Nanoparticulate vanadium oxide potentiated vanadium toxicity in human lung cells

Metal oxides may hold, as nanosized particles, a toxic potential to human health and the environment that is not present in the bulk material. Due to the high surface-to-volume ratio, small amounts can lead to strong oxidative damage within biological systems, impairing cellular functions as a consequence of their high surface reactivity. We report here on a new nanosized V2O3 material that has a needle-like structure with diameters of less than 30 nm and variable lengths. The potentiated toxicity of nanoscale vanadium oxide (V2O3) compared to bulk material is demonstrated here in human endo- and epithelial lung cells, and might be due to the higher catalytic surface of the particles. Reduction in cell viability is almost ten times stronger and starts with lowest concentrations of "nanoscaled" material (10 mu g/mL). Vanadium oxide leads to an induction of heme oxygenase 1 (HO-1) in a dose dependent manner in ECV304 cells whereas a reduction in protein levels can be observed for the epithelial cells (A549). Lipid peroxidation can be observed also for "nanoscaled" vanadium oxide to a much stronger extent in macrophages (RAW cells) than for bulk material. The observed effects can not only be explained by oxidation from V2O3 to V2O5 as there are significant differences between the novel nano vanadium and all used bulk materials (V2O3 and V2O5). It appears rather to be a nanoeffect of a high surface reactivity, here coupled with a yet unknown toxicity potentiating effect of a technically important catalyst.