Australian Centre for Microscopy & Microanalysis, The University of Sydney, Sydney, NSW 2006, Australia.
Biomaterials. 2011 Jul;32(20):4565-73. doi: 10.1016/j.biomaterials.2011.03.006. Epub 2011 Apr 1.
Nanoparticles with an iron core and gold shell (denoted "Fe@AuÓ") have been reported to limit cancer-cell proliferation and therefore have been proposed as a potential anti-cancer agent. However, the underlying mechanisms are still unknown. In this study, we used flow cytometry, confocal fluorescence microscopy, and transmission electron microscopy to analyse the morphological and functional alterations of mitochondria in cancerous cells and healthy cells when treated with Fe@Au. It was found that Fe@Au caused an irreversible membrane-potential loss in the mitochondria of cancer cells, but only a transitory decrease in membrane potential in healthy control cells. Production of reactive oxygen species (ROS) was observed; however, additions of common ROS scavengers were unable to protect cancerous cells from the Fe@Au-induced cytotoxicity. Furthermore, iron elements, before oxidation, triggered mitochondria-mediated autophagy was shown to be the key factor responsible for the differential cytotoxicity observed between cancerous and healthy cells.
具有铁核和金壳的纳米粒子(表示为“Fe@Au”)已被报道能抑制癌细胞增殖,因此被提议作为一种潜在的抗癌药物。然而,其潜在的机制尚不清楚。在这项研究中,我们使用流式细胞术、共聚焦荧光显微镜和透射电子显微镜来分析用 Fe@Au 处理后癌细胞和健康细胞中线粒体的形态和功能变化。结果发现,Fe@Au 导致癌细胞中线粒体的膜电位不可逆丧失,但健康对照细胞中的膜电位仅短暂下降。观察到活性氧(ROS)的产生;然而,添加常见的 ROS 清除剂并不能保护癌细胞免受 Fe@Au 诱导的细胞毒性。此外,氧化前的铁元素触发的线粒体介导的自噬被证明是导致癌细胞和健康细胞之间观察到的差异细胞毒性的关键因素。