6 Iodo-δ-lactone reproduces many but not all the effects of iodide

Thomasz, Lisa; Oglio, Romina; Dagrosa, María Alejandra; Krawiec, L.; Pisarev, Mario A.; Juvenal, Guillermo

doi:10.1016/j.mce.2010.03.012

Cited by 20 publications

(14 citation statements)

References 39 publications

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“…A decrease of Pax8 mRNA levels by I Ϫ was described by other authors, but this was under different conditions (33). The inhibition of iodide uptake by high doses of I Ϫ is extremely fast and was interpreted by Eng et al (22) to be a consequence of NIS internalization or protein turnover.…”

mentioning

confidence: 83%

Regulation of Thyroid Oxidative State by Thioredoxin Reductase Has a Crucial Role in Thyroid Responses to Iodide Excess

Leoni

Kimura

Santisteban

et al. 2011

Molecular Endocrinology

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The phenomenon that supraphysiological doses of iodide (I(-)) temporarily inhibit thyroid hormone synthesis is known as thyroid iodide autoregulation. Recovery of thyroid function has been attributed to sodium-iodide symporter (NIS) inhibition, but the diversity of available data makes it difficult to reach definitive conclusions. Iodide excess induces reactive oxygen species production and cell toxicity. However, the roles of the oxidative state of the cell and antioxidant selenoproteins in I(-) autoregulation have never been explored. Here we analyze the effects of high I(-) doses in rat thyroids and in PCCl3 cells in the period comprising I(-) autoregulation (i.e. 0-72 h after I(-) administration), focusing on NIS expression, redox state, and the expression and activity of selenoproteins. Our results show that NIS mRNA inhibition by I(-) does not occur at the transcriptional level, because neither NIS promoter activity nor Pax8 expression or its binding to DNA was modulated. Because I(-) uptake was inhibited much earlier than NIS protein, and no effect was observed on its subcellular localization, we suggest that I(-) is inhibiting NIS in the plasma membrane. The increased reactive oxygen species production leads to an increase in thioredoxin reductase mRNA levels and enzyme activity, which reduces the oxidative stress. Inhibition of thioredoxin reductase at either gene expression or activity levels prevented NIS recovery, thus illustrating a new role played by this selenoprotein in the regulation of cell homeostasis and consequently in I(-) autoregulation.

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mentioning

confidence: 83%

Regulation of Thyroid Oxidative State by Thioredoxin Reductase Has a Crucial Role in Thyroid Responses to Iodide Excess

Leoni

Kimura

Santisteban

et al. 2011

Molecular Endocrinology

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“…Moreover it was demonstrated that IL δ prevents goiter growth in rats (Pisarev et al, 1988 and that, in vitro, it inhibits thyroid cell proliferation in pigs (Dugrillon and Gärtner, 1995;Dugrillon et al, 1990), humans (Dugrillon et al, 1994) and FRTL-5 cells (Pisarev et al, 1992). Regarding 2-IHDA, in in vitro studies no growth suppressing effect could be demonstrated by measuring thymidine incorporation in primary cultures of dog thyroid cells (Panneels et al, 1994a) but we have demonstrated that it has an antigoitrogenic action (Thomasz et al, 2010a). Therefore the objective of this work was analyze the role of 2-IHDA on cell proliferation and to study the mechanisms involved in such regulation.…”

Section: Introductionmentioning

confidence: 72%

“…Regarding growth effects we have recently demonstrated that this compound has antigoitrogenic activity, decreasing the intracellular levels of cAMP, reducing the number of cells and the glandular epithelial height (Thomasz et al, 2010a). 2-IHDA was not only able to prevent the growth of MMI induced goiter, but also caused the involution of performed goiter.…”

Section: Discussionmentioning

confidence: 97%

Inhibitory effects of 2-iodohexadecanal on FRTL-5 thyroid cells proliferation

Thomasz

Coulonval

Salvarredi

et al. 2015

Molecular and Cellular Endocrinology

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“…It has been also demonstrated in in vivo and in vitro studies that the halogen inhibits iodide transport. NIS mRNA levels are also regulated by iodide [28][29][30] at a transcriptional step, although a regulation at a posttranscriptional level may be not discarded [31][32][33]. It is postulated that the decrease in NIS is responsible of the "escape" from the acute WolffChaikoff effect [29].…”

Section: Thyroid Functionmentioning

confidence: 99%

Thyroid: Iodine Beyond the Thyronines

Juvenal¹,

Thomasz²,

Oglio³

et al. 2011

curr chem biol

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Although thyroid gland function is mainly under the control of pituitary TSH, other factors may also play a role in this process. Iodine is not used only by the thyroid to synthesize thyroid hormones but also directly influences a number of parameters such as thyroid proliferation and function. Thyroid autoregulation has been related to intraglandular content of an unknown putative iodocompound. The thyroid is capable of producing different iodolipids such as 6-iododeltalactone (ILδ) and 2-iodohexadecanal (2-IHDA). Data from different laboratories have shown that these iodolipids can inhibit several thyroid parameters suggesting that these compounds may be the intermediates in the thyroid autoregulation process.

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6 Iodo-δ-lactone reproduces many but not all the effects of iodide

Cited by 20 publications

References 39 publications

Regulation of Thyroid Oxidative State by Thioredoxin Reductase Has a Crucial Role in Thyroid Responses to Iodide Excess

Regulation of Thyroid Oxidative State by Thioredoxin Reductase Has a Crucial Role in Thyroid Responses to Iodide Excess

Inhibitory effects of 2-iodohexadecanal on FRTL-5 thyroid cells proliferation

Thyroid: Iodine Beyond the Thyronines

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