The Effects of Disturbance on Hypothalamus-Pituitary-Thyroid (HPT) Axis in Zebrafish Larvae after Exposure to DEHP

Jia, Pan‐Pan; Ma, Yanbo; Lu, Chihua; Mirza, Zakaria A.; Zhang, Wei; Jia, Yongfang; Li, Weiguo; Pei, De‐Sheng

doi:10.1371/journal.pone.0155762

Cited by 79 publications

(30 citation statements)

References 54 publications

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“…Up-regulation of Tg and Slc5a5 transcript levels may promote thyroid development to compensate for the depressed T4 concentration, as also reported for polybrominated diphenyl ethers [163]. Transcriptional levels of deiodinases were more elevated in exposed zebrafish, in accordance with a study reporting that hypothyroidism caused by EDCs is associated with higher activity and expression of Dio2 [164]. On the other hand, a recent study reported a reduction of liver DIO1 activity in BPA-treated adult rats [102], which is a finding worth of note as decreased expression of DIO1 was observed in nearly all PTCs and is likely an early event in malignant TC [165].…”

Section: Discussionsupporting

confidence: 88%

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: Discussionsupporting

confidence: 88%

Bisphenols as Environmental Triggers of Thyroid Dysfunction: Clues and Evidence

Gorini

Bustaffa

Coi

et al. 2020

IJERPH

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“…Previous work suggests that environmental estrogens may also influence thyroid hormone signaling. Exposure to the plasticizer diethylhexyl phthalate (DEHP) increased total T3 levels in zebrafish larvae and upregulated thyroid signaling genes thyroglobulin (tg), transthyretin (ttr), and dio2 (55). DEHP exhibits estrogen-like activity, although the receptor by which it acts has not been determined.…”

Section: Discussionmentioning

confidence: 99%

G protein-coupled estrogen receptor regulates heart rate by modulating thyroid hormone levels in zebrafish embryos

Romano

Edwards

Souder

et al. 2016

Preprint

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Estrogens act by binding to estrogen receptors alpha and beta (ERα, ERβ), ligand-dependent transcription factors that play crucial roles in sex differentiation, tumor growth and cardiovascular physiology. Estrogens also activate the G protein-coupled estrogen receptor (GPER), however the function of GPER in vivo is less well understood. Here we find that GPER is required to maintain normal heart rate in zebrafish embryos. Acute exposure to estrogens increased heart rate in wildtype and in ERα and ERβ mutant embryos but not in GPER mutants. Nuclear estrogen receptor signaling remained normal in GPER mutant embryos, however GPER mutant embryos exhibited reduced basal heart rate while heart rate was normal in ERα and ERβ mutants. We detected GPER transcript in discrete regions of the brain but not in the heart. In the brain, we observed gper expression in cells lacking nuclear estrogen receptor activity, suggesting that GPER acts in the brain to regulate heart rate independently of nuclear estrogen receptor signaling. Our results demonstrate that estradiol plays a previously unappreciated role in the acute modulation of heart rate during zebrafish embryonic development and that GPER functions as an autonomous estrogen receptor in vivo to regulate basal heart rate.

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“…The maintenance and reproduction of zebrafish are referred to as our previous study [22]. Briefly, the wild type zebrafish (Danio rerio, AB strain) were maintained in a flow-through system with the condition of temperature (28 o C ± 0.5) and 14:10 (light: dark) photoperiod, and fed twice every day with the newly hatched brine shrimp (Artemia nauplii).…”

Section: Zebrafish Maintain and Long-term Exposure To Dehpmentioning

confidence: 99%

“…Zebrafish model possesses numerous advantages involving the short life span, transparent embryos, high similarity to the human genome, and diverse adaptability [21]. Thus, it usually applied as a credible animal model to evaluate the toxicity of various environmental pollutants including DEHP [22]. Moreover, the zebrafish model was recently used to study the functions and impacts of various pollutants on gut microbiota after acute or chronic exposure [23,24].…”

Section: Introductionmentioning

confidence: 99%

DEHP chronic exposure disturbs the gut microbial community and metabolic homeostasis: Gender-based differences in zebrafish

Pei

Jia

Xin

et al. 2020

Preprint

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Background: Di-(2-ethylhexyl) phthalate (DEHP), a predominant phthalate ester (PAE), exhibits various toxic potentials with environmental and human health risks. However, the chronic effects of DEHP exposure on gut microbiota and associated host’s health are still largely unexplored. Here, zebrafish were exposed to relative environmental levels (0-100 μg/L) of DEHP from embryos to adult (3.5 months), then the developmental indexes and microbiota as well as the related energy metabolites in gut tissues were checked to unveil the effects during the growth progress. Results: The results indicated that the composition of gut microbiota was different among male and female adult zebrafish, and DEHP disrupted the diversity and richness of the bacterial community. The histopathological analysis of intestinal tissues revealed the decrease of villus length and tunica muscularis thickness, especially the goblet cells per villi in male fish. Moreover, energy metabolites in gut tissues were actively increased at lower levels groups, which probably contribute to the condition factor of host. For immune-related genes, the expression levels of il-8 was increased both in female and male fish in the lowest concentration (10 μg/L), but the tlr-5 and il-1β genes were in the different response with significantly decreased in female fish. Conclusion: Taken all together, those results indicated that chronic exposure to DEHP led to zebrafish obesity with the disturbed bacterial community in the gut and related metabolism pathways. Those findings provided deep insights on the perturbation of gut microbiota, metabolic homeostasis, and gender-based differences by DEHP exposure.

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The Effects of Disturbance on Hypothalamus-Pituitary-Thyroid (HPT) Axis in Zebrafish Larvae after Exposure to DEHP

Cited by 79 publications

References 54 publications

Bisphenols as Environmental Triggers of Thyroid Dysfunction: Clues and Evidence

Bisphenols as Environmental Triggers of Thyroid Dysfunction: Clues and Evidence

G protein-coupled estrogen receptor regulates heart rate by modulating thyroid hormone levels in zebrafish embryos

DEHP chronic exposure disturbs the gut microbial community and metabolic homeostasis: Gender-based differences in zebrafish

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