Expression data from human olfactory neurosphere derived cells (hONS) established from adult donors treated with coated and uncoated ZnO nanoparticles
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE45322 | GEO | 2013/09/11
SECONDARY ACCESSION(S): PRJNA193532
REPOSITORIES: GEO
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Project description:ZnO nanoparticles can elicit a range of cytotoxic responses in different cells in vitro that may reflect either Zn2+ dissolution or nanoparticle-specific effects. Coating the ZnO nanoparticles may mitigate their cytotoxicity. We aimed to capture whole genome transcriptional profiles (up and down regulated) at time-points associated with distinct cytotoxic responses in cells treated with two types of uncoated (Nanosun, Z-COTE) or two types of coated (HP1, MAX) ZnO nanoparticles, compared to untreated cells. hONS cells were incubated with 25ug/ml ZnO nanoparticles (uncoated: Nanosun and Z-COTE; coated: MAX, HP1) for 2h and 6h and their expression profiles were compared to time-matched untreated cells.
2013-09-11 | E-GEOD-45322 | biostudies-arrayexpress
Project description:ZnO nanoparticles can elicit a range of perturbed cell responses in vitro. The liver is a target for ZnO nanoparticle-, or Zn2+ released from ZnO nanoparticles-induced accumulation and/or impact in vitro and in vivo. The response of human hepatic stellate cells to ZnO nanoparticles has not yet been assessed. We aimed to determine whether the presence of surface coatings could protect human hepatic stellate cells from ZnO nanoparticle-induced cytotoxicity. Primary human hepatic stellate cells were treated with one of two types of uncoated ZnO nanoparticles (Z-COTE or Nanosun), two types of coated ZnO nanoparticles (HP1, MAX), a mass equivalent of ZnSO4, or were left untreated. After 24 h, RNA was isolated and processed for whole genome transcriptional profiling, comparing the expresson profiles of treated cells to the untreated controls. Each treatment was prepared in duplicate.
2014-08-07 | E-GEOD-60159 | biostudies-arrayexpress
Project description:ZnO nanoparticles can elicit a range of perturbed cell responses in vitro. The liver is a target for ZnO nanoparticle-, or Zn2+ released from ZnO nanoparticles-induced accumulation and/or impact in vitro and in vivo. The response of human hepatic stellate cells to ZnO nanoparticles has not yet been assessed. We aimed to determine whether the presence of surface coatings could protect human hepatic stellate cells from ZnO nanoparticle-induced cytotoxicity.
2014-08-07 | GSE60159 | GEO
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.
2013-07-25 | GSE39330 | GEO
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.
2013-07-25 | E-GEOD-39316 | biostudies-arrayexpress
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).
2013-07-25 | E-GEOD-39330 | biostudies-arrayexpress
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, 1µg/ml and 10µg/ml after 6 and 24 hours of exposure. Interestingly, 2703 genes were significantly differentially expressed in HMDM upon exposure to 10µg/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.
2013-07-25 | GSE39316 | GEO
Project description:Zinc oxide (ZnO) nanoparticles are commonly used in sunscreens for their UV-filtering properties. Their growing use can lead to their release into ecosystems, raising question about their toxicity. Effects of these engineered nanomaterials (ENMs) on cyanobacteria, which are important primary producers involved in many biogeochemical cycles, are unknown. In this study, we investigated by several complementary approaches the toxicological effects of two marketed ZnO-ENMs (coated and uncoated) on the model cyanobacteria Synechococcus elongatus PCC 7942. It was shown that despite the rapid adsorption of ENMs on cell surface, toxicity is mainly due to labile Zn released by ENMs. Zn dissipates cell membrane potential necessary for both photosynthesis and respiration, and induces oxidative stress leading to lipid peroxidation and DNA damages. It leads to global downregulation of photosystems, oxidative phosphorylation, and transcription/translation machineries. This also translates into significant decrease of intracellular ATP content and cell growth inhibition. However, there is no major loss of pigments and even rather an increase in exposed cells compared to controls. A proposed way to reduce the environmental impact of Zn would be the improvement of the coating stability to prevent solubility of ZnO-ENMs.
2019-06-05 | GSE102914 | GEO
Project description:Abstract: Nanoparticles (NPs) are expected to make their way into the aquatic environment where sedimentation of particles will likely occur, putting benthic organisms at particular risk. Therefore, organisms such as Hyalella azteca, an epibenthic crustacean which forages at the sediment surface, is likely to have a high potential exposure. Here we show that Zinc Oxide (ZnO) NPs are more toxic to H. azteca compared with the corresponding metal ion, Zn2+. Dissolution of ZnO NPs contributes about 50% of the Zn measured in the ZnO NP suspensions, and cannot account for the toxicity of these particles to H. azteca. However, gene expression analysis is unable to distinguish between the ZnO NP exposures and Zinc Sulfate (ZnSO4) exposures at equitoxic concentrations. These results lead us to hypothesize that ZnO NPs provide and an enhanced exposure route for Zn2+ uptake into H. azteca, and possibly other sediment dwelling organisms. Our study supports the prediction that sediment dwelling organisms are highly susceptible to the effects of ZnO NPs and should be considered in the risk assessment of these nanomaterials. This experiment included four different treatments and an untreated control. Each treatment or control, consisted of ten independent replicates of twenty Hyalella azteca. Of these, six were randomly chosen to be used for the microarray analysis.
2013-07-24 | E-GEOD-49136 | biostudies-arrayexpress
Project description:Abstract: Nanoparticles (NPs) are expected to make their way into the aquatic environment where sedimentation of particles will likely occur, putting benthic organisms at particular risk. Therefore, organisms such as Hyalella azteca, an epibenthic crustacean which forages at the sediment surface, is likely to have a high potential exposure. Here we show that Zinc Oxide (ZnO) NPs are more toxic to H. azteca compared with the corresponding metal ion, Zn2+. Dissolution of ZnO NPs contributes about 50% of the Zn measured in the ZnO NP suspensions, and cannot account for the toxicity of these particles to H. azteca. However, gene expression analysis is unable to distinguish between the ZnO NP exposures and Zinc Sulfate (ZnSO4) exposures at equitoxic concentrations. These results lead us to hypothesize that ZnO NPs provide and an enhanced exposure route for Zn2+ uptake into H. azteca, and possibly other sediment dwelling organisms. Our study supports the prediction that sediment dwelling organisms are highly susceptible to the effects of ZnO NPs and should be considered in the risk assessment of these nanomaterials.
2013-07-24 | GSE49136 | GEO