Journal
TOXICOLOGY IN VITRO
Volume 28, Issue 5, Pages 926-931Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.tiv.2014.03.002
Keywords
Inflammation; Neutrophils; Apoptosis; Nanoparticle; ZnO; Protein synthesis
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Funding
- Institut de Recherche Robert-Sauve en Sante et en Securite du Travail (IRSST)
- Natural Sciences and Engineering Research Council of Canada (NSERC)
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Inflammation is one of the major toxic effects reported in the literature following nanoparticle (NP) exposure. Knowing the importance of neutrophils to orchestrate inflammation, it is surprising that the direct role of NPs on neutrophil biology is poorly documented. Here, we investigated if ZnO NPs can alter neutrophil biology. We found that ZnO NPs increased the cell size, induced cell shape changes, activated phosphorylation events, enhanced cell spreading onto glass, but did not induce the generation of reactive oxygen species (ROS). Treatment of neutrophils with ZnO NPs markedly and significantly inhibited apoptosis and increased de nova protein synthesis, as demonstrated by gel electrophoresis of metabolically [S-35]-labeled cells. Utilization of the protein synthesis inhibitor, cycloheximide, reversed such antiapoptotic effect. We conclude that ZnO NPs are activators of several human neutrophil functions and that they inhibit apoptosis by a de novo protein synthesis-dependent and ROS-independent mechanism. This is the first example that a NP acts on the neo-synthesis of polypeptides. (C) 2014 Elsevier Ltd. All rights reserved.
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