Influence of Estradiol on Thyroid: Serum Radioiodide Concentration Ratios of Gonadectomized and Hypophysectomized Rats

Boccabella, Anthony V.; Alger, Elizabeth A.

doi:10.1210/endo-74-5-680

Cited by 19 publications

(6 citation statements)

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“…Some previous reports indicate that estradiol might regulate thyroid function through a direct action on thyrocytes (34), apart from a possible effect on TSH secretion (35)(36)(37)(38). The administration of estradiol to ovariectomized and hypophysectomized rats leads to a higher thyroid radioiodide uptake (32,39), which supports the hypothesis of a direct effect of estrogen on the thyroid. More recently, the presence of estrogen receptors has been demonstrated in both human and rat thyroid glands (40,41).…”

Section: Estrogensupporting

confidence: 71%

The importance of sodium/iodide symporter (NIS) for thyroid cancer management

Carvalho

Ferreira

2007

Arq Bras Endocrinol Metab

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The thyroid gland has the ability to uptake and concentrate iodide, which is a fundamental step in thyroid hormone biosynthesis. Radioiodine has been used as a diagnostic and therapeutic tool for several years. However, the studies related to the mechanisms of iodide transport were only possible after the cloning of the gene that encodes the sodium/iodide symporter (NIS). The studies about the regulation of NIS expression and the possibility of gene therapy with the aim of transferring NIS gene to cells that normally do not express the symporter have also become possible. In the majority of hypofunctioning thyroid nodules, both benign and malignant, NIS gene expression is maintained, but NIS protein is retained in the intracellular compartment. The expression of NIS in non-thyroid tumoral cells in vivo has been possible through the transfer of NIS gene under the control of tissue-specific promoters. Apart from its therapeutic use, NIS has also been used for the localization of metastases by scintigraphy or PET-scan with 124 I. In conclusion, NIS gene cloning led to an important development in the field of thyroid pathophysiology, and has also been fundamental to extend the use of radioiodine for the management of non-thyroid tumors. A glândula tireóide tem capacidade de captar e concentrar iodeto, etapa fundamental na biossíntese dos hormônios tireóideos. O uso de iodo radioativo para fins de diagnóstico e terapia das doenças da tireóide vem sendo feito há muitos anos. Entretanto, somente após a clonagem do gene que codifica o cotransportador de sódio/iodeto (NIS) houve aumento significativo dos estudos relacionados ao mecanismo de transporte de iodeto. Os estudos sobre a regulação da expressão do NIS e a possibilidade de terapia gênica visando à transferência do gene NIS para células que normalmente não expressam esse transportador, foram também viabilizados. Na maior parte dos nódulos tireóideos hipofuncionantes, tanto benignos quanto malignos, a expressão do gene do NIS está presente, mas a proteína NIS fica retida no compartimento intracelular. A transferência do gene usando-se promotores tecido-específicos possibilitou a expressão do NIS em células tumorais não-tireóideas in vivo. Além do seu uso terapêutico, o NIS também vem sendo usado para a localização de metástases tumorais através da cintilografia ou do PET-scan usando-se 124 I. Em conclusão, a clonagem do NIS possibilitou enorme avanço na área de fisiopatologia tireóidea e foi também fundamental para estender o uso do radioiodo para tumores não tireóideos.

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Section: Estrogensupporting

confidence: 71%

The importance of sodium/iodide symporter (NIS) for thyroid cancer management

Carvalho

Ferreira

2007

Arq Bras Endocrinol Metab

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“…Estrogen increases the thyrotropin (TSH) response to thyrotropin-releasing hormone stimulation in ovariectomized rats (Chen & Walfish 1978). Additionally, the stimulatory effect of estradiol on thyroid radioiodine uptake in ovariectomized and hypophysectomized rats (Boccabella & Alger 1964) supports the hypothesis of a direct action of estrogen on the thyroid. Because ERs are expressed in both human and rat thyroid glands (Banu et al 2002, Arain et al 2003 and estradiol increases the proliferation rate of the FRTL-5 rat thyroid cell line independent of TSH (Furlanetto et al 1999), it is clear that this hormone also regulates thyrocytes through a direct action.…”

Section: Thyroid Function Regulation By Estrogenmentioning

confidence: 79%

Sexual dimorphism and thyroid dysfunction: a matter of oxidative stress?

Fortunato¹,

Ferreira²,

Hecht³

et al. 2014

Journal of Endocrinology

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Thyroid diseases, such as autoimmune disease and benign and malignant nodules, are more prevalent in women than in men, but the mechanisms involved in this sex difference is still poorly defined. H 2 O 2 is produced at high levels in the thyroid gland and regulates parameters such as cell proliferation, migration, survival, and death; an imbalance in the cellular oxidant-antioxidant system in the thyroid may contribute to the greater incidence of thyroid disease among women. Recently, we demonstrated the existence of a sexual dimorphism in the thyrocyte redox balance, characterized by higher H 2 O 2 production, due to higher NOX4 and Poldip2 expression, and weakened enzymatic antioxidant defense in the thyroid of adult female rats compared with male rats. In addition, 17b-estradiol administration increased NOX4 mRNA expression and H 2 O 2 production in thyroid PCCL3 cells. In this review, we discuss the possible involvement of oxidative stress in estrogenrelated thyroid pathophysiology. Our current hypothesis suggests that a redox imbalance elicited by estrogen could be involved in the sex differences found in the prevalence of thyroid dysfunctions.

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“…However, the prevalence of thyroid disease is higher among women [35]. Estrogens could either stimulate the TSH secretion, or directly activate the growth of thyroid cells [36][37][38].…”

Section: Discussionmentioning

confidence: 99%