量子点对Cu2+诱导L02细胞毒性的影响及机理研究

Effects and Mechanism of Quantum Dots on Cu2+ Induced L02 Cytotoxicity

量子点(QDs)和Cu^2+可能共存于肝脏,对肝细胞产生联合毒性,威胁人体健康。本研究以人胚肝细胞(L02)为研究对象,考察了低/无毒的QDs(3.6%的细胞致死率)对Cu^2+诱导L02细胞毒性的影响及相关机理,为其可能的健康和环境风险提供参考。结果显示,QDs的加入使得Cu^2+的细胞毒性有了很大的提高,细胞存活率最高下降了26.0%,两者表现为协同作用;另外QDs存在使得Cu^2+细胞蓄积量增大,伴随着Cu^2+天然解毒蛋白CTR1和ATP7A等表达水平的升高,从侧面印证了Cu^2+的蓄积量增加对细胞的影响;同时,QDs的存在使得细胞乳酸脱氢酶(lactate dehyfrogenase,LDH)泄露相对于Cu^2+单独处理组提高,暗示QDs可能破坏了细胞膜,导致Cu^2+在细胞内蓄积量增加,从而使细胞毒性增加,两者的联合毒性表现为协同作用。

Quantum dots nanoparticles(QDs)and Cu^2+may coexist in the liver,threatening human heath based on the hepatocytotoxicity induced by these two chemicals.In this study,human embryonic hepatocytes(L02)were used to investigate the effects of low/non-toxic QDs on Cu^2+-induced L02 cytotoxicity and the associated mechanism,which may provided a reference for health security and environmental risks assessment of QDs.The results showed that the addition of QDs greatly improved the individual Cu^2+-induced cytotoxicity,with cell survival rate decreased by 26.0%at the highest level,indicating the synergistic effects between these two chemicals.In addition,the presence of QDs increased the accumulation of Cu^2+in the cells,accompanied by the increase of Cu^2+detoxification-protein including CTR1 and ATP7A expression level,which partly confirm the higher Cu accumulation in the cells compared to the treatments without QDs addition.Simultaneously,the existence of QDs makes the lactate dehyfrogenase(LDH)leakage of cells higher than that of single Cu^2+treated groups,suggesting that QDs may damage the cell membrane,leading to increased accumulation of Cu^2+in the cell and the cytotoxicity was thus increased,so the synergistic effects of these two chemicals were observerd.