Cytotoxicity of vanadium dioxide nanoparticles to human embryonic kidney cell line: Compared with vanadium(IV/V) ions.

Vanadium dioxide (VO 2) is a class of thermochromic material with potential applications in various fields. Massive production and wide application of VO 2 raise the concern of its potential toxicity to human, which has not been fully understood. Herein, a commercial VO 2 nanomaterial (S-VO 2) was studied for its potential toxicity to human embryonic kidney cell line HEK293, and two most common vanadium ions, V(IV) and V(V), were used for comparison to reveal the related mechanism. Our results indicate that S-VO 2 induces dose-dependent cellular viability loss mainly through the dissolved V ions of S-VO 2 outside the cell rather than S-VO 2 particles inside the cell. The dissolved V ions of S-VO 2 overproduce reactive oxygen species to trigger apoptosis and proliferation inhibition via several signaling pathways of cell physiology, such as MAPK and PI3K-Akt, among others. All bioassays indicate that the differences in toxicity between S-VO 2 , V(IV), and V(V) in HEK293 cells are very small, supporting that the toxicity is mainly due to the dissolved V ions, in the form of V(V) and/or V(IV), but the V(V)'s behavior is more similar to S-VO 2 according to the gene expression analysis. This study reveals the toxicity mechanism of nanosized VO 2 at the molecular level and the role of dissolution of VO 2 , providing valuable information for safe applications of vanadium oxides. [Display omitted] • VO 2 NPs induced a dose-dependent toxicity to HEK293 cells. • VO 2 NPs overproduce ROS to trigger apoptosis and proliferation inhibition. • Dissolved V ions of VO 2 NPs outside cells contribute to cellular viability loss. • Differences in toxicity between S-VO 2 , V(IV), and V(V) are very small. [ABSTRACT FROM AUTHOR]