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作 者:张驰[1] 林辉[1] 魏巍[1] 刘爱林[1] 陈学敏[1] 鲁文清[1]
机构地区:[1]华中科技大学同济医学院公共卫生学院劳动卫生与环境卫生学系
出 处:《癌变.畸变.突变》2007年第2期93-95,共3页Carcinogenesis,Teratogenesis & Mutagenesis
基 金:国家自然科学基金重大项目资助(No40590393)
摘 要:背景与目的:探讨多氯联苯126(PCB126)对苯并(a)芘[B(a)P]遗传毒性的影响。材料与方法:设PCB126三个剂量(0.01、0.10、1.00nmol/L),B(a)P一个剂量(50μmol/L)组,设三甲基胆蒽(3-MC)为阳性对照,二甲基亚砜(DMSO)为溶剂对照,以各PCB126浓度染毒HepG2细胞48h后,再与B(a)P联合染毒24h。通过荧光分光光度法测定各组细胞CYP1A1酶活性(EROD);并采用胞质分裂阻滞法微核实验(CBMNT)分析各组细胞的微核率(MN‰),并计算核分裂指数(NDI)。结果:与溶剂对照相比,PCB126各浓度组和50μmol/L的B(a)P单独作用及联合作用均可诱导CYP1A1酶活性显著增加,其差异均具有统计学意义(P<0.05,P<0.01)。微核率显著升高仅见于50μmol/L的B(a)P单独作用组,与溶剂对照组相比差异有统计学意义(P<0.01)。0.10、1.00nmol/L的PCB126和50μmol/L的B(a)P联合作用时,与B(a)P单独作用相比,CYP1A1酶活性和微核率均显著升高,差异有统计学意义(P<0.05,P<0.01)。结论:PCB126在本试验条件下未显示出遗传毒性作用,但对B(a)P的遗传毒性作用具有一定的增强效应。BACKGROUND & AIM: To study effects of polychlorinated biphenyl PCB126 on B(a)P-induced genotoxicity. MATERIALS AND METHODS: HepG2 cells were treated either with different concentrations of PCB126 (0.01, 0.10, 1.00 mnol/L) alone, or with different concentrations of PCB126 for 48 h then with B(a) P (50 μmol/L) and PCB126 together for another 24 h. DMSO and 3-MC were used as solvent control and positive control, respectively. EROD activity and micronuclei(MN) formation were analyzed through fluorescence spectrophotometry and a cytokinesis-block micronucleus(CBMN) assay, respectively. The frequencies of MN(‰) and nuclei division index (NDI) were calculated. RESULTS: Comparing to solvent control, EROD levels increased markedly in HepG2 cells treated with PCB126 (0.01, 0.10, 1.00 nmol/ L) and B(a) P (50 μmol/ L) alone or together, and MN frequencies increased significantly only in HepG2 cells treated with B(a)P alone(P〈0.05, P〈0.01). Comparing to B(a)P treatment alone, the EROD levels and MN frequencies increased significantly in HepG2 cells treated with B(a)P and PCB126 (0.10, 1.00 nmol/L) together(P〈0.05, P〈 0.01) . CONCLUSION: PCB126 at certain concentrations showed no genotoxic effect in HepG2 cells, but it might enhance the genotoxic properties of B(a)P.
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