Zebrafish toxicogenomics and phenotypic analyses reveal molecular insights into bisphenol-A (BPA) early-life exposure toxicity.
Ontology highlight
ABSTRACT:
ORGANISM(S): Danio rerio
PROVIDER: GSE22634 | GEO | 2012/06/01
SECONDARY ACCESSION(S): PRJNA128191
REPOSITORIES: GEO
Similar Datasets
Project description:In this study, developing zebrafish were exposed to 500-4500 µg/L BPA for 7 days from 3 hours post-fertilization for a microarray experiment to obtain molecular insights into BPA early-life exposure toxicity. We analyzed a total of 18 arrays; five biological replicate arrays for zebrafish treated with 500 µg/L BPA, four biological replicate arrays for zebrafish treated with 1500 µg/L BPA, four biological replicate arrays for zebrafish treated with 4500 µg/L BPA against 5 biological replicate arrays for control fish. A common reference sample was used for both treated and control samples.
2012-05-31 | E-GEOD-22634 | biostudies-arrayexpress
Project description:To elucidate the molecular perturbations underlying the connection of low-dose prenatal BPA exposure to cardiometabolic diseases, we assessed the liver transcriptome in both male and female mouse offspring exposed to 5ug/kg/day BPA and corn oil (control) during gestation.
2020-12-01 | GSE155845 | GEO
Project description:Purpose: finding differential transcripts usage in environmentally harzardous chemical, bisphenol A (BPA) in human retinal cells Methods: transcriptome analysis by the RNA-seq via mRNA pull-down Results: We found that BPA increases cellular toxicity by the increasing of early apoptotic pathway in Y79 cells. Also, over thounds of retained intron events were detected from the RNA-seq analysis. Conclusions: Bisphenol A (BPA) increases early cytotoxic effects in Y79 cells through the early apoptotic pathway and changes the context of trascript through the splicing regulation mechanisms.
2021-02-16 | GSE146255 | GEO
Project description:Fly strain y[1]; bw[1]; e[4]; ci[1] ey[R] was obtained from the Bloomington Stock Center. Flies were reared in incubators at 25°C, 65% of relative humidity, and photoperiod of 12 hours. For gene expression analyses flies were reared in media containing BPA, high sugar, and BPA + high sugar (chronic exposure). After development, newly emerged adult male flies were collected, aged for 48 hours, and flash frozen in liquid nitrogen. We collected four replicas of each sample and stored tehm at -80°C. Total RNA was extracted from whole flies using TRIzol (Life Technologies). The synthesis of cDNA and its labeling with fluorescent dyes (Cy3 and Cy5) as well as hybridization reactions were carried out using 3DNA protocols and reagents (Genisphere). Slides were scanned using Axon 400B scanner (Axon Instruments) and GenePix Pro 6.0 software. Foreground fluorescence of dye intensities was normalized by the Loess method in Bioconductor / Limma. Dye "swaps," loop design.
2014-06-04 | E-GEOD-55670 | biostudies-arrayexpress
Project description:Fly strain y[1]; bw[1]; e[4]; ci[1] ey[R] was obtained from the Bloomington Stock Center. Flies were reared in incubators at 25°C, 65% of relative humidity, and photoperiod of 12 hours. For gene expression analyses flies were reared in media containing BPA, high sugar, and BPA + high sugar (chronic exposure). After development, newly emerged adult male flies were collected, aged for 48 hours, and flash frozen in liquid nitrogen. We collected four replicas of each sample and stored tehm at -80°C. Total RNA was extracted from whole flies using TRIzol (Life Technologies). The synthesis of cDNA and its labeling with fluorescent dyes (Cy3 and Cy5) as well as hybridization reactions were carried out using 3DNA protocols and reagents (Genisphere). Slides were scanned using Axon 400B scanner (Axon Instruments) and GenePix Pro 6.0 software. Foreground fluorescence of dye intensities was normalized by the Loess method in Bioconductor / Limma.
2014-06-04 | GSE55670 | GEO
Project description:Bisphenol A (BPA) is a widespread Endocrine Disrupter mainly used in food contact plastics. Several evidences support BPA adverse effects, especially on susceptible groups such as pregnant women. The present study considered placental development - relevant for pregnancy outcomes and fetal nutrition/programming - as a potential target of BPA. Pregnant CD-1 mice were administered per os with vehicle, 0.5 (BPA05) or 50 mg/kg (BPA50) body weight (bw)/die of BPA, from gestational day (GD) 1 to GD11. At GD12, BPA50 induced significant degeneration and necrosis of giant cells, increased vacuolization in the junctional zone in absence of glycogen accumulation and reduction of the spongiotrophoblast layer. BPA05 induced a significant nuclear accumulation of M-NM-2-catenin in trophoblasts of the labyrinthine and spongiotrophoblast layers, supporting an activation of the Wnt/M-NM-2-catenin pathway. Transcriptomic analysis indicated a BPA05 promotion and a BPA50 inhibition of blood vessels development and branching supported by the morphological observation of decreased and increased total vessels area in the labyrinth layers upon BPA05 and BPA50 treatments, respectively, with BPA50 also inducing a decrease in vessels number. These mechanisms involve, respectively, CREB and Wnt/M-NM-2-catenin pathways for BPA05 and AhR/ARNT pathway for BPA50, as deducted by the transcription factor binding analysis. These results show that BPA differently affects mouse placental development depending on the dose level. In particular, the 0.5 mg/kw bw, in the range of dose level used to set the Tolerable Daily Intake, may elicit not negligible alterations whose relevance for human health has to be carefully evaluated. Three conidtions experiment: Control, BPA 0.5 mg/kg bw die; BPA 50 mg/kg bw die. Biological replicates: three control replicates; four replicates per treatment. Technical replicates: 2 (dye swap) per biological replica
2014-12-15 | E-GEOD-63852 | biostudies-arrayexpress
Project description:Bisphenol-A (BPA) is one of the most widespread endocrine disrupting chemicals (EDC) used as the base compound in the manufacture of polycarbonate plastics. Although evidence points to consider exposure to BPA as a risk factor for the development of Diabetes, its actions on whole body metabolism and on pancreatic beta cells are still unclear. The aim of this study was to study the in vivo effects of BPA on mice pancreatic islets, particularly on how it could regulate ion channels expression and function. And thus, bringing mechanistic insight into the suggested association between BPA exposure and health disorders. We used microarrays to detail the global profile of gene expression to identified different groups of up and down-regulated genes in the work model, with a special focus on genes related to ion channel-mediated actions of BPA in mice pancreatic β-cells.
2019-02-09 | GSE126297 | GEO
Project description:Bisphenol A (BPA) is used in the plastic industry as the monomer of polycarbonates and epoxy resins. Heat and changes in pH conditions lead to its leakage from the plastics in which it is incorporated. This largely contributes to the widespread exposure of the general population to this environmental contaminant. The exposure levels in humans are likely below the Tolerable Daily Intake (TDI: 50 µg/kg/day) and well below the No Observable Adverse Effect Level (NOAEL: 5000 µg/kg/day) defined from reprotoxicity studies. However, several studies suggest that BPA could induce deleterious effects specifically at low, environmentally relevant, doses. BPA has been described as an endocrine disruptor with estrogenic activity. Recently, it has been shown that BPA exposure has an impact on metabolic functions including stimulation of adipogenesis and of insulin production by the pancreas. Here, we investigated the effects of oral exposure to low (TDI) and high (NOAEL) doses of BPA on mouse liver transcriptome. Liver gene expression was measured from CD-1 mice (6 mice/group) exposed for 28 days to bisphenol A at doses 0 (controls), 50 (TDI or low dose) or 5000 µg/kg/day (NOAEL or high dose) via food contamination.
2011-09-20 | E-GEOD-26728 | biostudies-arrayexpress
Project description:Bisphenol A (BPA) is a widespread Endocrine Disrupter mainly used in food contact plastics. Several evidences support BPA adverse effects, especially on susceptible groups such as pregnant women. The present study considered placental development - relevant for pregnancy outcomes and fetal nutrition/programming - as a potential target of BPA. Pregnant CD-1 mice were administered per os with vehicle, 0.5 (BPA05) or 50 mg/kg (BPA50) body weight (bw)/die of BPA, from gestational day (GD) 1 to GD11. At GD12, BPA50 induced significant degeneration and necrosis of giant cells, increased vacuolization in the junctional zone in absence of glycogen accumulation and reduction of the spongiotrophoblast layer. BPA05 induced a significant nuclear accumulation of β-catenin in trophoblasts of the labyrinthine and spongiotrophoblast layers, supporting an activation of the Wnt/β-catenin pathway. Transcriptomic analysis indicated a BPA05 promotion and a BPA50 inhibition of blood vessels development and branching supported by the morphological observation of decreased and increased total vessels area in the labyrinth layers upon BPA05 and BPA50 treatments, respectively, with BPA50 also inducing a decrease in vessels number. These mechanisms involve, respectively, CREB and Wnt/β-catenin pathways for BPA05 and AhR/ARNT pathway for BPA50, as deducted by the transcription factor binding analysis. These results show that BPA differently affects mouse placental development depending on the dose level. In particular, the 0.5 mg/kw bw, in the range of dose level used to set the Tolerable Daily Intake, may elicit not negligible alterations whose relevance for human health has to be carefully evaluated.
2014-12-15 | GSE63852 | GEO
Project description:Endocrine disrupting compounds (EDCs) have the potential to cause adverse effects on wildlife and human health. Two important EDCs are the synthetic estrogen 17a-ethynylestradiol (EE2) and bisphenol A (BPA) both of which are xenoestrogens (XEs) as they bind the estrogen receptor and disrupt estrogen physiology in mammals and other vertebrates. In recent years the influence of XEs on oncogenes, specifically in relation to breast and prostate cancer has been the subject of considerable study. In this study healthy primary human prostate epithelial cells (PrECs) were exposed to environmentally relevant concentrations of BPA (5nM and 25nM BPA) and interrogated using a whole genome microarray. Microarray data were analyzed using the Pipeline for Integrated Microarray Expression and Normalization Toolkit (PIMENTo) that provides (1) data pre-processing, (2) and normalization to remove the technical variability across arrays data, (3) data visualization, (4) background subtraction, (5) quality control, and (6) differential expression (DE) analysis using the Bioconductor package 'limma'. Exposure to 5 and 25nM BPA generated 8,876 and 9,525 differentially expressed (DE) genes respectively in treated PrECs. Exposure to EE2 had the greatest effect on the PrEC transcriptome (2,389 DE genes) and all three exposures shared 7,011 common DE genes. Together, the low and high dose of BPA affected 1,839 genes not shared with the EE2 exposure.
2021-01-01 | E-MTAB-7576 | biostudies-arrayexpress