Excess Iodide Inhibits the Thyroid by Multiple Mechanisms

Wolff, J.

doi:10.1007/978-1-4757-2058-7_8

Cited by 39 publications

(10 citation statements)

References 40 publications

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“…The thyroid gland has adaptation mechanisms that reduce iodide metabolism when the supply is abundant, thus avoiding thyrotoxicosis. There are several mechanisms which include a direct inhibitory effect of iodide in the thyroid itself and inhibition by iodide of its own organification (Wolff-Chaikoff effect), its transport, thyroid hormones secretion, cAMP formation in response to TSH, and several other metabolic steps [40]. We suggest that all the protective mechanisms may ensure the excessive iodide intake of the 10 HI group on Days 7, 14, and 28 be eliminated from urine.…”

Section: Discussionmentioning

confidence: 93%

Activation of the Nrf2-Keap 1 Pathway in Short-Term Iodide Excess in Thyroid in Rats

Wang

Abeysekera

et al. 2017

Oxidative Medicine and Cellular Longevity

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Wistar rats were randomly divided into groups of varying iodide intake: normal iodide; 10 times high iodide; and 100 times high iodide on Days 7, 14, and 28. Insignificant changes were observed in thyroid hormone levels (p > 0.05). Urinary iodine concentration and iodine content in the thyroid glands increased after high consumption of iodide from NI to 100 HI (p < 0.05). The urinary iodine concentration of the 100 HI group on Days 7, 14, and 28 was 60–80 times that of the NI group. The mitochondrial superoxide production and expressions of Nrf2, Srx, and Prx 3 all significantly increased, while Keap 1 significantly decreased in the 100 HI group when compared to the NI or 10 HI group on Days 7, 14, and 28 (p < 0.05). Immunofluorescence staining results showed that Nrf2 was localized in the cytoplasm in NI group. Although Nrf2 was detected in both cytoplasm and nucleus in 10 HI and 100 HI groups, a stronger positive staining was found in the nucleus. We conclude that the activation of the Nrf2-Keap 1 antioxidative defense mechanism may play a crucial role in protecting thyroid function from short-term iodide excess in rats.

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Section: Discussionmentioning

confidence: 93%

Activation of the Nrf2-Keap 1 Pathway in Short-Term Iodide Excess in Thyroid in Rats

Wang

Abeysekera

et al. 2017

Oxidative Medicine and Cellular Longevity

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“…In the biosynthesis of iodolactones, however, this may be of great relevance because of the known affinities of the enzyme systems involved in eicosanoid metabolism, which increase from u>9-to w3-fatty acids. Thyroid membranes are abundant in arachidonic acid and docosahexaenoic acid (19) and the availability of these essential fatty acids may play a role in the pattern of iodolactones formed and may influence the growth inhibitory effect of iodide (24). A significant inverse relation between the sum of arachidonic acid and docosahexaenoic acid serum concentrations and thyroid cancer risk has been found and an involvement of the iodolactone pathway was hypothesized as an inhibitory factor of tumor promotion (35).…”

Section: Discussionmentioning

confidence: 99%

δ-Iodolactones decrease epidermal growth factor-induced proliferation and inositol-1,4,5-trisphosphate generation in porcine thyroid follicles—a possible mechanism of growth inhibition by iodide

Dugrillon

Gärtner²

1995

European Journal of Endocrinology

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delta-Iodolactone (6-iodo-8,11,14-eicosatrienoic delta-lactone, delta-IL), an iodinated derivative of arachidonic acid, has been shown to be synthesized in thyroid tissue and to inhibit thyroid cell proliferation. It is discussed as a potential mediator of the autoregulatory pathway of iodide in cyclic adenosine-3',5'-monophosphate (cAMP)- and thyrotropin (TSH)-independent growth. We therefore further localized the action of iodide and of delta-IL in isolated porcine thyroid follicles. Epidermal growth factor (EGF) and 12-O-tetradecanoylphorbol-13-acetate (TPA) dose dependently stimulated thyroid cell proliferation, which could be inhibited by staurosporin (0.1-10 nmol/l). Iodide (2.5-40 mumol/l) as well as delta-IL (0.5-2 mumol/l) also dose dependently inhibited EGF- and TPA-induced proliferation. As the calcium ionophor A23187 (100 pmol/l) completely abolished the inhibitory effects of iodide and of delta-IL, this may indicate a mechanism of delta-IL at or proximal to the calcium-dependent activation of protein kinase C. The growth inhibitory effect was restricted to delta-iodolactones when delta-IL was compared to 6-iodo-8,11,14,17-eicosatetraenoic delta-lactone and 5-iodo-7,10,13,16,19-docosapentaenoic gamma-lactone. It could not be prevented with propylthiouracil and therefore deiodination and a different iodide action is unlikely. Inositol-1,4,5-trisphosphate (IP3) and cAMP were measured in extracts from isolated porcine thyroid follicles stimulated with EGF (10 ng/ml) or TSH (1.0 U/l) revealing comparable kinetics in IP3 generation, while cAMP formation was only stimulated by TSH. delta-Iodolactone (2 mumol/l) only decreased EGF-induced IP3 formation, whereas TSH-induced IP3 and cAMP formation was unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…There is evidence that iodine is a major mediator of thyroid autoregulation, involving numerous inhibitory actions (41). One of these is a decrease in cAMP formation in response to TSH, resulting in an inhibition of all cAMP-mediated stimulatory effects of TSH on the thyroid.…”

Section: Increased Thyroid Cell Responsiveness To Tshmentioning

confidence: 99%

Relevance of iodine intake as a reputed predisposing factor for thyroid cancer

Knobel

Medeiros‐Neto

2007

Arq Bras Endocrinol Metab

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Iodine is a trace element that is essential for the synthesis of thyroid hormone. Both chronic iodine deficiency and iodine excess have been associated with hypertrophy and hyperplasia of follicular cells, attributed to excessive secretion of TSH. This may be associated to thyroid cancer risk, particularly in women. Experimental studies have documented thyroid cancer induction by elevation of endogenous TSH, although in a small number of animals. Iodine deficiency associated with carcinogenic agents and chemical mutagens will result in a higher incidence of thyroid malignancy. Inadequate low iodine intake will result in increased TSH stimulation, increased thyroid cell responsiveness to TSH, increased thyroid cell EGF-induced proliferation, decreased TGFβ 1 production and increased angiogenesis, all phenomena related to promotion of tumor growth. Epidemiological studies associating iodine intake and thyroid cancer led to controversial and conflicting results. There is no doubt that introduction of universal iodine prophylaxis in population previously in chronic iodine-deficiency leads to a changing pattern of more prevalent papillary thyroid cancer and declining of follicular thyroid cancer. Also anaplastic thyroid cancer is practically not seen after years of iodine supplementation. Iodine excess has also been indicated as a possible nutritional factor in the prevalence of differentiated thyroid cancer in Iceland, Hawaii and, more recently, in China. In conclusion: available evidence from animal experiments, epidemiological studies and iodine prophylaxis has demonstrated a shift towards a rise in papillary carcinoma, but no clear relationship between overall thyroid cancer incidence and iodine intake.

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Excess Iodide Inhibits the Thyroid by Multiple Mechanisms

Cited by 39 publications

References 40 publications

Activation of the Nrf2-Keap 1 Pathway in Short-Term Iodide Excess in Thyroid in Rats

Activation of the Nrf2-Keap 1 Pathway in Short-Term Iodide Excess in Thyroid in Rats

δ-Iodolactones decrease epidermal growth factor-induced proliferation and inositol-1,4,5-trisphosphate generation in porcine thyroid follicles—a possible mechanism of growth inhibition by iodide

Relevance of iodine intake as a reputed predisposing factor for thyroid cancer

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