Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Embryo/ larval toxicity and key gene expression signatures of maternally transferred hexabromocyclododecane (HBCD) in Pimephales promelas

ABSTRACT: Hexabromocyclododecane (HBCD) is a brominated flame retardant that presents a threat to aquatic organisms as it can be maternally transferred and has been reported to hinder development and survival in early-life stage (ELS) fish. However, little is known to date regarding the molecular mechanisms that drive the toxicity of HBCD. This study examined the apical and molecular response patterns of maternally transferred HBCD in fathead minnow (Pimephales promelas) larvae at seven (whole transcriptome) and 14 (apical and physiological) days post-fertilization. The larvae sampled at 7dpf for whole transcriptomics analysis revealed dysregulation of pathways involved in membrane integrity (inhibition of calcium channel) and metabolic processes (downregulation of amino acid, glucose, and lipid biosynthesis), while the larvae reared for 14 days exhibited a significant decrease in survival at the highest treatment condition. These results indicate that maternal transfer of HBCD is of concern in fish, which may act through indirect mechanisms involving the inhibition of membrane transport leading to disruption in metabolic processes, collectively resulting in energy depletion and subsequently mortality.

ORGANISM(S): Pimephales promelas

PROVIDER: GSE212295 | GEO | 2022/09/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Embryo/ larval toxicity and key gene expression signatures of maternally transferred hexabromocyclododecane (HBCD) in Pimephales promelas

Project description:Embryo/ larval toxicity and key gene expression signatures of maternally transferred hexabromocyclododecane (HBCD) in Pimephales promelas

| PRJNA874903 | ENA

A combined transcriptomic and proteomic approach to identify toxicity pathways in early-life stages of Japanese medaka (Oryzias latipes) exposed to 1,2,5,6- tetrabromocyclooctane (TBCO)

Project description:Currently, the novel brominated flame retardant, 1,2,5,6-tetrabromocyclooctane (TBCO), is considered as a potential replacement for hexabromocyclododecane (HBCD). As such, use of TBCO could increase significantly in the near future. Therefore, this study investigated the toxicity of TBCO in order to assess its potential toxicological risks to aquatic organisms. Embryos of Japanese medaka (Oryzias latipes) were exposed to 10, 100 and 1,000 μg/L TBCO, and molecular responses were characterized by use of transcriptomics (RNAseq) and proteomics in embryos exposed to 100 μg/L TBCO that were collected on the day of hatch. TBCO was accumulated in embryos by 0.43-1.3×104 30 fold and the rate of accumulation was 1.7-1.8 day-131 . Number of days to hatch and success of hatching of embryos exposed to the two greatest concentrations of TBCO were impaired. Consistent with effects on hatching, proteins that were less abundant were enriched in pathways of embryo development and hatching. Responses of the transcriptome and proteome to TBCO also were used to predict adverse effects of TBCO. Functionally grouped gene ontology terms indicated that TBCO might impair contraction of cardiac muscle and vision, and these effects were confirmed by use of targeted bioassays designed to evaluate cardiac and visual performance. Results of this study provided a comprehensive understanding of effects of TBCO on medaka at early-life stages. Also, the study illustrated the power of “omics” approaches to explain and predict phenotypic responses to the exposure with chemicals.

2017-06-29 | PXD003823 | Pride

Hepatic transcriptomic alterations for 1,3,5,7,9,11-hexabromocyclododecane (HBCD) after 5-day exposure in rats

Project description:To identify liver transcripts differentially expressed due to treatment with 1,3,5,7,9,11-hexabromocyclododecane (HBCD), we collected RNA from male Harlan Sprague Dawley rats exposed to 0, 0.06, 0.641, 6.41, 64.1 or 641 mg/kg HBCD, 5 days after exposure for animals 7 weeks of age. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip array. A total of 1,2,1,23, and 247 gene transcripts were differentially expressed due to HBCD treatment after exposure to 0.06, 0.641, 6.41, 64.1 or 641 mg/kg HBCD (false discovery rate (FDR) < 0.05).

2020-07-15 | GSE153357 | GEO

A549 cell line gene expression profiling in response to HBCD

Project description:SurePrint G3 Human Gene Expression 8x60k oligonucleotide microarrays (Design ID: 028004,Agilent) were used to characterize gene expression profiles of A549 cells exposed to different concentrations of HBCD (hexabromocyclododecane) for 24 hours.

2014-10-01 | E-MTAB-2174 | biostudies-arrayexpress

HepG2/C3 cell line gene expression profiling in response to HBCD and DMBA

Project description:SurePrint G3 Human Gene Expression 8x60k oligonucleotide microarrays (Design ID: 039494,Agilent) were used to characterize gene expression profiles of HepG2/C3A cells exposed to HBCD (hexabromocyclododecane) or DMBA (dimethylbenzanthracene) for 24 hours.

2014-10-01 | E-MTAB-2173 | biostudies-arrayexpress

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

Impacts of Gestational FireMaster 550 (FM 550) Exposure on the Neonatal Cortex are Sex Specific and Largely Attributable to the Organophosphate Esters

Project description:To investigate the potential underlying neurotoxic effect of developmental exposure to flame retardant mixture, Fire Master 550, or it brominated and organophosphate we performed gene expression profiling in PND1 rat prefrontal cortex.

2022-08-20 | GSE211430 | GEO

Transcriptomic responses of human hepatocellular carcinoma cells (HepG2/C3A) to dust, flame retardants and dimethylbenzanthracene

Project description:Human HepG2/C3A cells were exposed to indoor dust reference material SRM2585; DMBA (dimethylbenzanthracene); HBCD (hexabromocyclododecane); two different mixtures of flame retardants (all dissolved in 0.1% DMSO) or 0.1% DMSO alone for 72h. RNA was prepared and labeled with Cy3 then hybridized to Agilent SurePrint G3 Human GE v2 8x60k Microarrays, Agilent design ID 039494.

2015-10-01 | E-MTAB-3324 | biostudies-arrayexpress

Medaka larvae were exposed to HBCD

Project description:Recently, omics techniques have been widely applied to the discovery of potential bio-markers and explore triggering mechanism. To get a more comprehensive diagnosis of HBCD impacts on marine medaka (Oryzias melastigma), the larvae (within 24 hours post-hatch) were exposed to gradient doses of HBCD. After exposure for 7 days, the profiles of genes expression were examined using a custom-commercial 26, 430-oligonucleotide arrays (4M-CM-^W44K) of Japanese medaka which is shared much genomic information with marine medaka.At the end of the treatment period, 30 larvae/sample were pooled for RNA extraction and labeled by One-Color. A total of twelve independent arrays: three control (DMSO), three low-concentration HBCD (0.2 nM) exposures, three medium-concentration HBCD (2 nM) exposures, and three high-concentration HBCD (20 nM) exposures. The larvae of marine medaka (within 24 hours post-hatch) were exposed to to 0 (control), 0.2nM, 2nM and 20nM of HBCD (dimethyl sulfoxide with a final concentration of 1:30000 v/v water) for 7 days. Each HBCD treatment had three replicates with 100 larvae for each Petri dish. At the end of the treatment period, 30 larvae/sample were pooled for RNA extraction. A total of twelve independent arrays: three control (DMSO), three low-concentration HBCD (0.2 nM) exposures, three medium-concentration HBCD (2 nM) exposures, and three high-concentration HBCD (20 nM) exposures.

2013-07-31 | E-GEOD-49362 | biostudies-arrayexpress

Medaka larvae were exposed to HBCD

2013-07-31 | GSE49362 | GEO