Hepatic transcriptomic alterations for tetrabromobisphenol A-bis(2,3-dibromopropyl ether) (TBBPA-DBPE) after 5-day exposure in rats
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PROVIDER: PRJNA642152 | ENA |
REPOSITORIES: ENA
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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).
2020-07-15 | GSE153363 | GEO
Project description:3,3’,5.5’-Tetrabromobisphenol A (TBBPA) is a widely used brominated flame-retardant utilized in the production of electronic devices and plastic paints. The objective of this study is to use zebrafish as a model and determine the effects of TBBPA exposure on early embryogenesis. We initiated TBBPA exposures (0, 10, 20 and 40μM) at 0.75 h post fertilization (hpf) and monitored early developmental events such as cleavage, blastula and epiboly that encompass maternal-to-zygotic transition (MZT) and zygotic genome activation (ZGA). Our data revealed that TBBPA exposures induced onset of developmental delays by 3 hpf (blastula). By 5.5 hpf (epiboly), TBBPA-exposed (10-20 μM) embryos showed concentration-dependent developmental lag by up to 3 stages or 100% mortality at 40 μM. Interestingly, while continued 0.75- 48 hpf TBBPA exposures (10 μM) led to severely deformed embryos, replacing exposure solution with chemical-free media at 6 hpf mitigated this effect, with 100% normal embryos at 48 hpf. To examine the genetic basis of TBBPA-induced delays, we conducted mRNA-sequencing on embryos exposed to 0 or 40 μM TBBPA from 0.75 hpf to 2, 3.5 or 4.5 hpf. Read count data showed that while TBBPA exposures had no overall impacts on maternal or maternal-zygotic genes, collective read counts for zygotically activated genes were lower in TBBPA treatment at 4.5 hpf compared to time-matched controls, suggesting that TBBPA delays ZGA. Gene ontology assessments for both time- and stage-matched differentially expressed genes revealed TBBPA-induced inhibition of chromatin assembly- a process regulated by histone modifications. Since acetylation is the primary histone modification system operant during early ZGA, we hypothesized that TBBPA inhibits histone acetylation, resulting in lack of open chromatin within promoters of zygotic genes and delaying ZGA. Therefore, we co-exposed embryos to 20 μM TBBPA and 100 μM N-(4-Chloro-3-(trifluoromethyl)phenyl)-2-ethoxybenzamide (CTB) -a histone acetyltransferase activator that promotes histone acetylation- and showed that TBBPA-CTB co-exposures from 0.75- 3 hpf significantly reversed TBBPA-only developmental delays, suggesting that TBBPA-induced phenotypes are indeed driven by repression of histone acetylation. Collectively, our work demonstrates that TBBPA disrupts ZGA and early developmental morphology, potentially by inhibiting histone acetylation. Future studies will focus on mechanisms of TBBPA-induced chromatin modifications.
2024-08-31 | GSE262783 | GEO
Project description:Vertebrate eye devlopment is partially regulated by thyroid hormones. TBBPA is a chemical that interacts with thyroid receptors. We investigated the effects of TBBPA on eye development of zebrafish. We expected TBBPA exposure to cause transcriptional changes of visual-system-related genes, which find their phenotypic anchoring in eye malformations and dysfunction, as observed in our previous studies. Additionally, the reversibility of effects after recovery in clean water for three days was investigated.
2019-05-09 | GSE121336 | GEO
Project description:Tetrabromobisphenol A bis (2-hydroxyethyl) ether (TBBPA-DHEE), a derivative of TBBPA, has been frequently detected in the environment. In this study, the median lethal concentration (LC50) of TBBPA-DHEE at 96 h post-fertilization (hpf) was 1.573 mg/L. Based on the reported environmental concentrations, we investigated the effects of TBBPA-DHEE on the nervous system of zebrafish embryos following exposure to varying concentrations (0, 20, 100, and 500 μg/L) for 4 to 144 hpf. Our results indicated that exposure to 100 μg/L at 144 hpf led to behavioral abnormalities in zebrafish. Furthermore, exposure to TBBPA-DHEE inhibited the development of the central nervous system and motor neurons in zebrafish. Real-time polymerase chain reaction (PCR) analysis revealed that exposure to TBBPA-DHEE significantly downregulated the expression levels of neurodevelopmental genes (shha, syn2a, elavl3, gfap, and gap43). Additionally, TBBPA-DHEE increased oxidative stress in zebrafish. Transcriptomic analysis demonstrated that exposure to TBBPA-DHEE affected the signaling pathways involved in neurodevelopment. Overall, this study demonstrated that TBBPA-DHEE may disrupt the early development of the nervous system, leading to abnormal motor behavior in zebrafish larvae, and provided novel insights into the potential mechanisms of TBBPA-DHEE neurotoxicity.
| S-EPMC11860782 | biostudies-literature
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.
2023-04-03 | GSE148518 | GEO
Project description:Tetrabromobisphenol A (TBBPA) biodegradation in acidogenic systems: one step further on where and who
| PRJEB49191 | ENA
Project description:Flame retardant tetrabromobisphenol A (TBBPA) disrupts histone acetylation and zygotic transcription during zebrafish embryogenesis
| PRJNA1093380 | ENA
Project description:Transcriptional profile of zebrafish eyes after exposure to 200 ug/L Tetrabromobisphenol A (TBBPA)
| PRJNA497088 | ENA
Project description:Tetrabromobisphenol A-bis(2,3-dibromopropyl ether) (TBBPA-BDBPE), a widely used flame retardant, has been frequently detected in various environmental compartments, but its health hazard remains largely unknown. Here, we investigated the adverse effects of TBBPA-BDBPE (50 and 1000 μg/kg/day) on postnatal testis development in CD-1 mice and the underlying mechanism. Following the first week of maternal exposure, neonatal mice in the high-dose group exhibited reduced seminiferous tubule area, fewer Sertoli cells and germ cells, and damaged microtubules in Sertoli cells; even microtubule damage was also observed in the low-dose group. When exposure extended to adulthood, male offspring in the high-dose group presented more remarkable alterations in reproductive parameters, including reduced sperm count; in the low-dose group, microtubule damage was also observable, along with blood-testis barrier impairment. Further molecular docking analysis and tubulin polymerization assay indicated that TBBPA-BDBPE could interact with tubulin and disrupt its polymerization. Moreover, we observed attenuated microtubules in mouse Sertoli cells in vitro (TM4) following TBBPA-BDBPE treatment, suggesting that TBBPA-BDBPE impaired testis development possibly by interfering with tubulin dynamics. This study not only highlights the male reproductive hazard of TBBPA-BDBPE but also greatly improved the understanding of the molecular mechanism for male reproductive toxicity of chemicals.
| S-EPMC11504584 | biostudies-literature
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.
2020-04-29 | GSE129412 | GEO