细胞毒性研究认为Cd2+的释放是硒化镉(CdSe)纳米粒子的细胞毒性机制之一,而Se2-阴离子在纳米粒子中的毒性机制未知。作者研究了硒代硫酸钠(selenosulfate(SSeO3)2-)对HL60细胞的细胞毒性作用,发现10μmol/L的硒代硫酸钠可以显著抑制细胞活力,诱导细胞凋亡,出现了染色质凝聚、DNA ladder和G0/G1凋亡亚峰。线粒体膜电位显著降低的同时,促凋亡蛋白Bax的免疫荧光增加。结果表明还原态的Se2-阴离子有显著的细胞毒性作用,可以诱导HL60细胞凋亡。同时也暗示Se2-阴离子的释放可能是含Se2-纳米粒子(比如硒化镉的量子点)细胞毒性的机制之一。
The effect of Cd2+ releasing in the cytotoxicity of nanoparticle cadmium selenide(CdSe)has been reported; how- ever, the role of Se2-ion remains unclear. In this study, the authors explored the cellular effects of selenosulfate(SSeO3)2-on HL60 cells. They found that 10 μmol/L selenosulfate significantly suppressed the cell viability, and induced apoptosis characterized by condensation of chromatin, DNA ladder and the sub-G0/G1 peak measured by flow cytometry. The mitochondrial membrane potential decreased and the immunofluorescence of pro-apoptosis protein Bax increased. The investigation reveals that the reductive Se2-ion may cause significant cytotoxicity, which suggests that the release of Se2- may be an alternative mechanism for the cytotoxic effects of Se2--containing nanoparticles such as quantum dots CdSe.