Tetrabromobisphenol A caused neurodevelopmental toxicity via disrupting thyroid hormones in zebrafish larvae

Zhu, Biran; Zhao, Gang; Yang, Lihua; Zhou, Bingsheng

doi:10.1016/j.chemosphere.2018.01.080

Cited by 79 publications

(42 citation statements)

References 35 publications

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“…Increased [89,128,129] or decreased [130,132,134,135] expression of Slc5a5, Tpo, Pax8, and Tg transcripts was dependent on the dose and window of exposure. Additionally, BPA and BPS appeared to interact with PAX8 and thyroid transcription factor 1 (TTF1) in silico [135].…”

Section: Zebrafishmentioning

confidence: 95%

“…Positive [37,38,128] and negative [37,38,[128][129][130][131] associations between exposure to BPs and T3 and/or T4 levels have been reported, depending on the chemical used, the dose tested, and the time of exposure. Reductions in T4 concentrations, when accompanied with higher TSH contents, may compensate hypothyroidism in zebrafish larvae and stimulate TH synthesis [38,129].…”

Section: Zebrafishmentioning

confidence: 99%

“…Similarly, BPs disrupting effects on thyroid gene expression vary according to the different experimental conditions, especially the duration of exposure [126]. Hence, transcription levels of genes implicated in thyroid cell function and proliferation (Tsh-r), TH activity (Trα, Trβ), and transport (Ttr) can be up- [37,68,126,130,132,133] or down-regulated [38,68,126,128,130,133]. The transcription of Hematopoietically expressed homeobox (Hhex) was up-regulated in larval fish following exposure to BPA or BPF, although it is important to note that the Hhex gene is expressed in early life, contributing to differentiation and development of the thyroid gland, as well as of other organs, such as the pancreas and liver [37].…”

Section: Zebrafishmentioning

confidence: 99%

“…BPs stimulated thyroid signaling increases expression of Corticotrophin-releasing hormone (Crh) mRNA in the hypothalamus [37,38,129] and of Tsh and Tshβ in the pituitary gland [89,128,130,[132][133][134], except for TBBPA, which down-regulated Tshβ mRNA in embryos [133].…”

Section: Zebrafishmentioning

confidence: 99%

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Bisphenols as Environmental Triggers of Thyroid Dysfunction: Clues and Evidence

Gorini

Bustaffa

Coi

et al. 2020

IJERPH

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Bisphenols (BPs), and especially bisphenol A (BPA), are known endocrine disruptors (EDCs), capable of interfering with estrogen and androgen activities, as well as being suspected of other health outcomes. Given the crucial role of thyroid hormones and the increasing incidence of thyroid carcinoma in the last few decades, this review analyzes the effects of BPS on the thyroid, considering original research in vitro, in vivo, and in humans published from January 2000 to October 2019. Both in vitro and in vivo studies reported the ability of BPs to disrupt thyroid function through multiple mechanisms. The antagonism with thyroid receptors (TRs), which affects TR-mediated transcriptional activity, the direct action of BPs on gene expression at the thyroid and the pituitary level, the competitive binding with thyroid transport proteins, and the induction of toxicity in several cell lines are likely the main mechanisms leading to thyroid dysfunction. In humans, results are more contradictory, though some evidence suggests the potential of BPs in increasing the risk of thyroid nodules. A standardized methodology in toxicological studies and prospective epidemiological studies with individual exposure assessments are warranted to evaluate the pathophysiology resulting in the damage and to establish the temporal relationship between markers of exposure and long-term effects.

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Section: Zebrafishmentioning

confidence: 95%

Section: Zebrafishmentioning

confidence: 99%

Section: Zebrafishmentioning

confidence: 99%

Section: Zebrafishmentioning

confidence: 99%

See 2 more Smart Citations

Bisphenols as Environmental Triggers of Thyroid Dysfunction: Clues and Evidence

Gorini

Bustaffa

Coi

et al. 2020

IJERPH

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“…Finally, considering neurotoxicity, several fish studies report effects of most Cat I FRs on locomotor activity and a couple of human studies report statistical associations between TPhP or TCEP exposure and neurobehavior/cognition in children [8,24,38]. Several animal studies analyzing the neurotoxic effects of TBBPA reached contradictory conclusions, ranging from LOAELs of 0.1 mg/kg/day in mice or 0.0064 µM in zebrafish to NOAELs of 1000 mg/kg/day in rats [16,26,32,46,47,50,77]. We also identified plausible AOPs for TPhP-, TBBPA-, TDCIPP-and TCEP-induced effects on neurobehavior/cognition.…”

Section: Plausible Aops For the Observed Aos Of Cat I Frsmentioning

confidence: 99%

Prioritization of hazards of novel flame retardants using the mechanistic toxicology information from ToxCast and Adverse Outcome Pathways

2019

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Background: Flame retardants (FRs) are used in most consumer products and textiles to comply with current flammability standards. After the restriction of polybrominated diphenyl ethers, a large number of chemically diverse replacement FRs are increasingly used, but the risk they represent is not yet properly evaluated and their toxicity pathways are still poorly understood. Approach:We collected in vivo toxicological information on 62 (including 52 non-regulated) FRs and established five prioritization categories (Cat I to V) based on data availability and toxicological concern. We then considered available in vitro toxicological data from ToxCast, as a complement to in vivo information. By combining these information sources, we then explored relevant toxicity mechanisms for nine selected FRs (Cat I) using the AOP (Adverse Outcome Pathway) framework. Results:For 20 FRs (Cat V), toxicological data on mammals were absent. Data available were scarce for another 22 FRs, of which 14 FRs (Cat II) may be of toxicological concern. We found substantial information for only ten replacement FRs, of which nine (Cat I) present some toxicological concern: tris-2-chloroethyl phosphate (TCEP), tris(1,3dichloropropyl)phosphate (TDCIPP), triphenyl phosphate (TPhP), tricresyl phosphate (TMPP), tetrabromobisphenol A (TBBPA), tri-n-butyl phosphate (TNBP), tri(2-butoxyethyl) phosphate (TBOEP), tris(1-chloro-2-propyl) phosphate (TCIPP), 2-ethylhexyl diphenyl phosphate (EHDPP). ToxCast results confirmed in vivo based categorization for several FRs and identified potential molecular targets. For the nine Cat I FRs, we identified several molecular targets, health outcomes and some potential AOPs. However, the complete toxicity pathways leading from molecular targets to adverse health outcomes are still unknown, with the exception of TBBPA-induced neurotoxicity. Conclusions:The approach presented in this study was particularly useful for the categorization of a large group of replacement FRs with relatively low data availability. We highlight priority compounds that critically need more toxicological studies or FRs for which regulatory measures could be envisaged. Our research also suggests that high toxicity indicated by ToxCast is particularly relevant for predicting higher hazard in vivo. Finally, we indicate several gaps and directions for future research, such as molecular targets that could be tested in vitro and health outcomes for cohort studies. which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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AOP Report: Thyroperoxidase Inhibition Leading to Altered Visual Function in Fish Via Altered Retinal Layer Structure

Gölz

Baumann

Pannetier

et al. 2022

Enviro Toxic and Chemistry

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Thyroid hormones (THs) are involved in the regulation of many important physiological and developmental processes, including vertebrate eye development. Thyroid hormone system–disrupting chemicals (THSDCs) may have severe consequences, because proper functioning of the visual system is a key factor for survival in wildlife. However, the sequence of events leading from TH system disruption (THSD) to altered eye development in fish has not yet been fully described. The development of this adverse outcome pathway (AOP) was based on an intensive literature review of studies that focused on THSD and impacts on eye development, mainly in fish. In total, approximately 120 studies (up to the end of 2021) were used in the development of this AOP linking inhibition of the key enzyme for TH synthesis, thyroperoxidase (TPO), to effects on retinal layer structure and visual function in fish (AOP‐Wiki, AOP 363). In a weight‐of‐evidence evaluation, the confidence levels were overall moderate, with ample studies showing the link between reduced TH levels and altered retinal layer structure. However, some uncertainties about the underlying mechanism(s) remain. Although the current weight‐of‐evidence evaluation is based on fish, the AOP is plausibly applicable to other vertebrate classes. Through the re‐use of several building blocks, this AOP is connected to the AOPs leading from TPO and deiodinase inhibition to impaired swim bladder inflation in fish (AOPs 155–159), together forming an AOP network describing THSD in fish. This AOP network addresses the lack of thyroid‐related endpoints in existing fish test guidelines for the evaluation of THSDCs. Environ Toxicol Chem 2022;41:2632–2648. © 2022 SETAC

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Tetrabromobisphenol A caused neurodevelopmental toxicity via disrupting thyroid hormones in zebrafish larvae

Cited by 79 publications

References 35 publications

Bisphenols as Environmental Triggers of Thyroid Dysfunction: Clues and Evidence

Bisphenols as Environmental Triggers of Thyroid Dysfunction: Clues and Evidence

Prioritization of hazards of novel flame retardants using the mechanistic toxicology information from ToxCast and Adverse Outcome Pathways

AOP Report: Thyroperoxidase Inhibition Leading to Altered Visual Function in Fish Via Altered Retinal Layer Structure

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