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Hepatic transcriptome of rats treated with vehicle or fipronil (3 mg/kg/d per os for 14 days)

ABSTRACT: Fipronil (CAS #: 120068-37-3), a widely used insecticide, has been described as a thyroid disruptor in rat inducing a marked increase in thyroxine (T4) clearance resulting in a decrease in T4 plasma concentration. These effects seem to require the bioactivation of fipronil via its biotransformation into fipronil sulfone by cytochromes P450 (CYP). Here, we hypothesized that fipronil-induced thyroid disruption may, at least in part, result from the induction of hepatic enzymes involved in the metabolism of thyroid hormones. Thus, we used microarrays to perform a genome-wide analysis of the effects of fipronil on gene expression in rat liver.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE39378 | GEO | 2013/08/22

SECONDARY ACCESSION(S): PRJNA170739

REPOSITORIES: GEO

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Hepatic transcriptome of rats treated with vehicle or fipronil (3 mg/kg/d per os for 14 days)

Project description:Fipronil (CAS #: 120068-37-3), a widely used insecticide, has been described as a thyroid disruptor in rat inducing a marked increase in thyroxine (T4) clearance resulting in a decrease in T4 plasma concentration. These effects seem to require the bioactivation of fipronil via its biotransformation into fipronil sulfone by cytochromes P450 (CYP). Here, we hypothesized that fipronil-induced thyroid disruption may, at least in part, result from the induction of hepatic enzymes involved in the metabolism of thyroid hormones. Thus, we used microarrays to perform a genome-wide analysis of the effects of fipronil on gene expression in rat liver. Liver gene expression was measured from female Wistar rats treated with vehicle (n = 7) or fipronil 3 mg/kg/day per os for 14 days (n = 8)

2013-08-22 | E-GEOD-39378 | biostudies-arrayexpress

Effect of fipronil on the thyroid gland transcriptome in the rat

Project description:Fipronil is a widely-used broad-spectrum phenylpyrazole insecticide. It has been shown that fipronil increases the hepatic metabolism of thyroid hormone in the rat, which may induce compensatory mechanisms at the level of the thyroid gland itself. Here, we studied the effect of fipronil on the transcriptome of the thyroid gland in the rat. Adult (2- to 3-month-old) female Wistar rats were treated per os with fipronil (3 mg/kg) or the vehicle alone for 14 days. The transcriptome of their thyroid gland was analyzed using Agilent 4x44K microarrays.

2016-09-07 | GSE75275 | GEO

Effect of fipronil on the thyroid gland transcriptome in the rat

2016-09-07 | E-GEOD-75275 | biostudies-arrayexpress

Thyroid hormone receptor beta is required for thyrotrpin regulation and thyroid hormone production.

Project description:Thyroid hormone receptor beta (THRB) is post-translationally modified by small ubiquitin-like modifier (SUMO). To investigate the biological role of THRB sumoylation, we generated a mouse model with a mutation that disrupts sumoylation at lysine 146 (K146Q). The THRB K146Q mutant mice had normal serum thyroxine (T4), markedly elevated serum thyrotropin (TSH) (81-fold above control), and enlargement of both the pituitary and the thyroid gland. The marked elevation in TSH, despite a normal serum T4 concentration, indicated blunted feedback regulation of TSH. TH profuction was 10-fold lower (per mg of thyroid tissue) in mutant mice compared to Wt mice.

2021-02-20 | GSE167105 | GEO

BRB-seq analysis of PFOS-induced thyroid hormone system disrupted rats reveal organ-specific effects

Project description:Perfluorooctanesulfonic acid (PFOS) is a persistent anthropogenic chemical that can affect the thyroid hormone system in humans. In experimental animals, PFOS exposure decreases thyroxine (T4) and triiodothyronine (T3) levels, without a compensatory upregulation of thyroid stimulating hormone (TSH). In adults, THs are regulated by the hypothalamus-pituitary-thyroid (HPT) axis, but also organs such as the liver and potentially the gut microbiota. PFOS and other xenobiotics can therefore potentially disrupt the TH system through various entry points of disruption. To start addressing this issue, we performed a PFOS exposure study to identify effects in multiple organs and pathways simultaneously.

2022-05-04 | GSE196133 | GEO

Brain hypothyroidism leads to immune tolerance in microglia in Alzheimer's disease [scRNA-seq]

Project description:An imbalance in thyroid hormones (THs) is associated with reversible dementia and Alzheimer’s disease (AD) pathogenesis. Whether hypothyroidism occurs in AD brains and how it affects AD pathology remain largely unknown. Here, we find that reduced conversion of thyroxine (T4) to tri-iodothyronine (T3) in the brain by decreased iodothyronine deiodinase 2 (DIO2) leads to hippocampal hypothyroidism in early AD model mice prior to TH changes in the blood. A TH deficiency causes immune tolerance with decreased phagocytic activity in microglia, thereby aggravating AD pathology. We demonstrate that microglial ecto-5’-nucleotidase (CD73) is reduced in the hypothyroid state and that its inhibition contributes to immune tolerance in microglia. Thus, our data define a molecular mechanism through which decreased conversion of T4 to T3 in the early AD brain, and consequent brain hypothyroidism causes microglial dysfunction and exacerbates AD pathology.

2023-09-01 | GSE219130 | GEO

Brain hypothyroidism leads to immune tolerance in microglia in Alzheimer's disease [RNA-seq]

2023-09-01 | GSE219129 | GEO

Expression data for brain samples in a metamorphosis assay for thyroid axis disruption

Project description:Thyroid hormones (TH), thyroxine (T4) and 3, 5, 3’-triiodothyronine (T3), play crucial roles in regulation of growth, development and metabolism in vertebrates and their action are targets for endocrine disruptive agents. Perturbations in TH action can contribute to the development of disease states and the U.S. Environmental Protection Agency is developing a high throughput screen using TH-dependent amphibian metamorphosis as an assay platform. Currently this methodology relies on external morphological endpoints and changes in central thyroid axis parameters. However, exposure-related changes in gene expression in TH-sensitive tissue types that occur over shorter time frames have the potential to augment this screen. This study aims to characterize and identify molecular markers in the tadpole brain. Using a combination of cDNA array analysis and real time quantitative polymerase chain reaction (QPCR), we examine the brain of tadpoles following 96 hours of continuous exposure to T3, T4, methimazole, propylthiouracil, or perchlorate. This tissue was more sensitive to T4 rather than T3, even when differences in biological activity were taken into account. This implies that a simple conversion of T4 to T3 cannot fully account for T4 effects on the brain and suggests distinctive mechanisms of action for the two THs. While the brain shows gene expression alterations for methimazole and propylthiouracil, the environmental contaminant, perchlorate, had the greatest effect on the levels of mRNAs encoding proteins important in neural development and function. Our data identify gene expression profiles that can serve as exposure indicators of these chemicals. Keywords: dose response

2007-05-12 | GSE7057 | GEO

Expression data for brain samples in a metamorphosis assay for thyroid axis disruption - inhibitors

2007-05-12 | GSE6964 | GEO

Expression data for hindlimb and tail samples in a metamorphosis assay for thyroid axis disruption - inhibitors

Project description:Thyroid hormones (TH), thyroxine (T4) and 3, 5, 3’-triiodothyronine (T3), play crucial roles in regulation of growth, development and metabolism in vertebrates and are targets for endocrine disruptive agents. Perturbations in TH action can contribute to the development of disease states and the U.S. Environmental Protection Agency is developing a high throughput screen using TH-dependent metamorphosis of the Xenopus laevis tadpole as an assay platform. Currently this methodology relies on external morphological endpoints and changes in central thyroid axis parameters. However, exposure-related changes in gene expression in TH-sensitive tissue types that occur over shorter time frames have the potential to augment this screen. Using a combination of cDNA array and real time quantitative polymerase chain reaction (QPCR) analyses, this study identifies molecular markers in tissues peripheral to the central thyroid axis. We examine the hindlimb and tail of tadpoles up to 96 hours of continuous exposure to T3, T4, methimazole, propylthiouracil, or perchlorate. Several novel biomarker candidates are indicated that include transcripts encoding importin, RNA helicase II/Gu, and defender against death protein, DAD1. In combination with previously-identified biomarker candidates, these transcripts will greatly augment the predictive and diagnostic power of the Xenopus metamorphosis assay for perturbation of TH action. Keywords: time course

2007-05-12 | GSE7051 | GEO

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