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1. Dallot, Constantin. Perturbation de la fonction thyroïdienne : mise en place d’une stratégie de criblage des produits chimiques : Thyroid function disruption : setting up a screening strategy for chemicals.

Degree: Docteur es, Interactions moléculaires et cellulaires, 2015, Nice

En dépit de la pression règlementaire croissante pour mieux détecter les produits chimiques potentiellement responsables de perturbations de la fonction thyroïdienne, les moyens de les cribler restent insuffisants et imparfaits. Un tel criblage implique l’utilisation de nombreux tests in vitro ciblant chacun l’un des divers mécanismes de toxicité potentiellement impliqué, ou des tests in vivo plus longs et plus contraignants. Trois modèles d’étude ont ainsi été évalués pour leur potentiel à simplifier les procédures de criblage actuellement préconisées. Le premier modèle d’étude qui a été proposé est un modèle in vivo d’exposition à court terme par voie orale de rats mâles adultes. Le suivi de l’expression de gènes permet de réaliser un criblage de la perturbation de la fonction thyroïdienne après 7 jours d’exposition seulement. Le second modèle d’étude qui a été retenu pour ce travail est la lignée cellulaire PCCl3 de thyrocytes de rats, identifiée comme un modèle potentiel pour le criblage de la toxicité thyroïdienne. Enfin, la pertinence pressentie de l’utilisation d’un modèle d’hépatocytes cryopréservés (LiverbeadsTM) a été confirmée pour l’identification des composés toxiques thyroïdiens chez le rongeur dont l’action est médiée par le foie. Trois modèles d’étude in vitro et in vivo utilisables lors des tests de criblage des produits chimiques perturbateurs de la fonction thyroïdienne ont donc été identifiés. L’évaluation de cette perturbation est rendue possible par l’utilisation de variations d’expression de gènes comme principal paramètre d’étude

Whereas disruption of thyroid hormone signaling by environmental chemicals is a growing concern, identifying thyroid toxicants in early screening studies remains a challenge. Indeed, several different molecular events can initiate a such disruption of the Hypothalamus-Pituitary-Thyroid (HPT) axis. Thus, the detection of thyroid toxicants implies to conduct systematically an important battery of in vitro assays, or long in vivo studies. In the aim to simplify the procedure for the screening of all the possible mode of actions (MoAs) involved, we assessed three models for their suitability to detect in a short term different thyroid toxicants by using changes in gene expression. We identified the possibility of discriminating thyroid toxicants from compounds that do not alter thyroid function, by using this approach, in a 7-day adult male rat assay. Regarding in vitro testing, we have established the proof of concept of discriminating direct-acting thyroid toxicants from compounds that do not affect thyroid function, on the basis of up-regulated expression of a set of genes as criteria of positivity, in an early screening in vitro assay based on PCCl3 rat thyroid cells. We also confirmed the relevance of the use of alginate-embedded cryopreserved hepatocytes (LiverbeadsTM) for the screening of liver-mediated thyroid toxicity in rodents. The present work allowed the identification of three models suitable for the early screening of the disruption of the thyroid…

Advisors/Committee Members: Cupo, Anny (thesis director).

Subjects/Keywords: Thyroïde; Toxicologie; Perturbateurs endocriniens; Criblage; Expression génique; Culture cellulaire; PCCl3; Rat; Thyroid; Toxicology; Endocrine disrupters; Screening; Gene expression; Cell culture; PCCl3; Rat

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Dallot, C. (2015). Perturbation de la fonction thyroïdienne : mise en place d’une stratégie de criblage des produits chimiques : Thyroid function disruption : setting up a screening strategy for chemicals. (Doctoral Dissertation). Nice. Retrieved from http://www.theses.fr/2015NICE4135

Chicago Manual of Style (16th Edition):

Dallot, Constantin. “Perturbation de la fonction thyroïdienne : mise en place d’une stratégie de criblage des produits chimiques : Thyroid function disruption : setting up a screening strategy for chemicals.” 2015. Doctoral Dissertation, Nice. Accessed April 17, 2021. http://www.theses.fr/2015NICE4135.

MLA Handbook (7th Edition):

Dallot, Constantin. “Perturbation de la fonction thyroïdienne : mise en place d’une stratégie de criblage des produits chimiques : Thyroid function disruption : setting up a screening strategy for chemicals.” 2015. Web. 17 Apr 2021.

Vancouver:

Dallot C. Perturbation de la fonction thyroïdienne : mise en place d’une stratégie de criblage des produits chimiques : Thyroid function disruption : setting up a screening strategy for chemicals. [Internet] [Doctoral dissertation]. Nice; 2015. [cited 2021 Apr 17]. Available from: http://www.theses.fr/2015NICE4135.

Council of Science Editors:

Dallot C. Perturbation de la fonction thyroïdienne : mise en place d’une stratégie de criblage des produits chimiques : Thyroid function disruption : setting up a screening strategy for chemicals. [Doctoral Dissertation]. Nice; 2015. Available from: http://www.theses.fr/2015NICE4135


Freie Universität Berlin

2. Schanze, Nancy. Role of the thyroid hormone metabolite 3-iodothyronamine in the regulation of the thyroid hormone homeostasis.

Degree: 2017, Freie Universität Berlin

3-Iodothyronamine (3-T1AM) is an endogenous thyroid hormone (TH) metabolite in humans and rodents, which can be formed in murine intestinal tissue by decarboxylation and deiodination from T4. A single injection of 50 mg/kg 3-T1AM leads to bradycardia and hypothermia in mice and Djungarian hamsters. These effects are opposite to the effects of an excess of the classic TH T3. It has also been demonstrated that the same 3-T1AM dose suppresses plasma T4 and TSH in rats, indicating interference with the hypothalamus pituitary thyroid (HPT) axis. The hypothesis of this doctoral thesis is that 3-T1AM is involved in the fine tuning of the TH homeostasis by direct action on the thyroid gland. Male C57BL/6 mice were intraperitoneally injected with 5 mg/kg 3-T1AM or the corresponding amount of solvent for 7 d daily. The mRNA expression of the TH synthesis genes sodium iodide symporter (Nis), thyroglobulin, and pendrin were reduced after 3-T1AM treatment, potentially leading to reduced TH biosynthesis. However, no involvement of the HPT axis was observed. This was attributed to unchanged expression of T3 responsive genes involved in the regulation of the HPT axis and unaltered TH serum concentrations. A functional effect of 3-T1AM treatment on the thyroid despite unchanged circulating TH was observed in the enlargement of thyroid follicular lumina. Experiments with the iodine-free 3-T1AM metabolite T0AM show that the latter exerts its own activity profile in mice under the same treatment conditions, but also affects thyroid gene expression and morphology. The findings of the mouse studies were complemented with in vitro studies in PCCL3 rat thyrocytes. 3-T1AM is taken up by PCCL3 cells and is intracellularly metabolized. The resulting metabolites T0AM and 3-iodothyroacetic acid (3-TA1) were secreted from the cells into the cell culture medium. Both, Nis expression and function in the form of iodide uptake were reduced by 3-T1AM in PCCL3 cells. A partial inhibition of Dio1 activity as well as glucose utilization were also observed. Mechanistically, 3-T1AM signaling via adrenergic or Taar1-mediated cAMP modulation could be largely excluded in this model, whereas a strong 3-T1AM-dependent increase in intracellular calcium was observed, which needs to be further characterized. T0AM could (partially) mediate the inhibitory effect of 3-T1AM on Nis in PCCL3 cells. In summary, 3-T1AM has the potential to interfere with the TH biosynthesis machinery at several levels and thus regulate the TH homeostasis by direct action on the thyroid gland. An in vitro model of functional thyroid follicles from murine embryonic stem cells, which was published in 2012, was implemented within the framework of the doctoral thesis and established in the laboratory. In this model, the direct effect of 3-T1AM on TH biosynthesis will be investigated in future studies. Advisors/Committee Members: w (gender), Prof. Dr. Josef Köhrle (firstReferee), Prof. Dr. Sigmar Stricker (furtherReferee).

Subjects/Keywords: 3-iodothyronamine; thyroid hormone; Iodine; sodium/iodide symporter; PCCL3; 500 Naturwissenschaften und Mathematik::570 Biowissenschaften; Biologie::572 Biochemie

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Schanze, N. (2017). Role of the thyroid hormone metabolite 3-iodothyronamine in the regulation of the thyroid hormone homeostasis. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-4405

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Schanze, Nancy. “Role of the thyroid hormone metabolite 3-iodothyronamine in the regulation of the thyroid hormone homeostasis.” 2017. Thesis, Freie Universität Berlin. Accessed April 17, 2021. http://dx.doi.org/10.17169/refubium-4405.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Schanze, Nancy. “Role of the thyroid hormone metabolite 3-iodothyronamine in the regulation of the thyroid hormone homeostasis.” 2017. Web. 17 Apr 2021.

Vancouver:

Schanze N. Role of the thyroid hormone metabolite 3-iodothyronamine in the regulation of the thyroid hormone homeostasis. [Internet] [Thesis]. Freie Universität Berlin; 2017. [cited 2021 Apr 17]. Available from: http://dx.doi.org/10.17169/refubium-4405.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Schanze N. Role of the thyroid hormone metabolite 3-iodothyronamine in the regulation of the thyroid hormone homeostasis. [Thesis]. Freie Universität Berlin; 2017. Available from: http://dx.doi.org/10.17169/refubium-4405

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

.