Metal and metal oxide nanoparticles have been widely used in catalytic, electronic and biomedical fields. It is necessary to investigate their toxicity and potential hazards to human and aquatic ecosystems. Zebrafish (Danio rerio), as a promising animal model, has been increasingly utilized to assess the toxicity of nanoparticles. Zebrafish has numerous characteristics for toxicity evaluation, such as short life cycle and high fecundity. This review describes the advantages of using zebrafish in the toxicity assessment of metal and metal oxide nanoparticles. Then we focus on the toxic effects, particularly the acute toxicity and the chronic ones, induced by nanoparticles in zebrafish. Target organ toxicities are also mentioned, including immunotoxicity, developmental toxicity, neurotoxicity, reproductive toxicity, cardiovascular toxicity and hepatotoxicity. The toxic effects of selected metal nanoparticles, including Au, Ag, Cu, and metal oxide nanoparticles such as TiO2, Al2O3, CuO, NiO and ZnO, as well as the underlying mechanisms of nanoparticles causing these effects, are also highlighted and described in detail. Furthermore, we introduce the general factors that affect nanoparticle‐induced toxicity in zebrafish. The drawbacks and advantages of using the zebrafish model in nanotoxicity studies are also argued. Finally, we suggest that the application of zebrafish to assess chronic toxicity of metal and metal oxide nanoparticles and the joint toxicity of metal and metal oxide nanoparticles and other pollutants could be hot topics in nanotoxicology.

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Ag2Se QD exposure activated microglia followed by pro-inflammatory cytokine IL-1β release in vivo and in vitro through NLRP3 inflammasome activation.

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Fine particulate matter (PM2.5)‐induced detrimental cardiovascular effects have been widely concerned, especially for endothelial cells, which is the first barrier of the cardiovascular system. Among potential mechanisms involved, reactive oxidative species take up a crucial part. However, source of oxidative stress and its relationship with inflammatory response have been rarely studied in PM2.5‐induced endothelial injury. Here, as a key oxidase that catalyzes redox reactions, NADPH oxidase (NOX) was investigated. Human umbilical vein endothelial cells (EA.hy926) were exposed to Standard Reference Material 1648a of urban PM2.5 for 24 h, which resulted in NOX‐sourced oxidative stress, endothelial dysfunction, and inflammation induction. These are manifested by the up‐regulation of NOX, increase of superoxide anion and hydrogen peroxide, elevated endothelin‐1 (ET‐1) and asymmetric dimethylarginine (ADMA) level, reduced nitric oxide (NO) production, and down‐regulation of phosphorylation of endothelial NO synthase (eNOS) with increased levels of inducible NO synthase, as well as the imbalance between tissue‐type plasminogen activator (tPA) and plasminogen activator inhibitor 1 (PAI‐1), and changes in the levels of pro‐inflammatory and anti‐inflammatory factors. However, administration of NOX1/4 inhibitor GKT137831 alleviated PM2.5‐induced elevated endothelial dysfunction biomarkers (NO, ET‐1, ADMA, iNOS, and tPA/PAI‐1), inflammatory factors (IL‐1β, IL‐10, and IL‐18), and adhesion molecules (ICAM‐1, VCAM‐1, and P‐selectin) and also passivated NOX‐dependent AKT and eNOS phosphorylation that involved in endothelial activation. In summary, PM2.5‐induced NOX up‐regulation is the source of ROS in EA.hy926, which activated AKT/eNOS/NO signal response leading to endothelial dysfunction and inflammatory damage in EA.hy926 cells.