摘要
目的研究多氯联苯1254对苯并(a)芘致HepG2细胞DNA损伤的影响。方法设11.5、23.0和46.0μmol/L多氯联苯1254剂量组,苯并(a)芘50μmol/L剂量组,10 m l/L二甲基亚砜为溶剂对照。用不同浓度多氯联苯1254预处理HepG2细胞,24 h后染毒,通过单细胞凝胶电泳和高效液相-电化学技术,检测细胞中的DNA链断裂和8-羟基脱氧鸟嘌呤核苷酸(8-OHdG)。结果50μmol/L苯并(a)芘诱导HepG2细胞中DNA O liver尾矩(OTM)值为1.66±0.21,8-OHdG含量为(23.31±6.02)8-OHdG/106dG,溶剂对照组OTM值为0.79±0.15,8-OHdG含量为(12.31±3.24)8-OHdG/106dG,两组比较差异均有统计学意义;11.5、23.0和46.0μmol/L单独处理组OTM值分别为0.88±0.20、1.01±0.15和1.10±0.16,8-OHdG含量分别为(19.57±7.57)、(22.80±9.16)和(31.74±9.25)8-OHdG/106dG,46.0μmol/L组与溶剂对照组比较,8-OHdG含量显著增加,差异有统计学意义;经11.5、23.0和46.0μmol/L的多氯联苯1254预处理,苯并(a)芘诱导的OTM值分别为2.14±0.22、2.43±0.32和2.71±0.31,8-OHdG含量分别为(32.50±3.81)、(49.23±16.66)和(60.36±18.04)8-OHdG/106dG,与苯并(a)芘单独作用组比较均显著增加,差异有统计学意义。结论多氯联苯1254能使苯并(a)芘诱导的HepG2细胞DNA损伤作用显著增强,表明多氯联苯1254对苯并(a)芘的遗传毒性作用具有一定的协同效应。
Objective To study the effect of polychlorinated biphenyl, Aroclor1254 on benzo（a） pyrene [ B （a）P ]-induced DNA damage in HepG2 ceils. Methods HepG2 ceils were pretreated with Aroclor1254 （11.5, 23 and 46 μmol/L） for 24 hours and then exposed to B（a）P （50 μmol/L）. DMSO （10 ml/L） was used as solvent control. Single cell gel electrophoresis （SCGE） and high-performance liquid chromatography-electrochemical detection （HPLC-EC） assays were applied to detect DNA single-strand breaks and 8-hydroxy-2＇-deoxyguanosine （8-OHdG） in HepG2 cells, respectively. Results Average Oliver tail moment （OTM） and 8-OHdG level in HepG2 ceils were significantly increased in B（a） P treated group （ 1.66 ± 0. 21 ）, （23. 31 ± 6. 02） 8-OHdG/10^6 dG than that in solvent control （0. 79 ± 0. 15 ）, （ 12. 31 ± 3.24） 8-OHdG/10SdG, respectively. In Aroclor 1254 treated group （11.5,23.0, 46. 0 μmol/L）, average OTM were 0. 88 ± 0. 20, 1.01 ± 0. 15 and 1.10 ± 0. 16, and 8-OHdG levels were （ 19. 57 ± 7.57）. （22. 80 ±9. 16） and （31.74 ±9.25） 8-OHdG/10^6dG, respectively. A concentration of 46μmol/L Aroclor1254 caused a significant increase of 8-OHdG level as compared with the solvent control. After pretreatment of HepG2 cells with Aroclor1254 （11.5, 23.0 and 46. 0 μ mol/L）, B（a）P induced more DNA strand breaks （OTM： 2. 14±0.22. 2.43±0.32and2.71 ±0.31） and8-OHdG [（32.50±3.81）, （49.23±16.66） and （60. 36 ± 18.04） 8-OHdG/10^6dG ] in HepG2 cells than B （a）P alone. Conclusion Aroclor1254 might enhance B （a）P-induced DNA damage in HepG2 cells, which should imply a synergistic effect of Aroclor125g on the genotoxicity of B（a）P.
出处
《中华预防医学杂志》
CAS
CSCD
北大核心
2006年第2期97-100,共4页
Chinese Journal of Preventive Medicine
基金
国家自然科学基金重大项目资助项目(40590393)
