Oxidative stress and EROD activity in Caco-2 cells upon exposure to chlorinated hydrophobic organic compounds from drinking water reservoirs

Our previous studies showed hydrophobic organic compounds (HOCs) in the sediments of drinking water reservoirs caused DNA damage in human cells (Caco-2) after chlorination. However, the main mechanisms remained unclear. This study compared oxidative damage and EROD activity in Caco-2 cells upon exposure to chlorinated HOCs, and the role of antioxidants (catalase, vitamin C and epigallocatechin gallate (EGCG)) in reducing the toxicities was examined. The result showed that chlorinated HOCs induced a 4-fold increase in production of reactive oxygen species (ROS) compared with HOCs. Antioxidants supplement significantly reduced ROS yields and DNA peroxidation. HOCs with relatively higher TEQbio were greatly reduced (about 98%) after chlorination, indicating dioxin-like toxicity is not the main factor inducing oxidative damage by chlorinated HOCs. Yet, ROS and the associated oxidative damage seem to be more responsible for causing DNA damage in the cells. Antioxidants including catalase, Vitamin C and EGCG showed protective effect against chlorination.