抄録
Objective: To explore the effect and mechanism of haze particulate matter PM2.5 on apoptosis in human bronchial epithelial cells (16-HBE).
Methods: The human bronchial epithelial cells (16-HBE) were exposed to 8, 16, 32, 64, 128 μg/mL haze particulate matter PM2.5 from Guangzhou. After 24, 48 and 72 h of incubation, the cell survival and apoptotic rate, DNA and oxidative damage were respectively determined.
Results: After 24, 48 and 72 h treated, compared with the negative control, the cell survival rates of 64, 128 μg/mL group decreased significantly (P<0.05), the cell total apoptotic rates and the concentration of 8-Hydroxy-2’-deoxyguanosine of 64, 128 μg/mL groups increased significantly (P<0.05), and the DNA Olive tail moment of all groups increased significantly (P<0.05); Compared with the 24 h group, the cell survival rates of all treated groups in 72 h decreased significantly (P<0.05), the cell survival rates increased significantly in 72 h except 8 μg/mL group (P<0.05), the concentration of 8-Hydroxy-2’-deoxyguanosine of 128 μg/mL group in 72 h increased significantly (P<0.05), and the DNA Olive tail moment of all groups in 48 and 72 h increased significantly (P<0.05).
Conclusion: Haze particulate matter PM2.5 can induce 16-HBE cell apoptosis in a dose and time dependent manner. Oxidative damage is one of the mechanisms of haze particulate matter PM2.5 induce cell apoptosis. Haze particulate matter PM2.5 can produce reactive oxygen species, lead to the imbalance between the ability of oxidation and the ability of antioxidation, finally bring into DNA oxidative damage, and then DNA strand break, induce cell apoptosis.
