Extensive applications of vanadium dioxide (VO2)-based materials raise concerns over the biosafety of VO2 exposure via various routes. To understand the effects of VO2 on people’s health, we used RNA sequencing (RNA-seq) technique to monitor the widespread changes in gene expression to reveal the toxicity mechanism of two commercial VO2 materials, nanoscale VO2 (S-VO2) and bulk VO2 (M-VO2) on Raw264.7 cell line, which represents the first cellular systems dealing with xenobiotics. Nanoscale S-VO2 displayed higher toxicity than bulk M-VO2, but both of VO2 particles inhibited the proliferation and induced the apoptosis in Raw264.7 cells with similar toxicity mechanisms. As shown by RNA-seq analysis and validated by biochemical assays, VO2 particles induced the endoplasmic reticulum stress accompanied with the release of calcium ions and the overproduction of reactive oxygen species, and then led to DNA damage, mitochondrial damage, autophagy and lysosomal damage, which finally resulted in apoptosis and proliferation inhibition, showing a decline in viability. The cellular uptake of VO2 particles and the dissolved species of VO2 jointly contributed to the observed toxicity. This systematic study reveals the toxicity mechanisms of VO2 materials at the transcriptome level, providing valuable data for their safe applications in the future.

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