The intensive use of metal-based nanoparticles results in their continuous release into the environment, leading to potential risks for human health and microbial ecosystems. Although previous studies have indicated that nanoparticles may be toxic to microorganisms, there is a scarcity of data available to assess the underlying molecular mechanisms of inhibitory and biocidal effects of nanoparticles on microorganisms. This study used physiological experiments, microscopy, live/dead staining, and the genome-wide RNA sequencing to investigate the multiple responses of Pseudomonas aeruginosa to the exposure of copper oxide nanoparticles (CuO NPs). The results for the first time show that CuO NPs induce lysogenic bacteriophage, which might render defective within a bacterial host. The presence of CuO NPs causes nitrite accumulation and great increases in N2O emissions. Respiration is likely inhibited as denitrification activity is depleted in terms of decreased transcript levels of most denitrification genes. Meanwhile, CuO NPs exposure significantly up-regulated gene expression for those coding for copper resistance, resistance-nodulation-division, P-type ATPase efflux, and cation diffusion facilitator transporters. Our findings offer insights into the interaction between environmental bacteria and CuO NPs at the transcriptional level and, thus, improve our understanding of potential risks of nanoparticles on microbial ecosystems and public health.
Keywords: bacteriophage; denitrification; emerging contaminations; genome-wide RNA sequencing; nanoparticles.