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Differential Gene Expression in Daphnia magna Suggests Distinct Modes of Action and Bioavailability for ZnO nanoparticles and Zn ions

ABSTRACT: Zinc Oxide nanoparticles (ZnO NPs) are being rapidly developed for use in consumer products, wastewater treatment and chemotherapy providing several possible routes for ZnO NP exposure to humans and aquatic organisms. Recent studies have shown that ZnO NPs undergo rapid dissolution to Zn+2, but the relative contribution of Zn+2 to ZnO NP bioavailability and toxicity is not clear. Gene expression profiling of D. magna exposed to ZnO NPs or ZnSO4 at equitoxic concentrations demonstrated that the particles cause toxicity through a distinct mechanism compared with Zn+2. D. magna were also exposed to a SiO NPs as a particle control at equimolar concentrations. The SiO NPs resulted in few differentially expressed genes and there was very little overlap between the genes affected by the ZnO NPs and the SiO NPs, suggesting that ZnO NPs cause a distinct pattern of differentially expressed genes. In the ZnO NP exposures, effects were observed to genes involved in cytoskeletal transport, cellular respiration and reproduction. Three biomarker genes including a multi-cystatin, ferritin and a C1q containing gene were confirmed as differentially expressed in a specific pattern by ZnO NP and provide a suite of biomarkers for identifying environmental exposure to ZnO NP and differentiating between NP and ionic exposure.

ORGANISM(S): Daphnia magna

PROVIDER: GSE22051 | GEO | 2010/12/31

SECONDARY ACCESSION(S): PRJNA128983

REPOSITORIES: GEO

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Differential Gene Expression in Daphnia magna Suggests Distinct Modes of Action and Bioavailability for ZnO nanoparticles and Zn ions

Project description:Zinc Oxide nanoparticles (ZnO NPs) are being rapidly developed for use in consumer products, wastewater treatment and chemotherapy providing several possible routes for ZnO NP exposure to humans and aquatic organisms. Recent studies have shown that ZnO NPs undergo rapid dissolution to Zn+2, but the relative contribution of Zn+2 to ZnO NP bioavailability and toxicity is not clear. Gene expression profiling of D. magna exposed to ZnO NPs or ZnSO4 at equitoxic concentrations demonstrated that the particles cause toxicity through a distinct mechanism compared with Zn+2. D. magna were also exposed to a SiO NPs as a particle control at equimolar concentrations. The SiO NPs resulted in few differentially expressed genes and there was very little overlap between the genes affected by the ZnO NPs and the SiO NPs, suggesting that ZnO NPs cause a distinct pattern of differentially expressed genes. In the ZnO NP exposures, effects were observed to genes involved in cytoskeletal transport, cellular respiration and reproduction. Three biomarker genes including a multi-cystatin, ferritin and a C1q containing gene were confirmed as differentially expressed in a specific pattern by ZnO NP and provide a suite of biomarkers for identifying environmental exposure to ZnO NP and differentiating between NP and ionic exposure. We exposed Daphnia magna to the 1/10 LC50 and LC25 of ZnO nanoparticles and Zn++ as ZnSO4 for 24-h. For each exposure condition, we performed 3 exposures and 2 technical replicates (as dye swap) for each exposure (6 microarrays total). All exposures were compared to a unexposed laboratory control

2010-12-31 | E-GEOD-22051 | biostudies-arrayexpress

Toxicity and transcriptomic analysis in Hyalella azteca suggests increased exposure and susceptibility of epibenthic organisms to Zinc Oxide Nanoparticles

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

Toxicity and transcriptomic analysis in Hyalella azteca suggests increased exposure and susceptibility of epibenthic organisms to Zinc Oxide Nanoparticles

2013-07-24 | E-GEOD-49136 | biostudies-arrayexpress

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

Project description: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

2014-03-01 | E-GEOD-54738 | biostudies-arrayexpress

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

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

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

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Transcriptomic study of PMA-differentiated THP-1 cells following exposure to zinc oxide nanoparticles NM110

Project description:To identify differentially expressed genes and key biological pathways that define toxicity following nanoparticles exposure, we performed microarray analyses on PMA-differentiated THP-1 macrophages exposed for 4 h to 8 µg/mL of NP ZnO (50 % cell viability) and to 2 µg/mL of NP ZnO (50 % cell viability divided by 4 ). This project has received funding from the European Union’s Horizon 2020 research and innovation programme under grant agreement No. 686098

2020-05-30 | GSE99435 | GEO

Continuous ZnO nanoparticle exposure induces melanoma-like skin lesions in epidermal barrier dysfunction model mice through anti-apoptotic effects mediated by the oxidative stress–activated NF-κB pathway

Project description:Increasing interest in the hazardous properties of zinc oxide nanoparticles (ZnO NPs), commonly used as ultraviolet filters in sunscreen, has driven efforts to study the percutaneous application of ZnO NPs to diseased skin; however, in-depth studies for epidermal barrier dysfunction remain lacking. Our epidermal barrier dysfunction model develops large gaps between keratinocytes due to keratinocyte-specific Cdc42 knockout, allowing ZnO NPs entry to the stratum basale of the epidermis, impacting melanocytes. ZnO NP application for 14 and 49 consecutive days induced melanoma-like skin lesions, dysregulated melanoma-associated gene expression, increased oxidative injury, inhibited apoptosis, and increased nuclear factor kappa B (NF-κB) p65 and Bcl-2 expression in melanocytes. Exposure to 5.0 µg·mL−1 ZnO NPs for 72 h increased cell viability, decreased apoptosis, and increased Fkbp51 expression in melanocytes, consistent with histological observations. The oxidative stress–mediated mechanism underlying the induction of anti-apoptotic effects was verified using the reactive oxygen species scavenger N-acetylcysteine. The entry of ZnO NPs into the stratum basale of skin with epidermal barrier dysfunction resulted in melanoma-like skin lesions and an anti-apoptotic effect induced by oxidative stress, activating the NF-κB pathway in melanocytes. These findings suggest that ZnO NPs are potentially carcinogenic for skin with a damaged barrier function.

2022-03-09 | GSE183662 | GEO

Modulation of intestinal proteome of juvenile common carp (Cyprinus carpio L.) after dietary exposure to ZnO nanoparticles

Project description:ZnO nanoparticles (NPs) are widely used in industrial and consumer products. Thus, understanding their interaction with biological systems is the key for their safe application. The aim of present study was to evaluate the toxicological effects on the intestine of common carp, Cyprinus carpio, after dietary exposure to ZnO NPs. To assess the toxicity of ZnO NPs and of their toxic mechanism to gastrointestinal tract, we applied label free protein quantification on carp intestine considering the fact that fish are on the top of food chain in aquatic ecosystems. Even though carp and zebrafish do not have five intestinal segments like mammals (Brugman, 2016), previous studies have revealed that intestinal anatomy and architecture in cyprinid teleost fish is closely related to mammals with functional homology (Curry, 1939). Therefore, the findings can also provide beneficial information to understand the mechanisms underlying NPs toxicity in mammals.

2017-09-25 | PXD006867 | Pride

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