Gd3+ complexes have a variety of medical applications. In order to shed light on the mechanism of hepatotoxicity of Gd3+ compounds, we investigated the effects of GdCl3 on human embryo liver cell strand (L02 cells). The experimental results showed that long-time exposure to GdC13 resulted in L02 cell apoptosis. The incubation of L02 cells with GdCl3 first induced increase in cellular reactive oxygen species (ROS) and decrease in mitochondrial inner membrane potential (△Ψm). It later resulted in the activation of poly (ADP-ribose) polymerase (PARP) and the release of mitochondrial apoptosis-inducing factor (AIF). The activation of caspase 3, however, was not observed.Antioxidants could significantly reduce GdCl3-induced decrease of △Ψm, release of AIF, and cell apoptosis. Although GdCl3 caused a significant increase in cell membrane permeability in L02, the change of cell membrane permeability was unlikely to be involved in GdCl3-induced cell apoptosis. Overall, our experimental results suggested that GdCl3 induced apoptosis of human embryo liver L02 cell line by ROS-mediated AIF pathway.