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 to DCE can cause severe toxic encephalopathy and has obvious toxic effects on the liver. However, the toxicity of DCE on the liver and its molecular mechanism 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. The DCE-exposed groups showed hepatic dysfunction relative to the control group. Moreover, apoptotic cells and decreased phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) were found in liver tissue of rats in 3 DCE-exposed groups. In vitro tests showed 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, incubating HepG2 cells with epidermal growth factor, an ERK1/2 activator, significantly increased apoptosis in HepG2 cells. In conclusion, our results suggest that DCE induces apoptosis in HepG2 cells by inhibiting ERK1/2 pathways.