Received for review May 12, 2006

Revised manuscript received September 17, 2006

Accepted September 18, 2006

Abstract:

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 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.

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