PLASMA INORGANIC IODIDE, A CHEMICAL REGULATOR OF NORMAL THYROID FUNCTION<sup>1</sup>

Wolff, J.; Chaikoff, I.L.

doi:10.1210/endo-42-6-468

Cited by 200 publications

(225 citation statements)

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“…Since its first description in 1937, the chemical analysis of iodide proposed by Sandell & Kolthoff (1937) was first applied to geological substrates such as rock, soil and water. Its application to human tissues and secretions became generalized about 40 y ago (Wolff & Chaikoff, 1948;Follis et al, 1962;Vought et al, 1964;Jolin & Escobar del Rey, 1965;Lauber, 1975;Bourdoux, 1988;Bürgi et al, 1990;Als et al, 1995;Haldimann et al, 1998) and several modes of presentation have been used for reporting data about iodine output. When precise 24 h urine collections could be obtained, iodine output was presented as an excretion in mg I/day or better mg I/24h.…”

Section: Introductionmentioning

confidence: 99%

Quantification of urinary iodine: a need for revised thresholds

et al. 2003

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Objective: To compare different possibilities of reporting the iodine supply in the same urine samples. Indeed, in field studies, urinary iodine concentration (I/L: mg I/L, mmol I/L, I/creatinine: mg I/g creatanine, mmol I/mol creatinine) is more readily available than excretion (I/24h mg I/24 h, mmol I/24h). However, confusion exists regarding the comparability of iodine supply based upon I/L, I/creatinine and I/24h, which for decades have been regarded as biochemically equivalent. Design: We compared I/24h, I/L and I/creatinine in accurate 24 h collections of urine and I/L and I/creatinine in 47 spot urine samples. Patients: A total of 13 subjects (Bern n ¼ 7, Brussels n ¼ 6) collected a total of 110 precise 24 h urine collections (Bern n ¼ 63, Brussels n ¼ 47). The subjects from Brussels also took a spot sample at the beginning of each 24 h collection. Results: Iodine supply in both places was mildly deficient according to the criteria of WHO; all but one collection indicated an intake of 40.39 mmol I/24h (450 mg I/24h). The same data presented as I/creatinine (or I/L) indicated an iodine intake of o0.39 (o50 mg I/24h) in 5% (24%) of the samples in Bern and 23% (57%) in Brussels. Similar findings were observed for 47 spot samples. Whatever the cut-off selected, I/creatinine and I/L were systematically lower than I/24h (Po0.0002). Creatinine showed smaller CV than volume but did not perform better in defining iodine intake. Conclusion: Considering I/24h as a reference, both I/creatinine and I/L clearly underestimate the iodine intake in subjects with adequate proteoenergetic intake. The significant deviations observed illustrate the urgent need for establishing separate ranges for I/24h, I/creatinine and I/L. In population studies, these deviations might even be larger.

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Section: Introductionmentioning

confidence: 99%

Quantification of urinary iodine: a need for revised thresholds

et al. 2003

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“…The inhibition of iodine organification is called the Wolff-Chaikoff (W-C) effect. Wolff and Chaikoff (22) and Wolff et al (23) further demonstrated that when rats maintained high levels of serum iodine for > 40 hr, the inhibition of iodine on organification in the thyroid ceased and the thyroid resumed its normal rate of hormone synthesis, preserving the euthyroid state.…”

Section: Thyroid Effects Of Excess Iodine Ingestionmentioning

confidence: 98%

Use of iodine for water disinfection: iodine toxicity and maximum recommended dose.

Backer

Hollowell

2000

Environ Health Perspect

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Iodine is an effective, simple, and cost-efficient means of water disinfection for people who vacation, travel, or work in areas where municipal water treatment is not reliable. However, there is considerable controversy about the maximum safe iodine dose and duration of use when iodine is ingested in excess of the recommended daily dietary amount. The major health effect of concern with excess iodine ingestion is thyroid disorders, primarily hypothyroidism with or without iodine-induced goiter. A review ofthe human trials on the safety ofiodine ingestion indicates that neither the maximum recommended dietary dose (2 mg/day) nor the mum recommended duration of use (3 weeks) has a firm basis. Rather than a clear threshold response level or a linear and temporal dose-response relationship between iodine intake and thyroid function, there appears to be marked individual sensitivity, often resulting from unmasking ofunderlying thyroid disease. The use of iodine for water disinfection requires a risk-benefit decision based on iodine's benefit as a disinfectant and the changes it induces in thyroid physiology. By using appropriate disinfection techniques and monitoring thyroid finction, most people can use iodine for water treatment over a prolonged period of time. Key worni goiter, iodine, thyroid disorders, thyroid hormones, water purification, water supply.

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“…Based on the expectation that the genomic organisation of human NIS (hNIS) would be highly homologous to rNIS, Smanik et al (1996) isolated cDNA encoding hNIS using primers to the cDNA/rNIS sequence [10]. The cDNA sequence predicted that rNIS was a 618 amino acid protein with a relative molecular mass of 65,196. Elucidation of the secondary structure of NIS protein was facilitated by the generation of a high affinity sitedirected polyclonal anti-NIS antibody (Ab) against the last 16 amino acids of the COOH terminus [11].…”

Section: Molecular Characterisation Of Nismentioning

confidence: 99%

“…Inhibition of thyroid function following administration of large doses of iodide is well-known. Wolff and Chaikoff (1948) first reported that iodide organification in the rat thyroid was blocked when plasma levels of iodide reached a critical high threshold, a phenomenon known as the acute Wolff-Chaikoff effect [65]. In the following year, Raben et al (1949) showed that this could be prevented with the administration of thiocyanate, a competitive inhibitor of iodide uptake, suggesting that the phenomenon was dependent on the intrathyroidal rather than the plasma concentration of iodide [66].…”

Section: Effect Of Iodide Therapy On Nis Functionmentioning

confidence: 99%

The Biology of the Sodium Iodide Symporter and its Potential for Targeted Gene Delivery

Hingorani¹

2010

CCDT

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The sodium iodide symporter (NIS) is responsible for thyroidal, salivary, gastric, intestinal and mammary iodide uptake. It was first cloned from the rat in 1996 and shortly thereafter from human and mouse tissue. In the intervening years, we have learned a great deal about the biology of NIS. Detailed knowledge of its genomic structure, transcriptional and post-transcriptional regulation and pharmacological modulation has underpinned the selection of NIS as an exciting approach for targeted gene delivery. A number of in vitro and in vivo studies have demonstrated the potential of using NIS gene therapy as a means of delivering highly conformal radiation doses selectively to tumours. This strategy is particularly attractive because it can be used with both diagnostic ( 99m Tc, 125 I, 124 I) and therapeutic ( 131 I, 186 Re, 188 Re, 211 At) radioisotopes and it lends itself to incorporation with standard treatment modalities, such as radiotherapy or chemoradiotherapy. In this article, we review the biology of NIS and discuss its development for gene therapy.

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PLASMA INORGANIC IODIDE, A CHEMICAL REGULATOR OF NORMAL THYROID FUNCTION¹

Cited by 200 publications

References 0 publications

Quantification of urinary iodine: a need for revised thresholds

Quantification of urinary iodine: a need for revised thresholds

Use of iodine for water disinfection: iodine toxicity and maximum recommended dose.

The Biology of the Sodium Iodide Symporter and its Potential for Targeted Gene Delivery

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PLASMA INORGANIC IODIDE, A CHEMICAL REGULATOR OF NORMAL THYROID FUNCTION1

Cited by 200 publications

References 0 publications

Quantification of urinary iodine: a need for revised thresholds

Quantification of urinary iodine: a need for revised thresholds

Use of iodine for water disinfection: iodine toxicity and maximum recommended dose.

The Biology of the Sodium Iodide Symporter and its Potential for Targeted Gene Delivery

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Product

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PLASMA INORGANIC IODIDE, A CHEMICAL REGULATOR OF NORMAL THYROID FUNCTION¹