A Critical Review of Polychlorinated Biphenyls Metabolism, Metabolites, and Their Correlation with Oxidative Stress

Abstract

Polychlorinated biphenyls (PCBs) are notorious persistent organic pollutants that were banned in the last century. However, PCBs still remain ubiquitous in the ecosystem due to their persistence and bioaccumulative potency against environmental and biological degradation. Albeit there is no longer the permission of commercial production of PCBs, they were continuously released into global biota via illegal disposal of e-waste or as byproducts of industrial supplies. The role of oxidative stress is often implicated in PCBs' toxicology. PCBs, especially coplanar ones, have a high affinity toward aryl hydrocarbon receptors and inducing CYP1A1, which is considered as a source of oxidative stress. Although commercial PCBs and coplanar individual PCBs, for example, PCB 77 and 126, induced oxidative stresses have been extensively investigated, PCB metabolite-induced oxidative stress has received less attention. PCBs can undergo phase I metabolism which metabolizes the parent PCBs into hydroquinone/semiquinone/quinone metabolites as a futile redox cycle, producing downstream reactive oxygen species (ROS) as byproducts. PCBs can also undergo phase II metabolism yielding methylsulfonyl metabolites that deplete glutathione and such. PCB metabolites induce oxidative stress generally via direct production of ROS or indirect scavenge antioxidant and inhibit antioxidant enzymes, disturbing cellular redox balance. This review aims to provide a critical summary of PCBs metabolism, PCBs parents, and daughter metabolite-induced oxidative stress. We especially focus on the connection between parent PCBs and downstream metabolites, to encourage research associated with PCB metabolite-induced oxidative stress.