Zinc oxide nanoparticles induce HIF-1α protein stabilization through increased reactive oxygen species generation from electron transfer chain complex III of mitochondria

While zinc oxide (ZnO) NPs are one of the most abundantly used nanomaterials in the cosmetic, medical, and electronics industries [1], In mammalian cells, the toxic effects of ZnO NPs have been demonstrated, including their role in inflammatory responses, endoplasmic reticulum stress, and apoptosis [2,3]. In addition, ZnO NPs could be absorbed into keratinocytes [4]. Although ZnO NPs exert their potential cytotoxic effects through generating reactive oxygen species (ROS) production and oxidative stress [5], the source/mechanism of ZnO NP-induced ROS production and ZnO NP-mediated signalling cascades in keratinocytes have not been delineated.