Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Effects of different types of wastewater on microbial degradation of 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) in anaerobic sediment.

PROVIDER: PRJNA438397 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6848120_1.fastq.gz	Fastqsanger.gz
	SRR6848120_2.fastq.gz	Fastqsanger.gz
	SRR6848121_1.fastq.gz	Fastqsanger.gz
	SRR6848121_2.fastq.gz	Fastqsanger.gz
	SRR6848122_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Whole brains and frontal lobes of rat offsprings exposed perinatally to low doses of 2,2',4,4'-tetrabromodiphenyl ether

Project description:Analysis of developmental toxicity of environmental toxin 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) at the level of gene expression. Dams of Wistar rats were exposed to environmentaly relevant doses of BDE-47 at gestation and lactation. Gene expression in total brains and frontal lobes was analysed in offspring on postnatal day 10.

2010-01-13 | GSE19867 | GEO

Comparative analysis between effects of thalidomide and environmental chemicals on neuronal differentiations in human sphere

Project description:To develop molecular indicators of neurodevelopmental disorders related to the exposure to external chemicals, we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to influence neuronal differentiation from embryonic stem cells. Thalidomide (TMD), bisphenol A (BPA), 4-hydroxy-2,2',3,4',5,5',6-heptachlorobiphenyl (4OH-PCB187) and 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) were exposed to human embryonic stem (ES) cell-derived sphere on day 3 after starting sphere formation for 72 hours. Gene expression analysis on the stage of sphere development showed chemical specific characteristics.

2020-05-28 | GSE151239 | GEO

Transcriptome profiling analysis of Mactra veneriformis exposed to BDE-47 by deep sequencing

Project description:RNA-seq provided a general overview of the gene expression profiles of the digestive glands of Mactra veneriformis exposed to 2, 2′,4,4′-tetrabromodiphenyl ether (BDE-47, a type of widely used brominated flame retardants).

2019-10-19 | GSE88918 | GEO

Perinatal Exposure to 2,2’,4’4’ –Tetrabromodiphenyl Ether Impairs Male Reproductive Health in Adult Rats

Project description:Toxicity of PBDE for male reproductive system was shown in several human and animal studies, however long lasting effects of perinatal exposures on male reproduction are yet poorly understood. In this study pregnant Wistar rats were exposed to 0.2 mg/kg 2,2’,4,4’-tetrabromodiphenyl ether (BDE-47) from gestation day 8 till postnatal day 21 and testis transcriptome was analyzed on postnatal day 120 in offspring. Exposed animals had significant change in testes transcriptome including suppression of genes essential for spermatogenesis and activation of immune response genes. In particular exposed animals had on average 4 fold decreased expression of protamine and transition protein genes in testes suggesting that histone-protamine exchange may be dysregulated in the course of spermatogenesis resulting in exposure legacy transfer to the next generation via aberrant sperm epigenome.

2019-08-10 | GSE85420 | GEO

Transcriptomic Analysis of Gonadal Adipose Tissue in Male Mice Exposed Perinatally to 2,2',4,4'- Tetrabromodiphenyl Ether (BDE-47)

Project description:Transcriptomic Analysis of Gonadal Adipose Tissue in Male Mice Exposed Perinatally to 2,2',4,4'- Tetrabromodiphenyl Ether (BDE-47)

| PRJNA445270 | ENA

Developmental Exposure to 2,2’,4, 4’ –Tetrabromodiphenyl Ether Induces Long-Lasting Changes in Liver Metabolism in Male Mice

Project description:Polybrominated diphenyl ethers (PBDEs) were used as flame-retardant additives in a wide range of polymers starting in 1965 and were recently withdrawn from commerce in North America and Europe. Generations that were exposed perinatally to the highest environmental doses of PBDE have now reached 5-20 years of age and in the U.S. account for 1/5 of the total population. Emerging data indicates long-term impairment of metabolic health by PBDE exposure in humans and laboratory animals. We hypothesize that exposure to PBDE during sensitive developmental windows may result in long-lasting changes in liver metabolism. In this study pregnant CD-1 mice were exposed to 0.2 mg/kg 2,2’,4,4’-tetrabromodiphenyl ether (BDE-47) from gestation day 8 till postnatal day 21 and liver RNA-seq was performed on the last day of dam exposure and on postnatal week 20 in male offspring. Several groups of metabolic genes, including ribosomal and mitochondrial genes were significantly upregulated at both time-points. Genes regulated via mechanistic target of rapamycin (mTOR pathway), the gatekeeper of metabolic homeostasis, were whether up- or down- regulated at both time-points. Thus, perinatal exposure to environmentally relevant doses of BDE-47 in laboratory mice results in long-lasting changes in liver metabolism. Our evidence suggests involvement of the mTOR pathway in the observed metabolic programming of liver.

2018-02-22 | GSE85221 | GEO

Liver of rat offsprings exposed perinatally to low doses of 2,2',4,4'-tetrabromodiphenyl ether

Project description:Background: Polybrominated diphenyl ethers are a group of flame-retardant chemicals appearing increasingly in the environment. Their health effects and mechanisms of toxicity are poorly understood.Objectives: We screened for the sensitive effects and mechanisms of toxicity of 2,2 ,4,4 -tetra-bromodiphenyl ether (BDE-47) by analyzing the gene expression profile in rats exposed to doses comparable to human exposure.Methods: Wistar dams were exposed to vehicle or BDE-47 (0.002 and 0.2 mg/kg body weight) every fifth day from gestation day 15 to postnatal day 20 by injections to caudal vein. Total RNA was extracted from the livers of pups and hybridized to the whole-genome RNA expression micro-arrays. The list of genes 2-fold differentially expressed was exported to PANTHER and Ingenuity Systems for analysis of enriched ontology groups and molecular pathways.Results: Oxidoreductase and transferase protein families were enriched in exposed rats as were these biological process categories: carbohydrate metabolism; electron transport; and lipid, fatty acid, and steroid metabolism. Four signaling pathways (cascades of activation of drug-metabolizing enzymes) and 10 metabolic pathways were significantly enriched. Drug-metabolizing enzymes appear to be regulated by BDE-47 through an aryl hydrocarbon receptorindependent mechanism. Direct interaction with retinoid X receptor or its upstream cascade may be involved. The main metabolic effects consisted of activation of metabolic pathways: alpha- and omega-oxidation of fatty acids, glycolysis, and starch hydrolysis.Conclusions: Altered expression of genes involved in metabolic and signaling pathways and functions of the organism occurs after perinatal exposure of rat offspring to BDE-47 at doses relevant for the general population.

2010-01-13 | GSE19868 | GEO

Insights into Brominated Flame Retardant Neurotoxicity: Mechanisms of Hippocampal Neural Cell Death and Brain Region-Specific Transcriptomic Shifts in Mice

Project description:Brominated Flame Retardants (BFRs) reduce flammability in a wide range of products including electronics, carpets, and paint, but leach into the environment to result in continuous, population-level exposure. Epidemiology studies have correlated BFR exposure with neurological problems, including alterations in learning and memory. This study investigated the molecular mechanisms mediating BFR-induced cell death in hippocampal cells and clarified the impact of HBCD exposure on gene transcription in the hippocampus, dorsal striatum, and frontal cortex of male mice. Hippocampal derived HT-22 cell exposure to tetrabromobisphenol-A (TBBPA), hexabromocyclododecane (HBCD), or 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) (current, phasing out, and phased out BFRs, respectively) induced time, concentration, and chemical-dependent cellular and nuclear morphological alterations indicative of apoptosis, which aligned with alterations in cell cycle and increases in annexin V staining. All three BFRs increased p53 and p21 expression; however, inhibition of p53 nuclear translocation using pifthrin-a did not decrease cell death. Transcriptomic analysis upon low (10 nM) and cytotoxic (10 μM) BFR exposure indicated that HBCD and BDE-47 altered genes mediating autophagy-related pathways. Further evaluation showed BFR exposure increased LC3-II conversion and autophagosome formation, and co-exposure with the autophagy inhibitor 3-methyladenine (3-MA) attenuated cytotoxicity. Transcriptomic assessment of select brain regions from subchronically HBCD-exposed male mice demonstrated alteration of genes mediating vesicular transport, with greater impact on the frontal cortex and dorsal striatum compared to the dorsal and ventral hippocampus. These data demonstrate that BFRs can induce chemical-dependent autophagy in neural cells in vitro and provide evidence that BFRs induce region-specific transcriptomic effects in the brain.

2024-07-28 | GSE242684 | GEO

Changes in rat sperm DNA methylation induced by age and by perinatal exposure to brominated flame retardant flame retardants 2,2’,4,4’-tetrabromodiphenyl ether (BDE-47)

Project description:Changes in rat sperm DNA methylation induced by age and by perinatal exposure to brominated flame retardant flame retardants 2,2’,4,4’-tetrabromodiphenyl ether (BDE-47)

| PRJNA554854 | ENA

Rattus norvegicus

Project description:Liver of rat offsprings exposed perinatally to low doses of 2,2',4,4'-tetrabromodiphenyl ether

| PRJNA121957 | ENA