Wei Wei, Zhang Chi, Lai Ruiping, Liu Ailin
Department of Occupational and Environmental Health, MOE Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Wei Sheng Yan Jiu. 2007 Mar;36(2):129-32.
To explore effects of polychlorinated biphenyl, PCB153 on DNA damage induced by benzo(a) pyrene (B[a]P) in HepG2 cells.
As target cell, HepG2 cells were treated at the concentrations of 0.1, 1, 10 and 100 micromol/L with PCB153 and at the concentrations of 12.5, 25, 50 and 100 micromol/L B[a]P respectively. DMSO was used as solvent control. Single cell gel electrophoresis (SCGE) was applied for quantitative analysis of DNA damage which was caused by treating alone or co-treating with PCB153 and B[a]P, CYP1A1 (EROD) and CYP2B1 (PROD) activities were detected by using fluorescence spectrophotometry.
When compared with the solvent control, the DNA oliver tail moments were increased significantly (P < 0.01) in HepG2 cells treated with all the concentrations of B[a]P, while no significant DNA damage was observed in HepG2 cells treated with all the concentrations of PCB153. When compared with B[a]P treated alone, the DNA oliver tail moments showed a increase tendency in HepG2 cells co-treated with PCB153 (0.1, 1, 10 micromol/L) and B[a]P (50 micromol/L). But DNA oliver tail moments were increased significantly only when co-treated with 10 micromol/L of PCB153 and 50 micromol/L of B[a]P (P <0.01), while decreased significantly after co-exposuring to 100 micromol/L of PCB153 and 50 micromol/L of B[a]P (P <0.01). All concentrations of PCB153 induced significant increase in EROD and PROD activities in HepG2 cells.
It was suggested that the enhancement of DNA damage induced by B[a]P could be associated with the increases of CYP1A1 and CYP2B1 activities induced by PCB153 in HepG2 cells.
探讨多氯联苯PCB153对苯并(a)芘(B[a]P)诱导的HepG2细胞DNA损伤的影响。
以HepG2细胞为靶细胞,分别用浓度为0.1、1、10和100 μmol/L的PCB153以及浓度为12.5、25、50和100 μmol/L的B[a]P处理。二甲基亚砜用作溶剂对照。采用单细胞凝胶电泳(SCGE)对单独或联合用PCB153和B[a]P处理引起的DNA损伤进行定量分析,用荧光分光光度法检测CYP1A1(EROD)和CYP2B1(PROD)活性。
与溶剂对照相比,所有浓度的B[a]P处理的HepG2细胞中DNA彗星尾矩均显著增加(P < 0.01),而所有浓度的PCB153处理的HepG2细胞中未观察到明显的DNA损伤。与单独用B[a]P处理相比,PCB153(0.1、1、10 μmol/L)和B[a]P(50 μmol/L)联合处理的HepG2细胞中DNA彗星尾矩呈增加趋势。但仅在10 μmol/L的PCB153和50 μmol/L的B[a]P联合处理时DNA彗星尾矩显著增加(P <0.01),而在100 μmol/L的PCB153和50 μmol/L的B[a]P共同暴露后显著降低(P <0.01)。所有浓度的PCB153均诱导HepG2细胞中EROD和PROD活性显著增加。
提示B[a]P诱导的DNA损伤增强可能与PCB153诱导的HepG2细胞中CYP1A1和CYP2B1活性增加有关。