeSH Terms: Antioxidants/metabolism; Blotting, Western; Carcinoma, Hepatocellular/metabolism; Cell Line, Tumor; Cell Survival/drug effects; Dose-Response Relationship, Drug; Estrogen Antagonists/toxicity*; Hepatocytes/drug effects*; Hepatocytes/enzymology; Humans; MAP Kinase Signaling System*; Mitogen-Activated Protein Kinases/biosynthesis*; Oxidative Stress; Polychlorinated Biphenyls/toxicity*; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Response Elements; Transcription Factor AP-1/metabolism

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