Department of Chemical and Biomolecular Engineering, National University of Singapore, 4 Engineering Drive 4, Singapore 117585, Singapore.
Department of Chemical and Biomolecular Engineering, National University of Singapore, 4 Engineering Drive 4, Singapore 117585, Singapore.
Biomaterials. 2014 Aug;35(25):6707-15. doi: 10.1016/j.biomaterials.2014.05.007. Epub 2014 May 28.
How silver nanomaterials (Ag NMs) could induce toxicity has been debated heatedly by many researchers. We utilized Ag nanoclusters (Ag NCs) with the same size and ligand protection but different core surface speciation. Ag(+)-rich NCs (Ag(+)-R NCs) and their counterpart, the reduced Ag(0)-rich NCs (Ag(0)-R NCs) are synthesized to represent possible dichotomous stages in silver nanomaterial degradation process. Here we show Ag(0)-R NCs induce higher cellular toxicity when compared to Ag(+)-R NCs. This cellular toxicity is brought about via the modulation of reactive oxygen species (ROS) in cells as a result of the more rapid release of Ag species from Ag(0)-R NCs and subsequent oxidation into Ag(+) in the lysosomal compartment. The weaker Ag(0)-R bond greatly potentiated the release of Ag species in the acidic and enzymatic processes within the lysosomes. Since lysosomes are absent in bacteria, increasing silver nanomaterials stability may lower toxicity in mammalian cells whilst not reducing their efficacy to fight bacteria; this redesign can result in a safer silver nanomaterial.
银纳米材料(Ag NMs)如何引起毒性一直是许多研究人员激烈争论的话题。我们利用具有相同尺寸和配体保护但核心表面形态不同的银纳米团簇(Ag NCs)。富银(Ag(+)-R NCs)和相应的富银(Ag(0)-R NCs)被合成,以代表银纳米材料降解过程中可能的两个阶段。我们发现,与 Ag(+)-R NCs 相比,Ag(0)-R NCs 诱导更高的细胞毒性。这种细胞毒性是由于 Ag(0)-R NCs 中 Ag 物种更快地释放,随后在溶酶体中氧化成 Ag(+),导致细胞内活性氧(ROS)的调节。Ag(0)-R 键较弱,极大地促进了溶酶体中酸性和酶促过程中 Ag 物种的释放。由于细菌中不存在溶酶体,增加银纳米材料的稳定性可能会降低哺乳动物细胞的毒性,而不会降低其对抗细菌的功效;这种重新设计可以得到更安全的银纳米材料。