Abstract:Types of the DNA damage in hepatic cells and the underlying mechanism in goldfish (Carassius auratus) exposed to monocrotophos were investigated in this study. Results showed that DNA damage in hepatic cells of goldfish was significantly increased by exposure of 0.01, 0.10, and 1.00mg/L monocrotophos for 24, 48, 96, and 168h, and reached maximum at 48h. Alkali-labile sites rather than single- or double-strand breaks were found, by using the alkaline, pH 12.1, and neutral comet assay, to be the main type of DNA damage induced by monocrotophos at 48h. Further, oxidative damage in DNA bases was verified by using the alkaline comet assay combined with Endo III or FPG enzyme. At 24h, glutathione peroxidase (GSH-Px) activities significantly decreased and malondialdehyde (MDA) concentrations significantly increased and exhibited peak values, indicating an over-production of reactive oxygen species (ROS) at short exposure duration (24h). However, superoxide dismutase (SOD) activities and GSH-Px activities significantly increased at 96~168h, and MDA concentrations showed a decreasing trend compared with those at 24h, suggesting a gradually decrease of ROS at 96~168h in the liver tissues. Accordingly, our results suggest that DNA damage induced by monocrotophos in hepatic cells of goldfish is possibly due to the inhibition of antioxidant enzymes activities and ROS scavenging.