FIG. 2.

APCs are resistant to oxidative stress. (A) Typical confocal microscopy images of reactive oxygen species (ROS), detected using the Mitotracker red tracer in APCs, human umbilical vein endothelial cells (HUVECs), and SVECs, under basal conditions (control) and after exposure to increasing doses of H₂O₂. (B) Line graph showing the average values of ROS in APCs, HUVECs, and SVECs (n=3 biological replicates per group, each assayed in triplicate). HUVECs and SVECs, but not APCs, exhibit a dose-dependent increase in ROS levels. Values represent fold change versus vehicle and are expressed as means±SEM. *p<0.05; **p<0.01 versus control in each group. (C–E) In situ detection of ROS in APCs, HUVECs, and SVECs, exposed to H₂O₂ (250 μM, 24 h) in the absence or presence of N-Acetyl Cysteine (NAC). NAC (1 mM, added 30 min before H₂O₂) prevents H₂O₂–induced oxidative stress in HUVECs and SVECs. Quantitative analysis of red fluorescence: Each bar is the mean±SEM of three independent experiments, *p<0.05 as indicated by the connecting line. (F) Effect of H₂O₂ on cell apoptosis: APCs, HUVECs, and SVECs were incubated with the indicated doses of H₂O₂ for 24 h. Apoptosis, as detected by Caspase 3/7 activity assay, was dose dependently increased in HUVECs and SVECs, but not in APCs. Each point is the mean±SEM of three independent experiments, *p<0.05 versus control in each group. To see this illustration in color, the reader is referred to the web version of this article at www.liebertpub.com/ars