Abstract
Polychlorinated biphenyls (PCBs) are infamous industry by-products or additives, and increasing evidences demonstrated that their exposure is associate with adverse effects on human health. Liver, as the dominate site for xenobiotic metabolism, is apt to be the primary target of PCBs insult. Although PCBs' hepatic toxic effects have been extensively studied, however, the biotransformation of PCBs in liver and the toxicities of associated PCB metabolites are neglected at some extent. Thus, we choose 2,3,5-trichloro-6-phenyl-[1,4]-benzoquinone (PCB29-pQ), a surrogate PCB29 metabolite, and evaluated its contribution on hepatotoxicity. In the current study, we discovered PCB29-pQ-induced lipid peroxidation and iron overload both in vivo and in vitro. Further mechanistic research confirmed iron overload is caused by reactive oxygen species (ROS)-driven hepcidin disorder in hepatic cells, and the increase of hepcidin is regulated by the translocation of nuclear factor erythroid 2-related factor 2 (Nrf2).