Ontology highlight
ABSTRACT:
PROVIDER: PRJNA603874 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10995500.fastq.gz | Fastqsanger.gz | |||
| SRR10995501.fastq.gz | Fastqsanger.gz | |||
| SRR10995502.fastq.gz | Fastqsanger.gz | |||
| SRR10995503.fastq.gz | Fastqsanger.gz | |||
| SRR10995504.fastq.gz | Fastqsanger.gz |
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Project description:Nanoparticles are compounds of emerging concern with largely unknown risks for human and ecological health. It is crucial to evaluate their potential biological impact to prevent unintended adverse effects on human health and the environment. We analyzed the transcriptional effects of polyvinylpyrrolidone-coated silver nanoparticles (PVP-AgNPs) and silver nitrate (AgNO3) on the fathead minnow (Pimephales promelas) to understand their potential toxicity and adverse outcomes. We also tested the feasibility of the fathead minnow as an alternative species to elucidate potential adverse effects on humans. Fathead minnow females were exposed to either 4 µg/L of AgNO3 or 70 µg/L of PVP-AgNPs for 96h. Microarray analyses were performed on liver and brain. Functional analysis identified potential toxicity pathways and molecular initiating events (MIEs) that were confirmed with functional assays. Data suggested that AgNO3 and PVP-AgNPs had both common and distinct transcriptional effects. The nanoparticles were linked to neurotoxicity and oxidative stress, and identified as a dopamine receptor antagonist. Silver nitrate was also identified as a potential neurotoxicant and was confirmed as adrenergic and cannabinoid receptors antagonist. While silver nitrate and PVP-AgNPs were both potential neurotoxicants, they appeared to act through different MIEs. Fathead minnow is a promising alternative species to elucidate potential adverse effects of relevance to human health. We analyzed the transcriptional effects of polyvinylpyrrolidone-coated silver nanoparticles (PVP-AgNPs) and silver nitrate (AgNO3) on the fathead minnow (Pimephales promelas) to understand their potential toxicity and adverse outcomes. FHM were obtained from Aquatic Biosystems (Fort Collins, CO), held in aerated dechlorinated tap water and fed three times daily with Zeigler® AquaTox Feed Gardners, PA, USA). Fathead minnow females were exposed to either 4 µg/L of AgNO3 or 70 µg/L of PVP-AgNPs (Luna Innovations, Blackburn, VA) for 96h at 24°C ± 1 with a 90% water change at 48 hours. Microarray analyses were performed on liver and brain.
2013-11-01 | E-GEOD-46520 | biostudies-arrayexpress
Project description:Despite considerable research effort devoted to the study of the effects of silver nanoparticles on mammalian cells in recent years, data on the potential long terms effects of this nanomaterial remain scarce, and centered on epithelial cells. The aim of this study was to explore the effects of silver nanoparticles on macrophages. To this end, RAW 264.7 murine macrophages were exposed to either 1 µg/ml silver nanoparticles for 20 days, i.e. a chronic exposure scheme, or to 20 µg/ml silver nanoparticles for 24 hours, i.e. an acute exposure scheme. A proteomic study was then conducted to study and compare the cellular responses to both exposure schemes. They proved to be essentially different, and stronger for the chronic exposure scheme. Targeted validation studies showed effects of chronic exposure to silver nanoparticles on detoxifying enzymes such as biliverdin reductase B, which was increased, and on central metabolism enzymes such as triose phosphate isomerase, which activity decreased under chronic exposure to silver nanoparticles. Chronic exposure to silver nanoparticles also induced a decrease of reduced glutathione content, a decreased phagocytic activity and reduced macrophages responses to lipopolysaccharide, as exemplified by nitric oxide and interleukin 6 production. Overall, chronic exposure to silver nanoparticles induced stronger effects than acute exposure on macrophages in the metabolic (glutathione level, mitochondrial potential) and functional (phagocytosis, cytokine production) parameters tested.
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Project description:Despite considerable research effort devoted to the study of the effects of silver nanoparticles on mammalian cells in recent years, data on the potential long terms effects of this nanomaterial remain scarce, and centered on epithelial cells. The aim of this study was to explore the effects of silver nanoparticles on macrophages. To this end, RAW 264.7 murine macrophages were exposed to either 1 µg/ml silver nanoparticles for 20 days, i.e. a chronic exposure scheme, or to 20 µg/ml silver nanoparticles for 24 hours, i.e. an acute exposure scheme. A proteomic study was then conducted to study and compare the cellular responses to both exposure schemes. They proved to be essentially different, and stronger for the chronic exposure scheme. Targeted validation studies showed effects of chronic exposure to silver nanoparticles on detoxifying enzymes such as biliverdin reductase B, which was increased, and on central metabolism enzymes such as triose phosphate isomerase, which activity decreased under chronic exposure to silver nanoparticles. Chronic exposure to silver nanoparticles also induced a decrease of reduced glutathione content, a decreased phagocytic activity and reduced macrophages responses to lipopolysaccharide, as exemplified by nitric oxide and interleukin 6 production. Overall, chronic exposure to silver nanoparticles induced stronger effects than acute exposure on macrophages in the metabolic (glutathione level, mitochondrial potential) and functional (phagocytosis, cytokine production) parameters tested.
2024-09-09 | PXD016051 | Pride
Project description:We examined effects of surface-coating (BPEI, CIT, PEG) of silver nanoparticles and time (6h, 12h, 24h) on gene expression in human liver cancer cells (HepG2)
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Project description:Nanoparticles are compounds of emerging concern with largely unknown risks for human and ecological health. It is crucial to evaluate their potential biological impact to prevent unintended adverse effects on human health and the environment. We analyzed the transcriptional effects of polyvinylpyrrolidone-coated silver nanoparticles (PVP-AgNPs) and silver nitrate (AgNO3) on the fathead minnow (Pimephales promelas) to understand their potential toxicity and adverse outcomes. We also tested the feasibility of the fathead minnow as an alternative species to elucidate potential adverse effects on humans. Fathead minnow females were exposed to either 4 µg/L of AgNO3 or 70 µg/L of PVP-AgNPs for 96h. Microarray analyses were performed on liver and brain. Functional analysis identified potential toxicity pathways and molecular initiating events (MIEs) that were confirmed with functional assays. Data suggested that AgNO3 and PVP-AgNPs had both common and distinct transcriptional effects. The nanoparticles were linked to neurotoxicity and oxidative stress, and identified as a dopamine receptor antagonist. Silver nitrate was also identified as a potential neurotoxicant and was confirmed as adrenergic and cannabinoid receptors antagonist. While silver nitrate and PVP-AgNPs were both potential neurotoxicants, they appeared to act through different MIEs. Fathead minnow is a promising alternative species to elucidate potential adverse effects of relevance to human health.
2013-11-01 | GSE46520 | GEO
Project description:Silver nanoparticles cause toxicity in exposed organisms and are an environmental health concern. The mechanisms of silver nanoparticle toxicity, however, remain unclear. We examined the effects of exposure to silver in nano-, bulk- and ionic forms on zebrafish embryos (Danio rerio) using a Next Generation Sequencing approach in an Illumina platform (High-Throughput SuperSAGE). Significant alterations in gene expression were found for all treatments and many of the gene pathways affected, most notably those associated with oxidative phosphorylation and protein synthesis, overlapped strongly between the three treatments indicating similar mechanisms of toxicity for the three forms of silver studied. Changes in oxidative phosphorylation indicated a down-regulation of this pathway at 24h of exposure, but with a recovery at 48h. This finding was consistent with a dose-dependent decrease in oxygen consumption at 24h, but not at 48h, following exposure to silver ions. Overall, our data provide support for the hypothesis that the toxicity caused by silver nanoparticles is principally associated with bioavailable silver ions in exposed zebrafish embryos. These findings are important in the evaluation of the risk that silver particles may pose to exposed vertebrate organisms. mRNA profiles of whole zebrafish embryos at 24 and 48 hours post-fertilisation (hpf) exposed to silver in nano, bulk and ionic forms were generated by deep sequencing using HT-SuperSAGE (Illumina GA2).
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Project description:Human diet emerges as a pivotal determinant of gut microbiota composition and function. Identification of the bacterial taxa targeted by diet derived factors with causal beneficial rather than detrimental effects on therapy and their mechanism of action is challenging but necessary for future clinical progress. The germ free mice colonized with human gut bacteria and four-plants derived nanoparticles uptaking bacteria were sorted with flow cytometry and identified with 16s rRNA next-generation sequencing.
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Project description:Colorectal cancer risk is associated with diets high in red meat. Heme, the pigment of red meat, induces cytotoxicity of colonic contents and elicits epithelial damage and compensatory hyperproliferation, leading to hyperplasia. Here we explore the possible causal role of the gut microbiota in heme-induced hyperproliferation. To this end, mice were fed a purified control or heme diet (0.5 μmol/g heme) with or without broad-spectrum antibiotics for 14 d. Heme-induced hyperproliferation was shown to depend on the presence of the gut microbiota, because hyperproliferation was completely eliminated by antibiotics, although heme-induced luminal cytotoxicity was sustained in these mice. Colon mucosa transcriptomics revealed that antibiotics block heme-induced differential expression of oncogenes, tumor suppressors, and cell turnover genes, implying that antibiotic treatment prevented the heme-dependent cytotoxic micelles to reach the epithelium. Our results indicate that this occurs because antibiotics reinforce the mucus barrier by eliminating sulfide-producing bacteria and mucin-degrading bacteria (e.g., Akkermansia). Sulfide potently reduces disulfide bonds and can drive mucin denaturation and microbial access to the mucus layer. This reduction results in formation of trisulfides that can be detected in vitro and in vivo. Therefore, trisulfides can serve as a novel marker of colonic mucolysis and thus as a proxy for mucus barrier reduction. In feces, antibiotics drastically decreased trisulfides but increased mucin polymers that can be lysed by sulfide. We conclude that the gut microbiota is required for heme-induced epithelial hyperproliferation and hyperplasia because of the capacity to reduce mucus barrier function. Mice were fed a Westernized high fat control diet, or the same diet supplemented with 0.5 µmol heme/g diet. One group of control and one group of heme mice received a mixture of broad spectrum Antibiotics (Abx) (ampicilin, neomycin and metronidazole) in their drinking water. After 14 days of intervention, mice were killed and gene expression was profiled in colon.
2015-08-03 | E-GEOD-40670 | biostudies-arrayexpress
Project description:Silver nanoparticles cause toxicity in exposed organisms and are an environmental health concern. The mechanisms of silver nanoparticle toxicity, however, remain unclear. We examined the effects of exposure to silver in nano-, bulk- and ionic forms on zebrafish embryos (Danio rerio) using a Next Generation Sequencing approach in an Illumina platform (High-Throughput SuperSAGE). Significant alterations in gene expression were found for all treatments and many of the gene pathways affected, most notably those associated with oxidative phosphorylation and protein synthesis, overlapped strongly between the three treatments indicating similar mechanisms of toxicity for the three forms of silver studied. Changes in oxidative phosphorylation indicated a down-regulation of this pathway at 24h of exposure, but with a recovery at 48h. This finding was consistent with a dose-dependent decrease in oxygen consumption at 24h, but not at 48h, following exposure to silver ions. Overall, our data provide support for the hypothesis that the toxicity caused by silver nanoparticles is principally associated with bioavailable silver ions in exposed zebrafish embryos. These findings are important in the evaluation of the risk that silver particles may pose to exposed vertebrate organisms.
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Project description:From the result of the gene expression analyses of human hepatoma cell line, HepG2, a number of genes associated with cell proliferation and DNA repair were distinctively up-regulated by Ag-nanoparticle exposure, suggesting that Ag-nanoparticles might stimulate cell proliferation and DNA damage, which are considered to be mechanisms playing an important role for carcinogenesis and tumor progression. The inductions of these genes involved in cell proliferation were also observed in PS-nanoparticles and Ag2CO3-exposed cells. In addition, the inductions of DNA repair-associated genes were also observed in Ag2CO3-exposure. These results suggest that both “nanoshape” and “silver” can cause the inductions of these gene expression patterns. Furthermore, cysteine, a strong ionic silver ligand partially abolished these gene expressions induced by silver nanoparticles. Ionic silver sourced from Ag-nanoparticles could not fully explain these gene expressions.
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