Objective To establish a model of long-term atrazine (ATR)-induced liver injury in mice and to evaluate the hepatotoxic effects induced by ATR. Methods C57BL/ 6-N male mice were randomly divided into a control group and 1. 5 mg / L and 150 mg / L ATR dose (ATR-L, ATR-H) groups. After 35 and 63 days, serum liver function biochemical indexes and inflammatory factors were detected, the hepatosomatic ratio was calculated, and the histopathology and ultrastructure of the liver were observed. Lipid peroxidation levels and antioxidant capacity, the activities of major phase I metabolic enzymes and phase II detoxification enzymes, and the expression of related proteins in liver tissues were detected. Results Compared with the control group, the ATR groups showed significant changes in the AST/ ALT ratio,levels of pro-inflammatory factors CCL2, TNF-α and IL-6, H2O2 content and activities of the metabolic enzymes NCR,CYT b5, and UDPGT ( P<0. 05). In the 150 mg / L ATR group, GGT content, peroxide levels ( as indicated by malondialdehyde), and CYP1A2 expression were significantly increased (P<0. 01), while GSH content was significantly decreased (P<0. 05), and hepatocyte injury and mitochondrial vacuolation were more serious when compared to control and 1. 5 mg / L groups. Conclusions In a mouse model of low-dose ATR liver injury, both 1. 5 mg / L and 150 mg / L ATR exposure induced liver injury in mice, with 150 mg / L ATR inducing the maximum metabolic toxicity in the liver after 63 days