Oxide-nanoparticles induce in vitro DNA damage and genomic instability in human peripheral blood cells.

The increasing application of nanotechnology has raised concerns regarding the genotoxic potential of engineered nanoparticles due to their unique physicochemical properties and biological interactions. The present study evaluated the genotoxic effects of four oxide nanoparticles-aluminium oxide (Al₂O₃NPs), iron oxide (Fe₃O₄NPs), silicon dioxide (SiO₂NPs), and titanium dioxide (TiO₂NPs)-in human peripheral blood cells using the alkaline comet and cytokinesis-block micronucleus (CBMN) assays. Sublethal concentrations were selected based on IC₅₀ values determined by a resazurin-based cell viability assay. The comet assay revealed a significant dose-dependent increase in DNA strand breaks for all nanoparticles, with TiO₂NPs inducing the highest levels of primary DNA damage, as reflected by the percentage of tail DNA. In contrast, SiO₂NPs produced the highest frequency of micronuclei in the CBMN assay, indicating pronounced chromosomal instability. Fe₃O₄NPs showed a significant increase in nucleoplasmic bridge formation at higher concentrations, while Al₂O₃NPs exhibited comparatively lower genotoxic effects. Overall, these findings demonstrate differential genotoxic responses among oxide nanoparticles, influenced by particle size and composition, and highlight their potential to induce genome instability even at sublethal exposure levels.