Abstract
The toxicity of CuO nanoparticles (NPs) to human lung epithelial (A549) cells was investigated in this study. CuO NPs (10-100 mg/L) had significant toxicity to A549 cells, whereas CuO bulk particles (BPs) showed much lower toxicity (24 h IC(50), 58 and 15 mg/L for CuO BPs and NPs, respectively). Transmission electron microscopic analysis demonstrated CuO NP entry into A549 cells and organelles, including lysosomes, mitochondria, and nucleus. Endocytosis was the primary pathway of CuO NPs uptake. CuO NPs (15 mg/L) induced mitochondrial depolarization, possibly mediated by reactive oxygen species (ROS) generation. Intracellular CuO NPs first generate ROS, which subsequently induces the expression of p38 and p53 and ultimately causes DNA damage (Comet assay). We confirm for the first time that the primary cytotoxic response is oxidative stress rather than DNA damage. A fraction of the CuO NPs was exported to the extracellular environment. In this study, centrifugal ultrafiltration tubes were successfully employed to determine the dissolved Cu(2+) from CuO NPs in the cell medium. Dissolved Cu(2+) ions contributed less than half of the total toxicity caused by CuO NPs, including ROS generation and DNA damage. This study provided useful data for understanding transport and toxicity of metal oxide NPs in human cells.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
