论文部分内容阅读
目的研究饮水含氮消毒副产物二氯乙腈(DCN)对体外培养的人肝癌HepG2细胞的氧化损伤和细胞周期的影响。方法二甲基亚砜(DMSO)溶解DCN,以DMSO处理为溶剂对照组,分别以0.8、4、20、100μmol/L DCN染毒HepG2细胞为处理组。应用Cell Counting Kit-8试剂盒检测细胞活力,相关试剂盒检测HepG2细胞内丙二醛(MDA)、超氧化物歧化酶(SOD)和还原型谷胱甘肽(GSH)的含量,并通过碘化丙啶(PI)标记的流式细胞技术检测细胞周期。结果 DCN引起HepG2细胞的IC50为230.53μmol/L;在染毒24 h条件下,与溶剂对照相比,100μmol/L的DCN可引起HepG2细胞内MDA含量上升(P<0.05)和SOD含量下降(P<0.01),各染毒组的DCN使HepG2细胞内GSH含量明显下降(P<0.05);在细胞活力75%以上的染毒剂量下对细胞周期无影响。结论低剂量的DCN可诱导HepG2细胞氧化损伤,使其脂质过氧化反应增强、抗氧化作用降低,但对细胞周期无影响。
Objective To study the effects of dichloroacetonitrile (DCN), a nitrogenous disinfectant by drinking water, on the oxidative damage and cell cycle of HepG2 cells cultured in vitro. Methods DCN was dissolved in dimethylsulfoxide (DMSO) and treated with DMSO as solvent control. HepG2 cells were treated with DCN at doses of 0.8, 4, 20 and 100 μmol / L, respectively. The cell viability was detected by Cell Counting Kit-8 kit. The contents of malondialdehyde (MDA), superoxide dismutase (SOD) and reduced glutathione (GSH) in HepG2 cells were detected by the kit, Propidium (PI) labeled flow cytometry was used to detect cell cycle. Results DCN induced HepG2 cells with IC50 of 230.53μmol / L. DCN at 100μmol / L increased the content of MDA in HepG2 cells (P <0.05) and decreased the content of SOD in HepG2 cells P <0.01). The content of GSH in HepG2 cells was significantly decreased in DCN group (P <0.05). No effect on cell cycle was observed when the cell viability was above 75%. Conclusion Low dose of DCN can induce oxidative injury in HepG2 cells, and enhance the lipid peroxidation, reduce the anti-oxidant effect, but have no effect on the cell cycle.