纳米硫化镉量子点细胞毒性作用机制

为初步探讨硫化镉量子点(CdS QDs)的细胞毒性作用机制,采用MTT毒性实验比较了CdS QDs和常规CdS对仓鼠肺细胞(CHL)的毒性效应以及细胞内外活性氧水平.结果表明,1)在较低暴露浓度(≤20μg·mL-1)时,CdS QDs细胞毒性显著高于常规CdS,而在较高暴露浓度(>20μg·mL-1)时,两者相差不大.2)在较低暴露浓度(≤40μg·mL-1)时,添加N-乙酰半胱氨酸(NAC)可显著降低CdS QDs的细胞毒性,而在较高暴露浓度(>40μg·mL-1)时,添加NAC对CdS QDs的细胞毒性没有明显影响.添加NAC对常规CdS细胞毒性没有显著影响.综合实验结果推测CdS QDs的细胞毒性与暴露剂量有关:在低浓度(<20μg·mL-1)时,主要是活性氧的氧化损伤作用;在中等浓度(20~40μg·mL-1)时,活性氧和Cd2+的释放共同作用;在高浓度(>40μg·mL-1)时,则是Cd2+的释放占主导地位.

The Cytotoxicity Mechanism of Unmodified Cadmium Sulfide Quantum Dots

In order to give a preliminary study of the cytotoxicity mechanism of unmodified cadmium sulfide quantum dots (CdS QDs), MTT assay was applied to compare different cytotoxicity effects between CdS QDs and microsized CdS on Chinese Hamster Lung Fibroblast (CHL)cells and Reactive Oxygen Species (ROS)levels in cells and outside. Results indicated that: 1)Compared with microsized CdS, CdS QDs showed a higher toxicity when they were at low concentrations (≤20μg·mL-1)but a similar toxicity was found when their concentrations were higher than 20μg·mL-1. 2)NAC could mitigate CdS QD-induced decrease of cell metabolic activity, especially when CdS QD concentrations were low (≤40μg· mL-1). But when CdS QD concentrations were higher than 40μg·mL-1, the effects were not apparent. However, for the cells treated with microsized CdS, NAC did not inhibit their damage. Synthesizing the above results, it could be speculated that the cytotoxicity of CdS QDs was concerned with the exposure dose of CdS QDs to the cells: when CdS QD concentrations were low (<20μg·mL-1), the ROS would be the main toxicity mechanism; when CdS QD concentrations were 20 ~40μg·mL -1, the ROS and the Cd2 + release together would be the toxicity mechanism; and when CdS QD concentrations were high(>40μg·mL-1), Cd2+ release would be the main toxicity mechanism.