量子点与Cu~(2+)对L02细胞毒性的协同作用机制:量子点可能的木马角色

量子点由于其广泛应用及可能的对环境的危害而引起关注,理解量子点对原有环境污染物诱导毒性的影响以及相关的机制对于控制量子点的环境风险具有重要意义.用2μg/mL(IC10)的QDs和2.5～20μg/mL(IC10～IC40)的Cu2+以及人胚肝细胞(L02)作为研究对象,通过EDX和量子点荧光光谱的变化确定了量子点和Cu2+的结合,量子点的存在提高了细胞内Cu2+含量,并进而由MTT和HE染色结果确定了相应的量子点存在下Cu2+诱导的细胞毒性的增加:细胞形态显著变化,存活率最大降低了3倍.由此,推测量子点在此过程中可能扮演了木马角色,吸附了Cu2+并携带其进入细胞,使得细胞内的Cu2+含量增加进而导致毒性提高.量子点在环境中的这种特征值得关注.

Mechanism of Quantum Dots Facilitating Cu2+-Induced Hepatic L02 Cells Toxicity: Possible Trojan-Horse Role of QDs

Concerns regarding the potential environmental impact of quantum dots (QDs) are raised for its extensive use. Understanding the influences of QDs on original environmental pollutants induced toxicity and obtaining information about the mechanism is crucial to evaluate potential ecological hazards posed by QDs. The effects of QDs on Cu2+ induced Hepatic L02 cells toxicity and the mechanisms were investigated. IC10 value of 2 microg/mL QDs and IC10-IC50 value of 2.5-20 microg/mL of CU2+ was used in this study. Firstly Luminescence emission spectrum of QDs showed 10 nm red shifts with addition of Cu2+ provide the interaction possibility of QDs and Cu2+, the further X-ray energy dispersive spectroscopy (EDX) analysis indicated binding of Cu2+ on QDs surface. Then the intracellular Cu2+ concentrations showed increase with addition of QDs, which is accompanied by loss of cell viability and morphology changes. The mechanism was therefore assumed as interaction of QDs-Cu2+ improved the intracellular Cu2+ level then cytotoxicity. QDs seemed to serve as Trojan-horse taking much more Cu2+ into cells via cheating cell membrane recognition, which imply the possible interactions with heavy metal ions will pose a significant influence on environment and human body.