Abstract

Particle size-dependent biological effects of silver nanoparticles (AgNPs) are of great interest; however, the mechanism of action of silver ions (Ag+) released from AgNPs concerning AgNP particle size remains unclear. Thus, we evaluated the influence of particle size (20, 40, 60, and 80 nm) on the acute 96-h bioaccumulation and toxicity (swim bladder damage) of AgNPs in zebrafish (Danio rerio) larvae, with a focus on the mechanism of action of Ag+ released from differently sized AgNPs. The 40- and 60-nm AgNPs were more toxic than the 20- and 80-nm versions in terms of inflammation and oxidative damage to the swim bladder, as indicated by inhibition of type 2 iodothyroxine deiodinase enzyme activity, mitochondrial injury, and reduced 30–50% adenosine triphosphate content. Furthermore, up-regulation and down-regulation of swim bladder development-related gene expression was not observed for pbx1a and anxa5, but up-regulation expression of shha and ihha was observed with no statistical significance. That 20-nm AgNPs were less toxic was attributed to their rapid elimination from larvae in comparison with the elimination of 40-, 60-, and 80-nm AgNPs; thus, less Ag+ was released in 20-nm AgNP-exposed larvae. Failed inflation of swim bladders was affected by released Ag+ rather than AgNPs themselves. Overall, we reveal the toxicity contribution of Ag+ underlying the observed size-dependent effects of AgNPs and provide a scientific basis for comprehensively assessing the ecological risk and biosafety of AgNPs.

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