Oxidative stress and mitochondria damage contribute to silica nanoparticle-induced cytotoxicity in human endothelial cells

Nanoparticles (NPs) have a wide variety of applications in material sciences, engineering and medicine. However, the inter- action of NPs with biological systems and the potential toxico- logical effects remain far from clear. Given the central role that the endothelium plays in cardiovascular (CV) homeostasis and the involvement of endothelial cell (EC) dysfunction in CV dis- eases pathogenesis, the EC represent an excellent model to investigate the impact of NPs on vascular (patho)physiology. Newly synthesized SiO2 NPs, functionalized or not with FITC, were characterized by fluorimetric analysis, SEM and TEM microscopy. Thereafter, cell viability, mitochondrial function, reactive oxygen species (ROS) and apoptosis were assessed in cultured human endothelial ECV304 cells under control and NPs exposed conditions. The cellular uptake of NPs and FITC- NPs was also investigated by fluorescence and TEM micros- copy. Exposure to NPs at dosage levels between 50 and 100 lg/ml decreased cell viability in a dose-dependent manner. Reduced mitochondrial membrane potential along with an increase in both the intracellular ROS level and intra-mitochon- drial oxidative stress were also observed in NPs-exposed cells. Fluorescence and TEM analysis revealed a dose-dependent uptake of NPs by ECV304 cells. In summary, exposure to NPs resulted in a dose-dependent cytotoxicity in cultured ECV304 cells that was associated with increased oxidative stress and mitochondria damage.