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 drinking control group, 1.5mg/L and 150mg/L ATR dose groups. Serum liver function biochemical indexes and inflammatory factors were detected after 35 and 63 d, hepatosomatic ratio was calculated, and histopathology and ultrastructure of the liver were observed. The levels of lipid peroxidation and antioxidant capacity, the activities of major phase I metabolic enzymes and phase II detoxification enzymes, the expression of related proteins in liver tissues were detected. Results Compared with control group, AST/ALT ratio, pro-inflammatory factors CCL2, TNF-α and IL-6, H2O2 content and the activities of metabolic enzymes NCR, CYPb5 and UDPGT in ATR groups had significant changes (P < 0.05). In 150mg/L ATR group, GGT content, MDA level of peroxide and CYP1A2 expression were significantly increased (P < 0.01), while GSH content was significantly decreased (P < 0.05). Moreover, hepatocyte injury and mitochondrial vacuolation were more serious. Conclusions In a mouse model of low-dose ATR- liver injury, both 1.5 mg/L and 150 mg/L atrazine exposure induced liver injury in mice, with 150 mg/L ATR inducing greater metabolic toxicity in the liver after 63 d.