1,2-Dichloroethane induced hepatotoxicity and apoptosis by inhibition of ERK 1/2 pathways

1,2-Dichloroethane (DCE) is a ubiquitous occupational environmental contaminant. Subacute exposure of DCE could cause severe toxic encephalopathy and obvious toxic effects on the liver. However, the toxicity of DCE on liver and the molecular mechanism still remain elusive. In the present study, we established a DCE-exposed animal model by inhalation in SD rats and used HepG2 cells in in vitro tests. Hepatic dysfunction was found in DCE-exposed groups compared with the control group. Moreover, apoptotic cells and the decreased phosphorylation of ERK1/2 were found in liver tissue of rats in three DCE-exposed groups. In in vitro tests, we also found that short-term exposure to DCE induced apoptosis in HepG2 cells. Furthermore, the incubation of cells with DCE significantly decreased the phosphorylation of ERK1/2 in a concentration-dependent manner. Additionally, the incubation of HepG2 cells with the ERK1/2 activator EGF significantly increased apoptosis in HepG2 cells. In conclusion, our results suggested that DCE induced apoptosis in HepG2 cells by inhibition of ERK1/2 pathways.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author