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Hepatic transcriptomic alterations for tetrabromobisphenol A-bis(2,3-dibromopropyl ether) (TBBPA-DBPE) after 5-day exposure in rats

ABSTRACT: Hepatic transcriptomic alterations for tetrabromobisphenol A-bis(2,3-dibromopropyl ether) (TBBPA-DBPE) after 5-day exposure in rats

PROVIDER: PRJNA642152 | ENA |

REPOSITORIES: ENA

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Hepatic transcriptomic alterations for tetrabromobisphenol A-bis(2,3-dibromopropyl ether) (TBBPA-DBPE) after 5-day exposure in rats

Project description:To identify liver transcripts differentially expressed due to treatment with tetrabromobisphenol A-bis(2,3-dibromopropyl ether) (TBBPA-DBPE), we collected RNA from male Harlan Sprague Dawley rats exposed to 0, 0.1, 0.94, 9.4, 94.3 or 943 mg/kg TBBPA.DBPE, 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 0,0,0,0,0, and 0 gene transcripts were differentially expressed due to TBBPA.DBPE treatment after exposure to 0.1, 0.94, 9.4, 94.3 or 943 mg/kg TBBPA.DBPE (false discovery rate (FDR) < 0.05).

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TBBPA, TBBPS and TCBPA disrupt hESCs hepatic differentiation and promote the proliferation of differentiated cells seemingly via up-regulating the FGF10 signaling pathway

Project description:Halogenated flame retardants (HFRs) Tetrabromobisphenol A (TBBPA), Tetrabromobisphenol S (TBBPS) and Tetrachlorobisphenol (TCBPA) are wildly applied in manufacturing industry to improve the fire safety of the products. Recent reports demonstrated that TBBPA, TBBPS and TCBPA can be detected in pregnant women serum at nanomolar-level. Considering TBBPA have also been detected in the cord serum and the structural similarity of the 3 HFRs, it is necessary to pay attention to their development toxicity. Liver is the important detoxic organ but also target of TBBPA since it has been demonstrated that TBBPA exposure lead to increased liver weight in mouse and rat. So the developmental hepatic toxicity of the 3 HFRs were studied in this current research with the transcriptomic and human embryonic stem cells hepatic differentiation based toxicity evaluation system. A hepatic differentiation specific lineage development map and cell lineage - gene expression annotations were made and used for easily assessing the lineage alternations caused by toxicant treatment. Together with GO and KEGG analysis, this study mainly demonstrated that, the 3 HFRs have many common disruptive effect on hepatic differentiation, while only TCBPA significantly inhibited hepatic differentiation. The up-regulation of genes related to cell cycle and FGF10 signaling pathway at relatively late stage of hepatic differentiation indicates the proliferation of hepatoblasts were promoted by the 3 HFRs, likely via up-regulating the FGF10 signaling pathway. The proliferating promoting effect may partly explain why liver gain weight in rodents exposed to TBBPA.

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Project description:We evaluated the hepatic developmental toxicity of TBBPA/TBBPS/TCBPA with a human embryonic stem cells (hESC) system. We found that TBBPA/TBBPS/TCBPA might adversely affect human hepatocyte-like cells specification from hESCs via mainly impairing definitive endoderm specifications, suggesting the early stages of embryonic development are susceptible to the three compounds.

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Environmentally relevant exposure to TBBPA and its analogues may not drastically affect human early cardiac development

Project description:Tetrabromobisphenol A (TBBPA) and its substitutes and derivatives have been widely used as halogenated flame retardants (HFRs), in the past few decades. As a consequence, these compounds are frequently detected in the environment, as well as human bodily fluids, especially umbilical cord blood and breast milk. This has raised awareness of their potential risks to fetuses and infants. In this study, we employed human embryonic stem cell differentiation models to assess the potential developmental toxicity of six TBBPA-like compounds, at human relevant nanomolar concentrations. To mimic early embryonic development, we utilized embryoid body-based 3D differentiation in presence of the six HFRs. Transcriptomics data showed that HFR exposure over 16 days of differentiation only interfered with the expression of a few genes, indicating those six HFRs may not have specific tissue/organ targets during embryonic development. Nevertheless, further analyses revealed that some cardiac-related genes were dysregulated. Since the heart is also the first organ to develop, we employed a cardiac differentiation model to analyze the six HFRs' potential developmental toxicity in more depth. Overall, HFRs of interest did not significantly disturb the canonical WNT pathway, which is an essential signal transduction pathway for cardiac development. In addition, the six HFRs showed only mild changes in gene expression levels for cardiomyocyte markers, such as NKX2.5, MYH7, and MYL4, as well as a significant down-regulation of some but not all the epicardial and smooth muscle cell markers selected. Taken together, our results show that the six studied HFRs, at human relevant concentrations, may impose negligible effects on embryogenesis and heart development. Nevertheless, higher exposure doses might affect the early stages of heart development.

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