Effects of TiO(2) and Co(3)O(4) Nanoparticles on Circulating Angiogenic Cells

BACKGROUND AND AIM: Sparse evidence suggests a possible link between exposure to airborne nanoparticles (NPs) and cardiovascular (CV) risk, perhaps through mechanisms involving oxidative stress and inflammation. We assessed the effects of TiO(2) and Co(3)O(4) NPs in human circulating angiogenic cells (CACs), which take part in vascular endothelium repair/replacement. METHODS: CACs were isolated from healthy donors’ buffy coats after culturing lymphomonocytes on fibronectin-coated dishes in endothelial medium for 7 days. CACs were pre-incubated with increasing concentration of TiO(2) and Co(3)O(4) (from 1 to 100 μg/ml) to test the effects of NP – characterized by Transmission Electron Microscopy – on CAC viability, apoptosis (caspase 3/7 activation), function (fibronectin adhesion assay), oxidative stress and inflammatory cytokine gene expression. RESULTS: Neither oxidative stress nor cell death were associated with exposure to TiO(2) NP (except at the highest concentration tested), which, however, induced a higher pro-inflammatory effect compared to Co(3)O(4) NPs (p<0.01). Exposure to Co(3)O(4) NPs significantly reduced cell viability (p<0.01) and increased caspase activity (p<0.01), lipid peroxidation end-products (p<0.05) and pro-inflammatory cytokine gene expression (p<0.05 or lower). Notably, CAC functional activity was impaired after exposure to both TiO(2) (p<0.05 or lower) and Co(3)O(4) (p<0.01) NPs. CONCLUSIONS: In vitro exposure to TiO(2) and Co(3)O(4) NPs exerts detrimental effects on CAC viability and function, possibly mediated by accelerated apoptosis, increased oxidant stress (Co(3)O(4) NPs only) and enhancement of inflammatory pathways (both TiO(2) and Co(3)O(4) NPs). Such adverse effects may be relevant for a potential role of exposure to TiO(2) and Co(3)O(4) NPs in enhancing CV risk in humans.