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Lewis E. Braverman - One of the best experts on this subject based on the ideXlab platform.
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Iodine-Induced Thyroid Dysfunction
The Thyroid and Its Diseases, 2019Co-Authors: Simone Leo, Lewis E. BravermanAbstract:Iodine is required for the synthesis of the thyroid hormones. Recommended daily iodine intake in adults is 150 μg daily, except in pregnant and lactating women who require higher amounts of iodine. The primary source of iodine is the diet, where iodine intake is predominantly obtained from dairy products, grains, and iodized salt. However, seaweed and other sources of iodine, including iodinated contrast media, nutritional supplements, and some medications, such as amiodarone and povidone-iodine, can be responsible for iodine excess. A healthy thyroid is able to adapt to iodine excess due to escape from the acute Wolff-Chaikoff Effect. However, iodine excess can induce hypothyroidism, hyperthyroidism, and thyroid autoimmunity. Iodine-induced hypothyroidism is due to failure to escape from the acute Wolff-Chaikoff Effect; it is typically transient and may not require treatment. Levothyroxine replacement therapy is necessary in some patients. Iodine-induced hyperthyroidism develops in patients with underlying autonomy of the thyroid, in which the iodine load acts as a substrate for the thyroid to produce excess amounts of thyroid hormones ( Jod-Basedow phenomenon). It is usually transient and requires only treatment with β-blockers. Patients with severe or persistent hyperthyroidism require treatment with antithyroid drugs. Prophylactic treatment to avoid the onset of thyroid dysfunction after exposure to iodine excess is generally not recommended.
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Amiodarone-Induced Thyroid Dysfunction
The Thyroid and Its Diseases, 2019Co-Authors: Lewis E. BravermanAbstract:Amiodarone is an antiarrhythmic drug, containing 37% iodine by weight, and with structural similarities to thyroid hormones. Amiodarone-induced thyroid dysfunction occurs in 15–20% of patients and includes amiodarone-induced hypothyroidism (AIH) and amiodarone-induced thyrotoxicosis (AIT). AIH is due to failure to escape from the acute Wolff-Chaikoff Effect and is easily treated with levothyroxine replacement without requiring amiodarone withdrawal. There are two types of AIT: type 1 AIT, a form of iodine-induced thyrotoxicosis that develops in patients with underlying thyroid disease exposed to the high iodine content of amiodarone, and type 2 AIT, a drug-induced destructive thyroiditis caused by a direct cytotoxic Effect of amiodarone. In some cases both pathogeneses coexist and these forms are called mixed forms. Differential diagnosis between AIT types is important since therapy differs. Type 1 AIT is treated with thionamide and in some cases by adding potassium perchlorate; type 2 AIT is treated with glucocorticoids; mixed forms may benefit from the combination of thionamide and glucocorticoids. Patients who are resistant to the other forms of treatment or who need a rapid restoration of euthyroidism should be treated by thyroidectomy. Radioactive iodine is usually not feasible, since these patients have a low radioiodine uptake. Monitoring of thyroid function should be performed before starting amiodarone and then every 3 months during amiodarone therapy and up to at least 2 years after amiodarone withdrawal.
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Role of iodine in thyroid physiology
Expert Review of Endocrinology & Metabolism, 2010Co-Authors: Angela M. Leung, Elizabeth N. Pearce, Lewis E. BravermanAbstract:Adequate levels of iodine, a trace element variably distributed on the earth, are required for the synthesis of the thyroid hormones thyroxine (T4) and triiodothyronine (T3). The iodide cycle consists of a series of transport, oxidation and coupling steps in thyroid follicular cells to produce thyroid hormone. The sodium/iodide symporter (NIS) transports iodide into the thyrocyte. Competitive inhibitors of NIS, such as perchlorate and thiocyanate, can decrease the entrance of iodide into the follicular cell. Pendrin is the primary protein that is responsible for iodide efflux out of the thyrocyte and into the follicular lumen. T4 is deiodinated in target tissues to produce the active form of thyroid hormone, T3, and other metabolites. Exposure to excessive iodine or chronic iodine deficiency may result in various clinical disorders. The Wolff–Chaikoff Effect and Jod-Basedow phenomenon describe mechanisms of thyroid autoregulation and dysregulation, respectively, during iodine excess. Population studies ha...
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The various Effects of amiodarone on thyroid function.
Thyroid, 2001Co-Authors: Fausto Bogazzi, Lewis E. Braverman, Luigi Bartalena, Maurizio Gasperi, Enio MartinoAbstract:Amiodarone, a benzofuranic-derivative iodine-rich drug used mostly for tachyarrhythmias, often causes changes in the peripheral metabolism of thyroid hormones mainly due to the inhibition of 5'-deiodinase activity: an increase in serum thyroxine and reverse triiodothyronine, and a decrease in serum triiodothyronine concentrations. Overt thyroid dysfunction, either amiodarone-induced thyrotoxicosis (AIT) or amiodarone-induced hypothyroidism (AIH), occurring in 14% to 18% of patients receiving long-term treatment, may develop both in apparently normal thyroid glands and in glands with preexisting abnormalities. AIH is mainly due to the failure to escape from the acute Wolff-Chaikoff Effect, and, in patients with thyroid autoimmune phenomena, to concomitant Hashimoto's thyroiditis. AIT is due to excess iodine-induced thyroid hormone synthesis (type I AIT) or to amiodarone-related destructive thyroiditis (type II AIT), although mixed forms often occur. Treatment of AIH consists of levothyroxine replacement th...
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Regulation of the sodium iodide symporter by iodide in FRTL-5 cells
European Journal of Endocrinology, 2001Co-Authors: Guemalli R. Cardona, Michael C. Previti, William W. Chin, Lewis E. BravermanAbstract:Objective: The acute decrease in iodide organification in the thyroid in response to excess iodide is termed the acute Wolff-Chaikoff Effect and normal organification resumes in spite of continued high plasma iodide concentrations (escape from the acute Wolff-Chaikoff Effect). We have recently reported that large doses of iodide given to rats chronically decrease the sodium/iodide symporter (NIS) mRNA and protein, suggesting that escape is due to a decrease in NIS and subsequent iodide transport. We have now studied the Effect of excess iodide on NIS in FRTL-5 cells to further explore the mechanisms whereby excess iodide decreases NIS. Design: FRTL-5 cells were employed and were incubated in the presence or absence of various concentrations of iodide. NIS mRNA and protein and the turnover of NIS were assessed. Methods: NIS mRNA was measured by Northern analysis, NIS protein by Western analysis and NIS turnover by pulse-chase labeling experiments. Results: Iodide (10 -3 mol/l) had no Effect on NIS mRNA in FRTL-5 cells at 24 and 48 h compared with cells cultured in the absence of iodide. However, excess iodide decreased NIS protein by 50% of control values at 24 h and by 70% at 48 h. This Effect of iodide was dose dependent. Pulse-chase experiments demonstrated that there was no Effect of iodide on new NIS protein synthesis and that the turnover of NIS protein in the presence of iodide was 27% faster than in the absence of added iodide. Conclusions: Excess iodide does not decrease NIS mRNA in FRTL-5 cells but does decrease NIS protein. suggesting that in this in vitro thyroid cell model iodide modulates NIS. at least in part, at a post-transcriptional level. This iodide-induced decrease in NIS protein appears to be due, at least partially. to an increase in NIS protein turnover.
Zainab Mahasneh - One of the best experts on this subject based on the ideXlab platform.
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The Wolff–Chaikoff Effect ameliorates heat stress in rats
Animal Biotelemetry, 2019Co-Authors: Hosam J. Al-tamimi, Amani Al-dawood, Zainab MahasnehAbstract:Background The thyroid gland contributes immensely to the basal metabolic rate, and hence, thermogenesis in mammals. Its response to the thermal environment is, however, slow and may require several days to adjust. A rapid thyrosuppressive mechanism (“Wolff–Chaikoff” phenomenon; WC) is inducible by high dietary iodine ingestion. The current study aimed to examine the WC on thermophysiology of rats exposed to acute heat stress (HS). Biotelemetry was used to assess real-time core body temperature ( T _core), locomotive activity (LA) and heart rate (HR) in rats ( N = 12). Animals were randomly assigned to two treatment groups: a control (CN) group had ad libitum access to tap water throughout the trial; a second group (KI) received potassium iodide (0.5%) in drinking water, 3 h before HS. Climatic conditions during the 10-day experimental period were set to 4 days at thermoneutrality (TN; T _a = 23.60 ± 0.05 °C), then HS ( T _a = 33.22 ± 0.25 °C, for 4 h) and finally back to TN until the end of trial. Serum samples were collected right after the HS, to measure free thyroxine (FT4), triiodothyronine (FT3) and total antioxidant capacity (TAO), from 12 other equivalent rats. Results The KI induced the WC, as evidenced with lower FT3 (1.66 and 1.91 ± 0.08 pg/mL) than the CN treatment, respectively. This momentary goitrogenic response by KI mitigated hyperthermia, compared to CN ( T _core maxima of 38.90 and 39.54 ± 0.09 °C). Furthermore, KI resulted in higher TAO than KI-free rats (238.30 and 198.80 ± 9.10 µM copper reducing equivalents). While instigating an instant suppression in LA, KI caused a delayed 25% elevation in HR along with a rebound in T _core, likely due to the “escape phenomenon.” Conclusions The employed WC protocol alleviated HS impact on rats. Research on other mammals awaits further investigation.
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The Wolff–Chaikoff Effect ameliorates heat stress in rats
Animal Biotelemetry, 2019Co-Authors: Hosam J. Al-tamimi, Amani Al-dawood, Zainab MahasnehAbstract:The thyroid gland contributes immensely to the basal metabolic rate, and hence, thermogenesis in mammals. Its response to the thermal environment is, however, slow and may require several days to adjust. A rapid thyrosuppressive mechanism (“Wolff–Chaikoff” phenomenon; WC) is inducible by high dietary iodine ingestion. The current study aimed to examine the WC on thermophysiology of rats exposed to acute heat stress (HS). Biotelemetry was used to assess real-time core body temperature (Tcore), locomotive activity (LA) and heart rate (HR) in rats (N = 12). Animals were randomly assigned to two treatment groups: a control (CN) group had ad libitum access to tap water throughout the trial; a second group (KI) received potassium iodide (0.5%) in drinking water, 3 h before HS. Climatic conditions during the 10-day experimental period were set to 4 days at thermoneutrality (TN; Ta = 23.60 ± 0.05 °C), then HS (Ta = 33.22 ± 0.25 °C, for 4 h) and finally back to TN until the end of trial. Serum samples were collected right after the HS, to measure free thyroxine (FT4), triiodothyronine (FT3) and total antioxidant capacity (TAO), from 12 other equivalent rats. The KI induced the WC, as evidenced with lower FT3 (1.66 and 1.91 ± 0.08 pg/mL) than the CN treatment, respectively. This momentary goitrogenic response by KI mitigated hyperthermia, compared to CN (Tcore maxima of 38.90 and 39.54 ± 0.09 °C). Furthermore, KI resulted in higher TAO than KI-free rats (238.30 and 198.80 ± 9.10 µM copper reducing equivalents). While instigating an instant suppression in LA, KI caused a delayed 25% elevation in HR along with a rebound in Tcore, likely due to the “escape phenomenon.” The employed WC protocol alleviated HS impact on rats. Research on other mammals awaits further investigation.
Andrzej Lewinski - One of the best experts on this subject based on the ideXlab platform.
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Protective Effect of KI in mtDNA in porcine thyroid: comparison with KIO_3 and nDNA
European Journal of Nutrition, 2015Co-Authors: Malgorzata Karbownik-lewinska, Jan Stepniak, Magdalena Milczarek, Andrzej LewinskiAbstract:Purpose Iodine, bivalent iron (Fe^2+), and hydrogen peroxide (H_2O_2), all significantly affecting the red-ox balance, are required for thyroid hormone synthesis. Intracellular iodine excess (≥10^−3 M) transiently blocks thyroid hormonogenesis (an adaptive mechanism called Wolff–Chaikoff Effect). The aim of the study was to evaluate the Effects of iodine, used as potassium iodide (KI) or potassium iodate (KIO_3), in concentrations corresponding to those typical for Wolff–Chaikoff Effect, on the level of oxidative damage to nuclear DNA (nDNA) and mitochondrial DNA (mtDNA) isolated from porcine thyroid under basal conditions and in the presence of Fenton reaction (Fe^2++H_2O_2 → Fe^3++^·OH + OH^−) substrates. Methods Thyroid nDNA and mtDNA were incubated in the presence of either KI or KIO_3 (2.5–50 mM), without/with FeSO_4 (30 µM) + H_2O_2 (0.5 mM). Index of DNA damage, i.e., 8-oxo-7,8-dihydro-2′-deoxyguanosine, was measured by HPLC. Results Neither KI nor KIO_3 increased the basal level of 8-oxodG in both nDNA and mtDNA. KI—in all used concentrations—completely prevented the damaging Effect of Fenton reaction substrates in mtDNA, and it partially prevented this damage in nDNA. KIO_3 partially prevented Fe^2++H_2O_2-induced oxidative damage in both DNA only in its highest used concentrations (≥25 mM). Conclusions Without additional prooxidative abuse, both iodine compounds, i.e., KI and KIO_3, seem to be safe in terms of their potential oxidative damage to DNA in the thyroid. The superiority of KI over KIO_3 relies on its stronger protective Effects against oxidative damage to mtDNA, which constitutes an argument for its preferential utility in iodine prophylaxis.
Malgorzata Karbownik-lewinska - One of the best experts on this subject based on the ideXlab platform.
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Protective Effect of KI in mtDNA in porcine thyroid: comparison with KIO_3 and nDNA
European Journal of Nutrition, 2015Co-Authors: Malgorzata Karbownik-lewinska, Jan Stepniak, Magdalena Milczarek, Andrzej LewinskiAbstract:Purpose Iodine, bivalent iron (Fe^2+), and hydrogen peroxide (H_2O_2), all significantly affecting the red-ox balance, are required for thyroid hormone synthesis. Intracellular iodine excess (≥10^−3 M) transiently blocks thyroid hormonogenesis (an adaptive mechanism called Wolff–Chaikoff Effect). The aim of the study was to evaluate the Effects of iodine, used as potassium iodide (KI) or potassium iodate (KIO_3), in concentrations corresponding to those typical for Wolff–Chaikoff Effect, on the level of oxidative damage to nuclear DNA (nDNA) and mitochondrial DNA (mtDNA) isolated from porcine thyroid under basal conditions and in the presence of Fenton reaction (Fe^2++H_2O_2 → Fe^3++^·OH + OH^−) substrates. Methods Thyroid nDNA and mtDNA were incubated in the presence of either KI or KIO_3 (2.5–50 mM), without/with FeSO_4 (30 µM) + H_2O_2 (0.5 mM). Index of DNA damage, i.e., 8-oxo-7,8-dihydro-2′-deoxyguanosine, was measured by HPLC. Results Neither KI nor KIO_3 increased the basal level of 8-oxodG in both nDNA and mtDNA. KI—in all used concentrations—completely prevented the damaging Effect of Fenton reaction substrates in mtDNA, and it partially prevented this damage in nDNA. KIO_3 partially prevented Fe^2++H_2O_2-induced oxidative damage in both DNA only in its highest used concentrations (≥25 mM). Conclusions Without additional prooxidative abuse, both iodine compounds, i.e., KI and KIO_3, seem to be safe in terms of their potential oxidative damage to DNA in the thyroid. The superiority of KI over KIO_3 relies on its stronger protective Effects against oxidative damage to mtDNA, which constitutes an argument for its preferential utility in iodine prophylaxis.
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Protective Effect of KI in mtDNA in porcine thyroid: comparison with KIO3 and nDNA
European Journal of Nutrition, 2014Co-Authors: Malgorzata Karbownik-lewinska, Jan Stepniak, Magdalena Milczarek, Andrzej LewińskiAbstract:Purpose Iodine, bivalent iron (Fe2+), and hydrogen peroxide (H2O2), all significantly affecting the red-ox balance, are required for thyroid hormone synthesis. Intracellular iodine excess (≥10−3 M) transiently blocks thyroid hormonogenesis (an adaptive mechanism called Wolff–Chaikoff Effect). The aim of the study was to evaluate the Effects of iodine, used as potassium iodide (KI) or potassium iodate (KIO3), in concentrations corresponding to those typical for Wolff–Chaikoff Effect, on the level of oxidative damage to nuclear DNA (nDNA) and mitochondrial DNA (mtDNA) isolated from porcine thyroid under basal conditions and in the presence of Fenton reaction (Fe2++H2O2 → Fe3++·OH + OH−) substrates.
Hosam J. Al-tamimi - One of the best experts on this subject based on the ideXlab platform.
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The Wolff–Chaikoff Effect ameliorates heat stress in rats
Animal Biotelemetry, 2019Co-Authors: Hosam J. Al-tamimi, Amani Al-dawood, Zainab MahasnehAbstract:Background The thyroid gland contributes immensely to the basal metabolic rate, and hence, thermogenesis in mammals. Its response to the thermal environment is, however, slow and may require several days to adjust. A rapid thyrosuppressive mechanism (“Wolff–Chaikoff” phenomenon; WC) is inducible by high dietary iodine ingestion. The current study aimed to examine the WC on thermophysiology of rats exposed to acute heat stress (HS). Biotelemetry was used to assess real-time core body temperature ( T _core), locomotive activity (LA) and heart rate (HR) in rats ( N = 12). Animals were randomly assigned to two treatment groups: a control (CN) group had ad libitum access to tap water throughout the trial; a second group (KI) received potassium iodide (0.5%) in drinking water, 3 h before HS. Climatic conditions during the 10-day experimental period were set to 4 days at thermoneutrality (TN; T _a = 23.60 ± 0.05 °C), then HS ( T _a = 33.22 ± 0.25 °C, for 4 h) and finally back to TN until the end of trial. Serum samples were collected right after the HS, to measure free thyroxine (FT4), triiodothyronine (FT3) and total antioxidant capacity (TAO), from 12 other equivalent rats. Results The KI induced the WC, as evidenced with lower FT3 (1.66 and 1.91 ± 0.08 pg/mL) than the CN treatment, respectively. This momentary goitrogenic response by KI mitigated hyperthermia, compared to CN ( T _core maxima of 38.90 and 39.54 ± 0.09 °C). Furthermore, KI resulted in higher TAO than KI-free rats (238.30 and 198.80 ± 9.10 µM copper reducing equivalents). While instigating an instant suppression in LA, KI caused a delayed 25% elevation in HR along with a rebound in T _core, likely due to the “escape phenomenon.” Conclusions The employed WC protocol alleviated HS impact on rats. Research on other mammals awaits further investigation.
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The Wolff–Chaikoff Effect ameliorates heat stress in rats
Animal Biotelemetry, 2019Co-Authors: Hosam J. Al-tamimi, Amani Al-dawood, Zainab MahasnehAbstract:The thyroid gland contributes immensely to the basal metabolic rate, and hence, thermogenesis in mammals. Its response to the thermal environment is, however, slow and may require several days to adjust. A rapid thyrosuppressive mechanism (“Wolff–Chaikoff” phenomenon; WC) is inducible by high dietary iodine ingestion. The current study aimed to examine the WC on thermophysiology of rats exposed to acute heat stress (HS). Biotelemetry was used to assess real-time core body temperature (Tcore), locomotive activity (LA) and heart rate (HR) in rats (N = 12). Animals were randomly assigned to two treatment groups: a control (CN) group had ad libitum access to tap water throughout the trial; a second group (KI) received potassium iodide (0.5%) in drinking water, 3 h before HS. Climatic conditions during the 10-day experimental period were set to 4 days at thermoneutrality (TN; Ta = 23.60 ± 0.05 °C), then HS (Ta = 33.22 ± 0.25 °C, for 4 h) and finally back to TN until the end of trial. Serum samples were collected right after the HS, to measure free thyroxine (FT4), triiodothyronine (FT3) and total antioxidant capacity (TAO), from 12 other equivalent rats. The KI induced the WC, as evidenced with lower FT3 (1.66 and 1.91 ± 0.08 pg/mL) than the CN treatment, respectively. This momentary goitrogenic response by KI mitigated hyperthermia, compared to CN (Tcore maxima of 38.90 and 39.54 ± 0.09 °C). Furthermore, KI resulted in higher TAO than KI-free rats (238.30 and 198.80 ± 9.10 µM copper reducing equivalents). While instigating an instant suppression in LA, KI caused a delayed 25% elevation in HR along with a rebound in Tcore, likely due to the “escape phenomenon.” The employed WC protocol alleviated HS impact on rats. Research on other mammals awaits further investigation.
