Interaction between silver nanoparticles of 20nm (AgNP20) and human neutrophils: induction of apoptosis and inhibition of de novo protein synthesis by AgNP20 aggregates

Cytotoxic and proinflammatory properties of silver nanoparticles (AgNPs) have been reported in few studies but the direct interaction between AgNPs and neutrophils, which play a key role in inflammation, has never been documented. Here, we examined the role of AgNPs with a starting size of 20nm (AgN...

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Veröffentlicht in:Journal of applied toxicology 2014-04, Vol.34 (4), p.404
Hauptverfasser: Poirier, Michelle, Simard, Jean-Christophe, Antoine, Francis, Girard, Denis
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Sprache:eng
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Zusammenfassung:Cytotoxic and proinflammatory properties of silver nanoparticles (AgNPs) have been reported in few studies but the direct interaction between AgNPs and neutrophils, which play a key role in inflammation, has never been documented. Here, we examined the role of AgNPs with a starting size of 20nm (AgNP20) in human neutrophils. Using dynamic light scattering for the characterization of NPs suspended under identical conditions to those used for in vitro experiments, we found that, at 10µgml-1, 92% of AgNP20 possess a diameter of 17.1nm but, at 100µgml-1, a tri-modal size distribution with large aggregates was observed (> 500nm). Neutrophil cell size increased when treated with AgNP20 and transmission electronic microscopy experiments revealed that AgNP20 can rapidly interact with the cell membrane, penetrate neutrophils, localize in vacuole-like structures, and be randomly distributed in the cytosol after 24h. Treatment with 100µgml-1 AgNP20 for 24h (but not 10µgml-1) increased the neutrophil apoptotic rate and inhibited de novo protein synthesis. We conclude that AgNP20 induced apoptosis and can act as potent inhibitors of de novo protein synthesis at 100, but not 10µgml-1 in human neutrophils. Copyright © 2013 John Wiley & Sons, Ltd. The aim of this study was to investigate the potential effect of AgNP20 on human neutrophil cell biology. AgNP20 were found to induce human neutrophil apoptosis by a de novo protein synthesis-dependent and reactive oxygen species-independent mechanism. [PUBLICATION ABSTRACT]
ISSN:0260-437X
1099-1263
DOI:10.1002/jat.2956