Fig. 4.

Pin1 overexpression attenuates arsenic-induced intracellular ROS production, mitochondrial dysfunction and apoptosis in L02 cells. (A) Changes in intracellular ROS levels in the different treatment groups. (B) Changes in the mitochondrial membrane potential (ΔΨm) in the different treatment groups. (C) Changes in intracellular ATP levels in the different treatment groups. (D) Mitochondrial damage, as indicated by the specific fluorescence probe MitoTracker red, was mitigated by Pin1 plasmid transfection. Scale bar: 10 or 1 μm. (E) Pin1 plasmid transfection suppressed arsenic-induced apoptosis, as analyzed by flow cytometry. (F) Quantification of apoptotic cells in the different treatment groups. The data are presented as the mean ± SEM of four independent experiments. ^*P < .05, ^**P < .01 vs. the control group. ^#P < .05, ^##P < .01 vs. the arsenic group.