Intestinal injury alters tissue distribution and toxicity of ZnO nanoparticles in mice.

The fast growing applications of ZnO nanoparticles (NPs) in food sector and other fields enhance the exposure possibility of human beings to ZnO NPs including via oral administration route. Although the oral toxicity of ZnO NPs has been studied, most of the research was performed on the normal animal models. Therefore, the understanding of the biological consequence of ZnO NPs on the population with diseases, especially gastrointestinal disease, is extremely limited. In this study, a mice model of inflammatory bowel disease (IBD) induced by indomethacin has been developed to comprehensively investigated the bioeffects of ZnO NPs on the specific population. The effect of the intestinal inflammation/injury on the distribution and toxicity of orally administrated ZnO NPs (nZnO, 20 nm × 100 nm and mZnO, ∼200 nm) in mice were analyzed. The results showed that there was a difference in the distribution of Zn and the essential trace elements (Fe and Cu) between the IBD mice and the normal mice. We also observed an obvious size effect. Higher hepatic Zn was detected in the IBD mice post-exposure to ZnO NPs, especially bigger ZnO NPs. In addition, the histopathological examination of main organs and biological parameters analysis showed that ZnO NPs caused slight toxicity to the liver and kidneys in the IBD mice. Our findings highlight the importance of the health status of animals on the bioeffects of nanomaterials.