Endosulfan upregulates AP-1 binding and ARE-mediated transcription via ERK1/2 and p38 activation in HepG2 cells

Highlights ► Endosulfan increased ERK1/2 and p38 activities in HepG2 cells. ► Endosulfan-induced increase in c-Jun phosphorylation upregulated AP-1 activity. ► Endosulfan activated ARE-mediated transcription.

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Bibliographische Detailangaben
Veröffentlicht in:	Toxicology (Amsterdam) 2012-02, Vol.292 (1), p.23-32
Hauptverfasser:	Song, Min Ok, Lee, Chang-Ho, Yang, Hyun Ok, Freedman, Jonathan H
Format:	Artikel
Sprache:	eng
Schlagworte:	antioxidants AP-1 ARE Biological and medical sciences Emergency Endosulfan Endosulfan - toxicity Enzyme Activation - drug effects Enzyme Activation - physiology enzyme activity ERK gene expression regulation glutathione Hep G2 Cells hepatotoxicity HepG2 human cell lines Humans Medical sciences mitogen-activated protein kinase Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 1 - physiology Mitogen-Activated Protein Kinase 3 - metabolism neurotoxicity oxidative stress p38 p38 Mitogen-Activated Protein Kinases - metabolism p38 Mitogen-Activated Protein Kinases - physiology Pesticides, fertilizers and other agrochemicals toxicology phosphorylation signal transduction teratogenicity Toxicology Transcription Factor AP-1 - metabolism Transcription, Genetic - drug effects Transcription, Genetic - physiology Transcriptional Activation - drug effects Transcriptional Activation - physiology Up-Regulation - drug effects Up-Regulation - physiology
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Beschreibung
Zusammenfassung:	Highlights ► Endosulfan increased ERK1/2 and p38 activities in HepG2 cells. ► Endosulfan-induced increase in c-Jun phosphorylation upregulated AP-1 activity. ► Endosulfan activated ARE-mediated transcription.
ISSN:	0300-483X 1879-3185
DOI:	10.1016/j.tox.2011.11.013