Previous studies have proved that the environmental toxicant, inorganic arsenic, 
activates nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in many 
different cell types. This study tried to explore the hepatic Nrf2 pathway upon 
arsenic treatment comprehensively, since liver is one of the major target organs 
of arsenical toxicity. Our results showed that inorganic arsenic significantly 
induced Nrf2 protein and mRNA expression in Chang human hepatocytes. We also 
observed a dose-dependent increase of antioxidant response element- (ARE-) 
luciferase activity. Both the mRNA and protein levels of NAD(P)H:quinone 
oxidoreductase 1 (NQO1) and heme oxygenase-1 (HO-1) were all upregulated 
dramatically. On the other hand, entry and accumulation of Nrf2 protein in the 
nucleus, while exportting the transcriptional repressor BTB and CNC homology 1 
(Bach1) from nucleus to cytoplasm, were also confirmed by western blot and 
immunofluorescence assay. Our results therefore confirmed the arsenic-induced 
Nrf2 pathway activation in hepatocytes and also suggested that the translocation 
of Bach1 was associated with the regulation of Nrf2 pathway by arsenic. Hepatic 
Nrf2 pathway plays indispensable roles for cellular defenses against arsenic 
hepatotoxicity, and the interplay of Bach1 and Nrf2 may be helpful to understand 
the self-defensive responses and the diverse biological effects of arsenicals.