Objective Coke oven emissions (COE) are primary industrial and environmental pollutant, including large amounts of carcinogenic and mutagenic polycyclic aromatc hydrocarbons (PAHs). Exogenous chemicals are absorbed into hematological system first, and may cause blood cell damage. However, few studies have reported the damage to hematological system induced by COE and related mechanism. This study is designed to investigate the damage and biological mechanism of hematological cells exposed to organic extracts of coke oven emissions (OE-COE).
Methods COE were collected at the top area of a coke oven and extracted to prepare OECOE. HL-60 cells were collected in logarithmic growth phase and cultured with OE-COE for 4 days at concentrations of 0, 2.5, 5, 10, and 20 mg/L to establish continuous exposure models. Afer exposure, cell survival rate was detected by CCK-8, cell apoptosis and necrosis by flow cytometry, DNA damage by comet assay, and the expression levels of inhibitor of nuclear factor-kappa B (NF-κB) (IκBα), phosphorylaton IκBα, NF-κB p65, and phosphorylaton NF-κB p65 by Western blot.
Results Afer 4 days of contnuous exposure, with the dosage increase of OE-COE, the relatve survival rate of HL-60 cells was decreased signifcantly (P < 0.001), especially the relatve survival rate of the 20 mg/L group which was decreased to 38.63%. The relatve apoptosis rates of HL-60 cells in the 5, 10, and 20 mg/L groups were 1.22 (P>0.05), 2.51 (P>0.05), and 13.97 (P < 0.05) tmes higher than that of the control group; the relatve necrosis rates of HL-60 cells in the 5, 10, and 20mg/L groups were 1.23 (P>0.05), 1.16 (P>0.05), and 2.88 (P < 0.05) tmes higher than that of the control group. The relatve percentages of tail DNA of HL-60 cells in the 10mg/L and 20mg/L groups were 2.05 (P < 0.05) and 2.40 (P < 0.05) tmes higher than that of the control group, and were also higher than those of the 2.5 and 5 mg/L groups (P < 0.05). The relatve expression levels of IκBα, phosphorylaton IκBα, NF-κB p65, and phosphorylaton NF-κB p65 proteins in the 5 and 10 mg/L groups were higher than those of control group (P < 0.05).
Conclusion OE-COE contnuous exposure could induce DNA damage in HL-60 cells, and the actvaton of NF-κB might be one of the mechanisms of DNA damage afer OE-COE exposure.
DownLoad: