Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22253800_1.fastq.gz | Fastqsanger.gz | |||
| SRR22253800_2.fastq.gz | Fastqsanger.gz | |||
| SRR22253801_1.fastq.gz | Fastqsanger.gz | |||
| SRR22253801_2.fastq.gz | Fastqsanger.gz | |||
| SRR22253802_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:3,3’-Dichlorobiphenyl (PCB-11) is a non-legacy PCB congener widely detected in environmental samples and has been detected in human serum, but its toxicity potential is poorly understood. Zebrafish statically exposed to 4,500 µg/L PCB-11 at 24 hours post fertilization (hpf) were collected at 96 hpf for RNA sequencing.
2019-08-22 | GSE118955 | GEO
Project description:In order to investigate the underlying mechanisms of PCB 153 mediated toxicity to Atlantic cod (Gadus morhua), we analyzed the liver proteome of fish exposed to various doses of PCB 153 (0, 0.5, 2 and 8mg/kg body weight) for two weeks and examined the effects on expression of liver proteins using quantitative proteomics. Label-free mass spectrometry enabled quantification of 1272 proteins, and 78 were differentially regulated between PCB 153 treated samples and controls. Two proteins downregulated due to PCB 153 treatment, Glutathione S-transferase theta 1 (GSTT1) and sulfotransferase family protein 1 (ST2B1), were verified using selected reaction monitoring (SRM). Supported by bioinformatics analyses, we concluded that PCB 153 perturbs lipid metabolism in the Atlantic cod liver and that increased levels of lipogenic enzymes indicate increased synthesis of fatty acids and triglycerides.
2017-01-17 | PXD004362 | Pride
Project description:Exposure to high fat diet (HFD) and persistent organic pollutants including polychlorinated biphenyls (PCBs) is associated with liver injury in human populations and with non-alcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH) in animal models. Exposure of HFD-fed male mice to the non-dioxin-like (NDL) PCB mixture Aroclor1260 or to dioxin-like (DL) PCB126 or to the combination caused steatohepatitis and differentially altered the liver proteome with pathways involving epigenetic regulation of gene expression. Here unbiased RNA sequencing of miRNA (miRNA-seq) and subsequent network analysis to characterize the biological pathways altered by HFD and PCB exposure compared to HFD alone. Distinct miRNA expression patterns reveald a potential role of miRNAs in the pathogenesis of NAFLD. These results demonstrate miRNA and transcriptome pathways in PCB-related hepatic inflammation and fibrosis in a mouse model of NAFLD.
2024-04-23 | GSE195829 | GEO
Project description:As part of a larger study on neurodevelopmental effects of lower chlorinated PCB 11, we characterized PCB 11 distribution in postweaning mouse dams orally developmentally exposed to PCB 11 via the diet. We used and liquid chromatography tandem mass spectrometry (LC MS/MS) based proteomics to map changes in hepatic protein levels following PCB 11 exposure, gas chromatography tandem mass spectrometry (GC MS/MS) to quantify PCB 11 and its metabolites in brain, liver, and serum; and liquid chromatograph-high resolution mass spectrometry (LC HRMS) to screen serum for additional PCB 11 metabolites. The accompanying dataset contains raw and processed files from the proteomic analysis only, including protein identification from AMICA, and network interaction data from STRING.
2025-11-10 | MSV000099827 | MassIVE
Project description:(Abstract) Toxicogenomics has great potential for enhancing our understanding of environmental chemical toxicity, hopefully leading to better-informed human health risk assessments. This study employed toxicogenomic technology to reveal species differences in response to two prototypical aryl hydrocarbon receptor (AHR) agonists, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and the polychlorinated biphenyl (PCB) congener PCB 126. Dose responses of primary cultures of rat and human hepatocytes were determined using species-specific microarrays sharing over 4,000 gene orthologs. Forty-seven human and 79 rat genes satisfied dose response criteria for both chemicals and were subjected to further analysis including the calculation of EC50 and the relative potency (REP) of PCB 126 for each gene. Only 5 responsive orthologous genes were shared between the two species, yet the geometric mean of the REPs for all rat and human modeled responsive genes were 0.06 (95% Confidence Interval (CI); 0.03-0.1) and 0.002 (95% CI; 0.001-0.005), respectively, suggesting broad species differences in the initial events that follow AHR activation but precede toxicity. This indicates that there are species differences in both the specific genes that responded and the agonist potency and relative potency for those genes. This observed insensitivity of human cells to PCB 126 is consistent with more traditional measurements of AHR activation (i.e., CYP1A1 enzyme activity) and suggests that the species difference in PCB 126 sensitivity is likely due to certain aspects of AHR function. That a species divergence also exists in this expanded AHR-regulated gene repertoire is a novel finding and should help when extrapolating animal data to humans. Experiment Overall Design: Primary hepatocyte cultures, separated into 2 pools of 3 female Sprague Dawley rats each, were treated with vehicle (0.5% DMSO), TCDD (-14 to -6.5 log10 M) , or PCB 126 (-12 to -5 log10 M) for 48h. Total RNA was extracted and screened with RG-U34A microarrays for dose response.
2009-09-17 | E-GEOD-14554 | biostudies-arrayexpress
Project description:(Abstract) Toxicogenomics has great potential for enhancing our understanding of environmental chemical toxicity, hopefully leading to better-informed human health risk assessments. This study employed toxicogenomic technology to reveal species differences in response to two prototypical aryl hydrocarbon receptor (AHR) agonists, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and the polychlorinated biphenyl (PCB) congener PCB 126. Dose responses of primary cultures of rat and human hepatocytes were determined using species-specific microarrays sharing over 4,000 gene orthologs. Forty-seven human and 79 rat genes satisfied dose response criteria for both chemicals and were subjected to further analysis including the calculation of EC50 and the relative potency (REP) of PCB 126 for each gene. Only 5 responsive orthologous genes were shared between the two species, yet the geometric mean of the REPs for all rat and human modeled responsive genes were 0.06 (95% Confidence Interval (CI); 0.03-0.1) and 0.002 (95% CI; 0.001-0.005), respectively, suggesting broad species differences in the initial events that follow AHR activation but precede toxicity. This indicates that there are species differences in both the specific genes that responded and the agonist potency and relative potency for those genes. This observed insensitivity of human cells to PCB 126 is consistent with more traditional measurements of AHR activation (i.e., CYP1A1 enzyme activity) and suggests that the species difference in PCB 126 sensitivity is likely due to certain aspects of AHR function. That a species divergence also exists in this expanded AHR-regulated gene repertoire is a novel finding and should help when extrapolating animal data to humans. Experiment Overall Design: Primary hepatocyte cultures derived from 3 human donors were treated with vehicle (0.5% DMSO), TCDD (-14 to -6.5 log10 M) , or PCB 126 (-12 to -5 log10 M) for 48h. Total RNA was extracted and screened with HG-U133A microarrays for dose response.
2009-09-05 | E-GEOD-14553 | biostudies-arrayexpress
Project description:Exposure to Polychlorinated Biphenyls (PCBs) is known to cause serious health effects in human both in pre- and post-natal period. The knowledge of gene expression will help us to develop early disease or disorder biomarkers for PCB induced health effects. We used microarrays to detail the global gene expression profile underlying the effects of high PCB exposure from the cord blood of the PCB-exposed newborn in Slovakia to understand the molecular mechanism of PCB related toxic effect and its functional implications during fetal development.
2017-01-01 | GSE32420 | GEO
Project description:The effects exerted by three mixtures of Polychlorinated Biphenyls (PCB), one featuring dioxin-like (DL) and two featuring non dioxin-like (NDL) congeners, on human fetal corpora cavernosa cells representative of a major male endocrine-sensitive organ, have been evaluated by gene expression profiling. PCB congeners concentrations used were derived from human internal exposure data to explore the impact of the adult body burden on a fetal tissue. Cell exposure were performed for 72h mimicking a chronic exposure. Experiment conditions: control, three treatments with PCB-Mix1, PCB-Mix2 or PCB-Mix3. Biological replicates: 3 control replicates, 3 replicates per treatment. Technical replica: 2 (dye swap) per biological replica. Direct comparison design (control vs treated samples) in 12/16 arrays (biological replicates 1 and 2); Loop design in 4/16 arrays (biological replicate 3).
2010-11-09 | E-GEOD-25193 | biostudies-arrayexpress
Project description:(Abstract) Toxicogenomics has great potential for enhancing our understanding of environmental chemical toxicity, hopefully leading to better-informed human health risk assessments. This study employed toxicogenomic technology to reveal species differences in response to two prototypical aryl hydrocarbon receptor (AHR) agonists, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and the polychlorinated biphenyl (PCB) congener PCB 126. Dose responses of primary cultures of rat and human hepatocytes were determined using species-specific microarrays sharing over 4,000 gene orthologs. Forty-seven human and 79 rat genes satisfied dose response criteria for both chemicals and were subjected to further analysis including the calculation of EC50 and the relative potency (REP) of PCB 126 for each gene. Only 5 responsive orthologous genes were shared between the two species, yet the geometric mean of the REPs for all rat and human modeled responsive genes were 0.06 (95% Confidence Interval (CI); 0.03-0.1) and 0.002 (95% CI; 0.001-0.005), respectively, suggesting broad species differences in the initial events that follow AHR activation but precede toxicity. This indicates that there are species differences in both the specific genes that responded and the agonist potency and relative potency for those genes. This observed insensitivity of human cells to PCB 126 is consistent with more traditional measurements of AHR activation (i.e., CYP1A1 enzyme activity) and suggests that the species difference in PCB 126 sensitivity is likely due to certain aspects of AHR function. That a species divergence also exists in this expanded AHR-regulated gene repertoire is a novel finding and should help when extrapolating animal data to humans.
2009-08-19 | GSE14554 | GEO