Abstract
First, our results showed that exposure to empty ENPs induced a decrease of cellular viability in NR8383 cells, and an increase of cellular viability and growth in THP-1 cells using, WST-1 and trypan blue. Expression of genes involved in oxidative damage (NCF1), inflammation (NFKB, TNFA, IL6, IL1B), autophagy (ATG16L), and apoptotic balance (PDCD4, BCL2, CASP8) was analyzed by RT-qPCR. ATG16L, BCL2, and TNFAwere up-regulated in NR8383 cells, which is consistent with an induction of autophagy and inflammation. On the other hand, NCF1, NFKB, and IL1B were down-regulated in THP-1 cells,whichmaycontribute to explain the increaseof cellular viability. Second, NPswere likely internalized by THP-1 as shown by TEM and flow cytometry after 2h using different pathways of endocytosis like clathrine and caveoline. Third, transcriptome analysis by microarray of THP-1, either exposed or not to GSNO-loaded ENPs, has shown a significant dose and time-dependent variation of the expression of genes belonging to the clusters “proliferation”, “cell structure”, “mitochondria” and “metabolic processes”. Thus, (i) the cytotoxicity of NPs is model dependent and (ii) mechanistic toxicology should be the corner stone for the evaluation of NPs harmfulness.
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