论文部分内容阅读
目的探讨2,2’,4,4’-四溴联苯醚(2,2’,4,4’-tetrabromodiphenyl ether,BDE-47)的L02肝细胞毒性效应。方法采用CCK8法检测BDE-47的肝细胞毒性效应,确定时间-剂量-效应关系。选取3个剂量组:高(80μmol/L)、中(20μmol/L)和低剂量(5μmol/L)的BDE-47染毒细胞,同时设立一个空白对照组和一个溶剂对照组,试剂盒检测各剂量组超氧化物歧化酶(SOD)、丙二醛(MDA)、乳酸脱氢酶(LDH)和谷胱甘肽S-转移酶(GST)的表达,SPSS 13.0进行统计分析。结果 BDE-47具有明显的肝细胞毒性(与对照组相比,P<0.01),染毒时间在12～72 h时呈现时间-剂量-效应关系,并发现BDE-47染毒肝细胞12 h的半数抑制浓度为80μmol/L,为其显著作用时间点;BDE-47染毒L02肝细胞后,细胞外的LDH表达增加,细胞内MDA含量增加;而细胞内GST和SOD酶活力则呈现低浓度BDE-47染毒时升高而高浓度时降低。结论 BDE-47对L02肝细胞具有一定的细胞毒性,并能够导致细胞氧化应激损伤。这可能是其生物毒性效应的重要机制之一。
Objective To investigate the hepatotoxic effects of L02 on 2,2 ’, 4,4’-tetrabromodiphenyl ether (BDE-47). Methods CCK8 method was used to detect the hepatotoxicity of BDE-47 and to determine the time-dose-response relationship. Three doses of BDE-47 cells (80μmol / L, 20μmol / L) and low dose (5μmol / L) were selected and a blank control group and a solvent control group were set up The levels of superoxide dismutase (SOD), malondialdehyde (MDA), lactate dehydrogenase (LDH) and glutathione S-transferase (GST) in each dose group were analyzed by SPSS 13.0. Results BDE-47 had obvious hepatotoxicity (P <0.01 compared with the control group), and the time-dose-response relationship was observed between 12 and 72 hours after exposure to BDE-47. The half inhibitory concentration was 80μmol / L, which was the significant time point. After L02 hepatocytes were exposed to BDE-47, the extracellular LDH expression increased and the intracellular MDA content increased; while the intracellular GST and SOD enzyme activity showed low Concentration BDE-47 increased while exposed to high concentrations. Conclusion BDE-47 has certain cytotoxicity on L02 hepatocytes and can induce cell oxidative stress injury. This may be one of the important mechanisms of its bio-toxic effects.