Transcriptional responses of continuously cultured Nitrosomonas europae to chonic TiO2 nanoparticle stress
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PROVIDER: PRJNA435938 | ENA |
REPOSITORIES: ENA
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Project description:To further explore the biotoxicity mechanisms of TiO2 nanoparticles (NPs) and the recovery potentials of the impaired Nitrosomonas europaea (N. europaea, ATCC 19718) cells, a genome-sequenced model ammonia oxidizing bacterium (AOB) commonly detected in the activated sludge of biological wastewater treatment plants, the whole-genome microarray analysis was applied to retrieve the induced transcriptional responses during the long-term exposure, after the toxicity effects and the recovery potentials were assessed at both physiological and metabolic levels.
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Project description:To further explore the biotoxicity mechanisms of zinc oxide nanoparticles (ZnO NPs) and the recovery strategies of the accordingly impaired Nitrosomonas europaea (N. europaea, ATCC 19718) cells, a genome-sequenced model ammonia-oxidizing bacterium (AOB) commonly detected in the activated sludge of biological wastewater treatment plants, whole-genome microarray analysis was applied to retrieve the induced transcriptional responses, after their physiological and metabolic activities were revealed. The whole-genome expressions were measured after exposure to 50 ppm ZnO NPs and 12-hrs recovery incubation when the ammonia removal rate (ARA) declined by 10% in the chemostat bioreactor. Three independent experiments were performed for each experiment.
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Project description:Functional gene expressions of continuously cultured Nitrosomonas europae after ZnO nanoparticles exposure and recovery incubation
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Project description:A comprehensive in vitro assessment of two commercial metal oxide nanoparticles, TiO2 and ZnO, was performed using human monocyte-derived macrophages (HMDM), monocyte-derived dendritic cells (MDDC), and T cell leukemia-derived cell line (Jurkat). TiO2 nanoparticles were found to be non-toxic whereas ZnO nanoparticles caused dose-dependent cell death. Subsequently, global gene expression profiling was performed to identify signaling pathways underlying the cytotoxicity caused by ZnO nanoparticles. Analysis was done with doses, 1M-BM-5g/ml and 10M-BM-5g/ml after 6 and 24 hours of exposure. Interestingly, 2703 genes were significantly differentially expressed in HMDM upon exposure to 10M-BM-5g/ml ZnO nanoparticles, while in MDDCs only 12 genes were affected. In Jurkat cells, 980 genes were differentially expressed. It is noteworthy that the gene expression of metallothioneins was upregulated in all the three cell types. In addition to the common ZnO-inducible changes, a notable proportion of the genes were regulated in a cell type-specific manner. Using a panel of ZnO nanoparticles, we obtained an additional support that the cellular response to ZnO nanoparticles is caused by particle dissolution. Gene ontology analysis revealed that the top biological processes disturbed in HMDM and Jurkat cells were regulating cell death and growth. In addition, genes controlling immune system development were affected. Bioinformatics assessment showed that the top human disease category associated with ZnO-responsive genes in both HMDM and Jurkat cells was cancer. Overall, the study revealed novel genes and pathways for mediating ZnO nanoparticle-induced toxicity and demonstrated the value of assessing nanoparticle responses through combined transcriptomics and bioinformatics approach. Altogether 90 samples were analyzed originating from three biological replicates of HMDM, MDDC or Jurkat cells containg untreated control cells, ZnO or TiO2 treated cells with doses 1M-BM-5g/ml and 10M-BM-5g/ml. The sample timepoints were 6 hours and 24 hours.
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