Gadolinium induced apoptosis of human embryo liver L02 cell line by ROS-mediated AIF pathway

Abstract

Gd 3+ complexes have a variety of medical applications. In order to shed light on the mechanism of hepatotoxicity of Gd 3+ compounds, we investigated the effects of GdCl 3 on human embryo liver cell strand (L02 cells). The experimental results showed that long-time exposure to GdCl 3 resulted in L02 cell apoptosis. The incubation of L02 cells with GdCl 3 first induced increase in cellular reactive oxygen species (ROS) and decrease in mitochondrial inner membrane potential (Δψ m). 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 GdCl 3-induced decrease of Δψ m, release of AIF, and cell apoptosis. Although GdCl 3 caused a significant increase in cell membrane permeability in L02, the change of cell membrane permeability was unlikely to be involved in GdCl 3-induced cell apoptosis. Overall, our experimental results suggested that GdCl 3 induced apoptosis of human embryo liver L02 cell line by ROS-mediated AIF pathway.