Mitigation of Metal Oxide Nanotoxicity with Functional Fibrils ^†

The toxicity of metal oxide nanoparticles has been a central research topic over the past two decades, owing to the domestic and industrial applications of this vast class of nanomaterials [1]. In the literature, ion release has been implicated as a primary cause for metal oxide nanotoxicity, coupled with the distinct physicochemical properties (e.g., large surface area, ready diffusion and dissolution, and strong adsorption) of nanoparticles, in comparison with bulk materials [2,3]. However, few solutions have been proposed thus far for overcoming the toxicity of metal oxide nanoparticles in vitro and in vivo. In this study, we engineered functional amyloid fibrils [4] using beta lactoglobulin (blg), a major whey protein, and demonstrated a scheme of ion sequestration by blg amyloid fibrils co-incubated with CuO or ZnO nanoparticles, using inductively coupled plasma mass spectrometry (ICP-MS). Our computer modeling revealed that blg fibrils possessed multiple binding sites for Cu²⁺ and Zn²⁺, while strong binding of the metal ions often occurred at the Cys-121 residues of the fibrils. In addition, our cell viability and reactive oxygen species assays implicated blg amyloid fibrils as a functional nanomaterial with minimal toxicity. This study offered a facile engineering strategy for remediating the toxicity of metal oxide nanoparticles for facilitating their safe biological and environmental applications.