2,4-Dichlorophenol induces DNA damage through ROS accumulation and GSH depletion in goldfish Carassius auratus.

2,4-Dichlorophenol (2,4-DCP) is one of the most abundant chlorophenols in the aquatic environment and has been frequently detected in surface waters. Although ecological and cellular toxicity of 2,4-DCP has aroused the public concern, few reports focus on the genotoxicity, especially on DNA double strand breaks (DSBs), of 2,4-DCP in fish. The present study aims to explore the genotoxic effect of 2,4-DCP on DSBs in goldfish Carassius auratus and to further elucidate its potential mechanism. The results showed that 2,4-DCP significantly induced DSBs (detected by neutral comet assay) in erythrocytes and hepatocytes of goldfish in a dose-dependent manner, indicating a genotoxicity of 2,4-DCP on fish. The total antioxidant capability (T-AOC) and the content of reduced glutathione (GSH) were significantly decreased, while the level of reactive oxygen species (ROS) was significantly increased in a dose-dependent manner in erythrocytes and hepatocytes, suggesting an oxidative stress caused by 2,4-DCP in fish. N-acetyl-L-cysteine (NAC), a precursor of GSH and a ROS scavenger, significantly impaired 2,4-DCP-induced ROS overproduction and DSBs, which proves that ROS accumulation and GSH depletion are involved in 2,4-DCP-induced DNA damage in fish. Environ. Mol. Mutagen., 2018. © 2018 Wiley Periodicals, Inc.