Background Although zinc oxide nanoparticles (ZnO NPs) have been widely used, there has been an increasing number of reports on the toxicity of ZnO NPs. However, study on the underlying mechanisms under in vivo conditions is insufficient. Methods In this study, we investigated the toxicological profiles of ZnO NPs in MRC5 human lung fibroblasts in vitro and in an in vivo model using the fruit fly Drosophila melanogaster . A comprehensive study was conducted to evaluate the uptake, cytotoxicity, reactive oxygen species (ROS) formation, gene expression profiling and genotoxicity induced by ZnO NPs. Results For in vitro toxicity, the results showed that there was a significant release of extracellular lactate dehydrogenase and decreased cell viability in ZnO NP-treated MRC5 lung cells, indicating cellular damage and cytotoxicity. Generation of ROS was observed to be related to significant expression of DNA Damage Inducible Transcript ( DDIT3 ) and endoplasmic reticulum (ER) to nucleus signaling 1 ( ERN1 ) genes, which are ER stress-related genes. Oxidative stress induced DNA damage was further verified by a significant release of DNA oxidation product, 8-hydroxydeoxyguanosine (8-OHdG), as well as by the Comet assay. For the in vivo study using the fruit fly D. melanogaster as a model, significant toxicity was observed in F1 progenies upon ingestion of ZnO NPs. ZnO NPs induced significant decrease in the egg-to-adult viability of the flies. We further showed that the decreased viability is closely associated with ROS induction by ZnO NPs. Removal of one copy of the D. melanogaster Nrf2 alleles further decreased the ZnO NPs-induced lethality due to increased production of ROS, indicating that nuclear factor E2-related factor 2 (Nrf2) plays important role in ZnO NPs-mediated ROS production. Conclusion The present study suggests that ZnO NPs induced significant oxidative stress-related cytotoxicity and genotoxicity in human lung fibroblasts in vitro and in D. melanogaster in vivo. More extensive studies would be needed to verify the safety issues related to increased usage of ZnO NPs by consumers.

摘要：采用溶胶鄄凝胶组装方法制备了 Nafion/SiO 2 胶体, 并涂附于烧结的 316L 不锈钢(SS鄄316L)金属微纤网络, 形成了空隙率为 60%-75%(渍, 体积分数)的整体式微纤结构化的 Nafion/SiO 2 固体酸催化剂. 使用傅里叶变换红 外光谱(FT鄄IR), 热重分析(TGA), 扫描电子显微镜(SEM)及 NH 3 吸附法对微纤结构化的 Nafion/SiO 2 催化剂进行 了表征. 结果显示, 溶胶鄄凝胶组装方法可以明显促进 Nafion 的分散, 导致酸性中心的暴露量显著增加; 结构化的 Nafion/SiO 2 催化剂以 200-400nm 颗粒堆积而成的多孔涂层形式存在. 在一种集换热、混合、 催化(反应)功能于 一体的微反应器中, 考察了整体式微纤结构化的 Nafion/SiO 2 固体酸催化剂催化苯硝化的反应性能.Nafion 在 SiO 2 中的组装量为 20%(w, 质量分数), 金属微纤网络上 Nafion/SiO 2 担载量为 36.3%(w)的优化催化剂上,75 益 时苯转化率为 44.7%, 硝基苯选择性可达 99.9%. 相近转化率下,Nafion/SiO 2 固体酸单位酸中心的催化效能约为 硫酸的 600 倍.

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