Polychlorinated biphenyl quinone-induced genotoxicity, oxidative DNA damage and γ-H2AX formation in HepG2 cells.

Our previous study has demonstrated that PCB quinone is cytotoxic in HepG2 cells (Toxicology in Vitro 26 (2012) 841-848). However, it is not clear whether PCB quinone is also carcinogenic (or mutagenic). In the current study, we investigated the genotoxicity of PCB quinone (2,3,5-trichloro-6-phenyl-[1,4]benzoquinone, PCB29-pQ) in HepG2 cells using single cell gel electrophoresis (SCGE) assay and micronucleus (MN) assay. We found PCB29-pQ exposure significantly increased olive tail moment (OTM) and micronuclei (MN) frequencies in HepG2 cells. These data suggested that PCB29-pQ caused DNA strand breaks and chromosome breaks. We further investigated whether the genotoxicity of PCB29-pQ is associated with the generation of reactive oxygen species (ROS). Using enzyme-linked immunosorbent assay for 8-hydroxydeoxyguanosine (8-OHdG) detection, we demonstrated that the level of oxidative DNA damage was significantly evaluated with PCB29-pQ exposure concentration and time dependently. Moreover, γ-H2AX appeared after the treatment of PCB29-pQ in HepG2 cells, may indicate double strand breaks (DSBs). In addition, the pretreatment of ROS scavengers inhibited the genotoxicity of PCB29-pQ significantly. In conclusion, our data suggested that PCB29-pQ causes genotoxic effects in HepG2 cells, probably via ROS-induced oxidative DNA damage.