It has not been well explored how NPs may induce some adverse effects on the biological systems. In this research, the interaction of cobalt oxide NPs (Co3O4 NPs) with tau protein and PC-12 cell line, as nervous system models, was investigated with several approaches including fluorescence spectroscopy, CD spectroscopy, docking study, MTT, LDH, AO/EB dual staining, and flow cytometry assays. Fluorescence investigation displayed that Co3O4 NPs spontaneously mediate the formation of a static complex with tau protein through hydrogen bonds and van der Waals forces. Docking study also revealed that Ser and Gln residues play important roles in the formation of hydrogen bonds between tau and Co3O4 NPs. Far UV-CD measurement determined that Co3O4 NPs changed the unfolded structure of tau protein toward a more folded conformation. Moreover, Co3O4 NPs demonstrated to stimulate the reduction of PC-12 cell viability through membrane leakage, fragmentation of DNA, apoptosis, and necrosis. In conclusion, Co3O4 NPs may trigger marked alterations on the tertiary and secondary structure of tau protein. Also, the dose of Co3O4 NPs is the crucial factor which induces their adverse effects on the cells. Because, all side effects of NPs are not well explored, additional detailed experiments are more needed.

译文

尚未很好地探讨NPs如何对生物系统产生某些不利影响。在这项研究中,氧化钴NPs (Co3O4 NPs) 与tau蛋白和PC-12细胞系 (作为神经系统模型) 的相互作用通过多种方法进行了研究,包括荧光光谱,CD光谱,对接研究,MTT,LDH,AO/EB双重染色和流式细胞仪检测。荧光研究表明,Co3O4 np通过氢键和范德华力自发介导与tau蛋白形成静态复合物。对接研究还表明,Ser和Gln残基在tau和Co3O4 np之间的氢键形成中起重要作用。Far uv-cd测量确定Co3O4 np将tau蛋白的未折叠结构改变为更折叠的构象。此外,Co3O4 np通过膜渗漏、DNA断裂、凋亡和坏死刺激PC-12细胞活力的降低。总之,Co3O4 np可能会触发tau蛋白的三级和二级结构发生明显变化。此外,Co3O4 NPs的剂量是诱导其对细胞产生不利影响的关键因素。由于NPs的所有副作用都没有得到很好的探索,因此更需要进行更详细的实验。

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