Metallic nanoparticles (NPs) have potential applications in industry and medicine, but they also have the potential to cause many chronic pulmonary diseases. Mechanisms for their cytotoxicity, glucose and energy metabolism responses need to be fully explained in lung epithelial cells after treatment with metallic nanoparticles. In our study, two different metallic nanoparticles (Fe2 O3 and ZnO) and two cell-based assays (BEAS-2B and A549 cell lines) were used. Our findings demonstrate that ZnO nanoparticles, but not Fe2 O3 nanoparticles, induce cell cycle arrest, cell apoptosis, reactive oxygen species (ROS) production, mitochondrial dysfunction and glucose metabolism perturbation, which are responsible for cytotoxicity. These results also suggest that the glucose metabolism and bioenergetics had a great potential in evaluating the cytotoxicity and thus were very helpful in understanding their underlying molecular mechanisms.
Keywords: ROS; cell cycle arrest; cytotoxicity; glucose metabolism; mitochondrial dysfunction; nanoparticles.
Copyright © 2015 John Wiley & Sons, Ltd.