Oxidative stress induced by ultrafine carbon black particles can elicit apoptosis in vivo and vitro.

Although carbon black (CB) particles have potential hazards to human health, the toxicological studies on CB are still limited. The purpose of this study was to investigate the effect of oxidative stress induced by ultrafine CB particles on apoptosis in vivo and vitro. Male C57BL/6 mice were inhalation exposed to CB for 28 days, and 16HBE cells were treated by CB particles and also added antioxidant (NAC). Antioxidant enzymes activities (CAT, SOD, GSH-Px) and ROS in the lungs and cells were evaluated. Apoptosis-related proteins (Bcl-2, Bax, Cleaved Caspase-3, pro-Caspase-3, Caspase-7, Caspase-8, Caspase-9, PARP-1) were tested by Western blot (WB), immunohistochemistry (IHC), and real-time PCR. The reduction of antioxidant enzymes activities and the addition of ROS in CB exposure groups were observed, and the gene and apoptosis-related proteins levels were increased in CB exposure mice. The results of CB-treated 16HBE cells were consistent with those of mice, and apoptosis rate was increased in CB-treated 16HBE cells. When the cells were treated with NAC, ROS induced by CB decreased, SOD and CAT activities of CB-treated 16HBE cells were increased. Apoptosis rate of 16HBE cells treated with NAC and CB was significantly decreased, and the expression of C-Caspase-3 was also decreased. Therefore, oxidative stress induced by ultrafine CB particles can elicit apoptosis in vivo and vitro. Antioxidants can significantly reduce oxidative damage and apoptosis induced by CB.