The physicochemistry of capped nanosilver predicts it biological activity in brain endothelial (RBEC4) cells
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE47543 | GEO | 2013/05/31
SECONDARY ACCESSION(S): PRJNA206022
REPOSITORIES: GEO
Similar Datasets
Project description:This study uses the RBEC4 cell model to examine if nanosilver of different sizes (10nm and 75nm) and cappings (citrate and polyvinylpyrrolidone(PVP)) affect its cellular permeability and genomic response. RBEC4 cells (95% confluent) were screeened for changes in gene expression after 18 hour exposure to 1.0 ppm of PVP or citrate coated nanosilver particles at 10 or 75 nanometer sizes. Analysis indicated that the cellular transcription profile alter by nanosilver 10nm+PVP was distinct from it 75nm counterpart and both sizes of citrate-coated particles.
2013-05-31 | E-GEOD-47543 | biostudies-arrayexpress
Project description:Global gene expression indicated that N27 neurons exposed to each nanoAg material (1.0 ppm, 18 hr) responded primarily to PVP coated nanoAg of both sizes with affected pathways largely associated with mitochondrial dysfunction (PVP 75 nm nanoAg) and Nrf-2 mediated oxidative stress (PVP 10 nm nanoAg) pathways. N27 rat dopaminergic neurons were exposed to non-cytoxic (0.5-5.0 ppm) concentrations of nanoAg of different sizes (10 nm, 75 nm) and “cappings” (PVP, citrate).
2013-06-20 | E-GEOD-48087 | biostudies-arrayexpress
Project description:Global gene expression indicated that N27 neurons exposed to each nanoAg material (1.0 ppm, 18 hr) responded primarily to PVP coated nanoAg of both sizes with affected pathways largely associated with mitochondrial dysfunction (PVP 75 nm nanoAg) and Nrf-2 mediated oxidative stress (PVP 10 nm nanoAg) pathways.
2013-06-20 | GSE48087 | GEO
Project description:Silver exposure is toxic to fish due to disturbances of normal gill function. A proposed toxicity mechanism of silver nanoparticles (AgNP) is derived from the release of silver ions, similar to silver nitrate (AgNO3). However, some datasets support the fact that AgNP can have unique toxic effects that are mediated at the gill. To determine if differences between AgNO3 and AgNP toxicities exist, fathead minnows were exposed to 20 nm PVP- or citrate-coated silver nanoparticles (PVP-AgNP; citrate-AgNP) at the nominal concentration of 200 μg/L or AgNO3 at nominal 6 μg/L for 96 hr. This nominal concentration was applied to approximate the dissolved fraction of Ag in the AgNP suspensions. Mucus production in the water was measured. While mucus production was initially significantly increased in the first 4 h of exposure in all silver treatments compared to control, a decrease in mucus production was observed following 24-96 h of exposure. To determine which genes/pathways are driving this shift in mucus production, gills were dissected and microarray analysis was performed. Hierarchal clustering of differentially expressed genes revealed that all samples distinctly clustered by treatment. There were 109 differentially expressed genes shared among all Ag treatments compared to controls. However, there were 185, 423, and 615 differentially expressed genes unique to AgNO3, PVP-AgNP, and citrate-AgNP, relative to control. While functional analysis indicated several common enriched pathways, such as aryl hydrocarbon receptor signaling, this analysis also indicated some unique pathways between nanosilver and AgNO3. Our results show that AgNO3, PVP-AgNP, and citrate-AgNP exposure affected mucus production in fish gills and also lead to common and unique transcriptional changes.
2015-06-01 | GSE64259 | GEO
Project description:To investigate the differently expressed genes upon the nanosilver particle (nAg) exposure.
2016-01-31 | GSE43331 | GEO
Project description:Metatranscriptome analysis of maize rhizosphere microbiome under nanosilver exposure
| PRJEB22046 | ENA
Project description:Flooding stress has a negative impact on the soybean cultivation in early growth stages. In order to understand the effect of nanosilver on the soybean growth under flooding stress, quantitative proteomics technique was used.
2016-12-14 | PXD001579 | Pride
Project description:We used microarrays to determine transcptional responses to silver nanoparticles (AgNPs) in the mouse liver following oral ingestion. Liver is a major target organ for AgNP accumulation after oral or intravenous exposure. Given that physicochemical properties of AgNPs such as surface coating may influence transcriptional responses to exposure, we evaluated AgNPs with two different surface coatings such as citrate (cit) and polyvinylpirrolidone (PVP). We identified common and unique mRNA and lncRNA expression profiles for cit-AgNPs and PVP-AgNPs. PVP-AgNPs induced a more robust transctiptional response characterized by a 2-fold higher number of differentially expressed mRNAs and lncRNAs.
2020-08-28 | GSE139560 | GEO
Project description:BACKGROUND:Silver nanoparticles (AgNP) have garnered much interest due to their antimicrobial properties, becoming one of the most utilized nano-scale materials. However, any potential evocable cardiovascular injury associated with exposure has not been reported to date. We have previously demonstrated expansion of myocardial infarction after intratracheal (IT) instillation of carbon-based nanomaterials. We hypothesized pulmonary exposure to Ag core AgNP induces a measureable increase in circulating cytokines, expansion of cardiac ischemia-reperfusion (I/R) injury and is associated with depressed coronary constrictor and relaxation responses. Secondarily, we addressed the potential contribution of silver ion release on AgNP toxicity. METHODS:Male Sprague-Dawley rats were exposed to 200 ?l of 1 mg/ml of 20 nm citrate-capped Ag core AgNP, 0.01, 0.1, 1 mg/ml Silver Acetate (AgAc), or a citrate vehicle by intratracheal (IT) instillation. One and 7 days following IT instillation the lungs were evaluated for inflammation and the presence of silver; serum was analyzed for concentrations of selected cytokines; cardiac I/R injury and coronary artery reactivity were assessed. RESULTS:AgNP instillation resulted in modest pulmonary inflammation with detection of silver in lung tissue and alveolar macrophages, elevation of serum cytokines: G-CSF, MIP-1?, IL-1?, IL-2, IL-6, IL-13, IL-10, IL-18, IL-17?, TNF?, and RANTES, expansion of I/R injury and depression of the coronary vessel reactivity at 1 day post IT compared to vehicle treated rats. Silver within lung tissue was persistent at 7 days post IT instillation and was associated with an elevation in cytokines: IL-2, IL-13, and TNF? and expansion of I/R injury. AgAc resulted in a concentration dependent infarct expansion and depressed vascular reactivity without marked pulmonary inflammation or serum cytokine response. CONCLUSIONS:Based on these data, IT instillation of AgNP increases circulating levels of several key cytokines, which may contribute to persistent expansion of I/R injury possibly through an impaired vascular responsiveness.
| S-EPMC4780684 | biostudies-literature
Project description:The widespread use of silver nanoparticles (Ag-NPs) in consumer and medical products provides strong motivation for a careful assessment of their environmental and human health risks. Recent studies have shown that Ag-NPs released to the natural environment undergo profound chemical transformations that can affect silver bioavailability, toxicity, and risk. Less is known about Ag-NP chemical transformations in biological systems, though the medical literature clearly reports that chronic silver ingestion produces argyrial deposits consisting of silver-, sulfur-, and selenium-containing particulate phases. Here we show that Ag-NPs undergo a rich set of biochemical transformations, including accelerated oxidative dissolution in gastric acid, thiol binding and exchange, photoreduction of thiol- or protein-bound silver to secondary zerovalent Ag-NPs, and rapid reactions between silver surfaces and reduced selenium species. Selenide is also observed to rapidly exchange with sulfide in preformed Ag(2)S solid phases. The combined results allow us to propose a conceptual model for Ag-NP transformation pathways in the human body. In this model, argyrial silver deposits are not translocated engineered Ag-NPs, but rather secondary particles formed by partial dissolution in the GI tract followed by ion uptake, systemic circulation as organo-Ag complexes, and immobilization as zerovalent Ag-NPs by photoreduction in light-affected skin regions. The secondary Ag-NPs then undergo detoxifying transformations into sulfides and further into selenides or Se/S mixed phases through exchange reactions. The formation of secondary particles in biological environments implies that Ag-NPs are not only a product of industrial nanotechnology but also have long been present in the human body following exposure to more traditional chemical forms of silver.
| S-EPMC3508364 | biostudies-literature