Unknown,Transcriptomics,Genomics,Proteomics

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The effect of ZnO nanoparticles on gene expression patterns in Daphnia magna

ABSTRACT: There is still a lot of contradiction on whether metal ions are solely responsible for the observed the toxicity of ZnO and CuO nanoparticles to aquatic species. While most tests have studied nanoparticle effects at organismal levels (e.g. mortality, reproduction), effects at suborganismal levels may clarify the role of metal ions, nanoparticles and nanoparticle aggregates. In this study, the effect of ZnO, CuO nanoparticles and zinc, copper salts was tested on the gene expression levels in Daphnia magna. D. magna was exposed during 96 hours to 10% immobilization concentrations of all chemicals, after which daphnids were sampled for a differential gene expression analysis using microarray. When comparing the nanoparticle exposed daphnids (ZnO or CuO) to the metal salt exposed daphnids (zinc or copper salt), the microarray results showed no significantly differentially expressed genes. These results indicate that the toxicity of the tested ZnO and CuO nanoparticles to D. magna caused is solely caused by toxic metal ions. 4 replicate exposures of ZnO nanoparticles, ZnCl2, Blank (for Zn); 4 replicate exposures of CuO nanoparticles, CuCl2.2H2O, Blank (for Cu); Individual reference design with swapped dyes for zinc (e.g. ZnO-REFZn; REFZn-bl) and copper exposure (e.g. CuO-REFCu; REFCu-bl); Zinc reference sample is a mixture of equal aliquots of ZnO nanoparticle, ZnCl2 and blank; Copper reference sample is a mixture of equal aliquots of CuO nanoparticle, CuCl2.2H2O and blank

ORGANISM(S): Daphnia magna

SUBMITTER: Nathalie Adam

PROVIDER: E-GEOD-54736 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

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, 1ug/ml and 10ug/ml after 6 and 24 hours of exposure. Interestingly, 2703 genes were significantly differentially expressed in HMDM upon exposure to 10ug/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. Nanoparticles used in the study: ZnO-1 commercial (IBU-tec advanced materials AG), ZnO-2 (mandelic acid coated ZnO-1), ZnO-3 (mercaptopropyl-trimethoxysilane coated ZnO-1), ZnO-4 (methoxyl coated ZnO), ZnO-5 (diethylene glycol modified ZnO) and ZnO-9 (folic acid modified ZnO). Detailed particle production and characterization data can be found from the articles: Buerki-Thurnherr et al. 2012 Nanotoxicology and Tuomela et al. Altogether 71 samples were analyzed: 3 biological replicates of HMDM samples (untreated control, 10ug/ml of ZnO-1, 6 and 24 hours), 3 biological replicates of MDDC samples (untreated control, 6 and 24 hours), 7 biological replicates of MDDC samples (10ug/ml of ZnO-1, 24 hours), 3 replicates of Jurkat cells (untreated control, 10ug/ml of ZnO-1, 6 and 24 hours), 3 replicates of Jurkat cells (untreated control, 10ug/ml of ZnO-2, ZnO-3, ZnO-5 or ZnO-9, or 10, 25, 50 or 100ug/ml of ZnO-4, 24 hours).

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, 1ug/ml and 10ug/ml after 6 and 24 hours of exposure. Interestingly, 2703 genes were significantly differentially expressed in HMDM upon exposure to 10ug/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. Nanoparticles used in the study: ZnO-1 commercial (IBU-tec advanced materials AG), ZnO-2 (mandelic acid coated ZnO-1), ZnO-3 (mercaptopropyl-trimethoxysilane coated ZnO-1), ZnO-4 (methoxyl coated ZnO), ZnO-5 (diethylene glycol modified ZnO) and ZnO-9 (folic acid modified ZnO). Detailed particle production and characterization data can be found from the articles: Buerki-Thurnherr et al. 2012 Nanotoxicology and Tuomela et al.

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The effect of ZnO nanoparticles on gene expression patterns in Daphnia magna

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