In vitro study on the joint hepatoxicity upon combined exposure of cadmium and BDE-209

Abstract

Joint toxicity is an important issue during the risk assessment of environmental pollutants. Contamination of heavy metals and persistent organic pollutants (POPs) under the environmental and biological settings poses substantial health risk to humans. Although previous studies demonstrated the co-occurrence of cadmium and decabrominated diphenyl ether (BDE-209) in environmental mediums, food chains and even human body, their potentially joint toxicities remain elusive thus far. Our investigation here with respect to the hepatotoxicity in vitro clearly demonstrated that combined exposure of cadmium and BDE-209 aggravated the injuries in hepatocytes, which was evidenced by the additive effects on the induction of remarkable morphological alternations, LDH release, cell apoptosis and necrosis, impairment of mitochondrial activity and transmembrane potential. Enhanced ROS production was one of the mechanisms for cell apoptosis and death upon joint treatment. Additionally, more cadmium-treated cells underwent apoptosis than BDE-209-treated cells while more ROS was generated with BDE-209 treatment, indicating that other mechanisms might be involved in cadmium-induced apoptosis. Our results would be helpful for evaluating the joint-hepatotoxicity upon combined exposure of cadmium and BDE-209 as well as investigating the underlying mechanisms.