Abstract: In order to study the histopathological and ultrastructure changes in hepatic cells, twentyfour SD rats were divided into four groups with one control and three experimental groups; Dimethoate was administrated daily intragastrically to SD rats in four groups with concentration of 0, 1, 6 and 30 mg·kg-1 body weight respectivelyMeanwhile,Dimethoate was added to hepatocyte culture fluid of rats with final concentration of 0，3，10，30，100 and 300 μmol·L-1 in each in vitro treatment After 12 and 24 h, apoptosis rate was analyzed by Annexin V/PI method; intracellular Ca2+ concentration, reactive oxygen species (ROS) and mitochondria membrane potential (Δψm) changes were analyzed by Fluo2/AM, Dichlorofluorescin diacetate (DCFHDA ) and rhodamine 123 method respectively to study the effects of Dimethoate on liver cell apoptosis The results showed that adipose degeneration and apoptosis were observed by histopathological and ultrastructure examination After 12 and 24 h exposure, cell apoptosis rate increased significantly; experimental groups (apart from the group with 3 mmol·L-1) had significant (P<005 or P<001) differences with control group and followed dose proportionality. Intracellular Ca2+ concentration in group with 3 mmol·L-1 was significantly (P<001) higher than that of control group, and then the concentration decreased with increasing dosage. Intracellular ROS level increased with increasing dosage and time of exposure in the range of 3-100 μmol·L-1; however, ROS level decreased slightly in group with 300 μmol·L-1. Apart from group with 3 μmol·L-1, the differences between control group and experimental groups were significant (P<001). Δψm decreased continuously apart from group with 300 μmol·L-1 after 24 h exposure.The Δψm of 30-300 μmol·L-1 groups were significantly lower than that of control (P＜001). It was concluded that low dosage of Dimethoate can induce liver cell apoptosis, and intracellular Ca2+, ROS and Δψm may participate in this process.