Iodine

About: Iodine is a research topic. Over the lifetime, 8936 publications have been published within this topic receiving 139981 citations. The topic is also known as: I & element 53.

Fluoride Exposure Induces Inhibition of Sodium/Iodide Symporter (NIS) Contributing to Impaired Iodine Absorption and Iodine Deficiency: Molecular Mechanisms of Inhibition and Implications for Public Health

Abstract: The sodium iodide symporter (NIS) is the plasma membrane glycoprotein that mediates active iodide transport in the thyroid and other tissues, such as the salivary, gastric mucosa, rectal mucosa, bronchial mucosa, placenta and mammary glands. In the thyroid, NIS mediates the uptake and accumulation of iodine and its activity is crucial for the development of the central nervous system and disease prevention. Since the discovery of NIS in 1996, research has further shown that NIS functionality and iodine transport is dependent on the activity of the sodium potassium activated adenosine 5′-triphosphatase pump (Na+, K+-ATPase). In this article, I review the molecular mechanisms by which F inhibits NIS expression and functionality which in turn contributes to impaired iodide absorption, diminished iodide-concentrating ability and iodine deficiency disorders. I discuss how NIS expression and activity is inhibited by thyroglobulin (Tg), tumour necrosis factor alpha (TNF-α), transforming growth factor beta 1 (TGF-β1), interleukin 6 (IL-6) and Interleukin 1 beta (IL-1β), interferon-γ (IFN-γ), insulin like growth factor 1 (IGF-1) and phosphoinositide 3-kinase (PI3K) and how fluoride upregulates expression and activity of these biomarkers. I further describe the crucial role of prolactin and megalin in regulation of NIS expression and iodine homeostasis and the effect of fluoride in down regulating prolactin and megalin expression. Among many other issues, I discuss the potential conflict between public health policies such as water fluoridation and its contribution to iodine deficiency, neurodevelopmental and pathological disorders. Further studies are warranted to examine these associations.

Strong association of high urinary iodine with thyroid nodule and papillary thyroid cancer

Abstract: This study demonstrates a strong association of high urinary iodine with thyroid nodules and papillary thyroid cancer as well as aggressive cancer features, suggesting that high urinary iodine is a risk factor for thyroid cancer. The risk of high iodine intake for thyroid cancer has been suggested but not established. The objective of the study was to evaluate the relationship between urine iodine levels and thyroid nodule and thyroid cancer. We preoperatively tested fasting urine iodine in 154 thyroid nodule patients and correlated the results with pathological diagnoses and compared with 306 subjects as normal control. The median urine iodine (MUI) was 331.33 μg/L in patients with benign thyroid nodules versus 466.23 μg/L in patients with papillary thyroid cancer (PTC) (P = 0.003), both of which were in the excessive iodine state and higher than the MUI of 174.30 μg/L in the control group (P 300 μg/L) was seen in 62.75 % of patients with benign thyroid nodules and 66.99 % of patients with PTC, both of which were significantly higher than the iodine excessive rate of 19.93 % in the control group (P < 0.001). Moreover, MUI in patients with PTC with lymph node metastasis was significantly higher than that of PTC patients without lymph node metastasis (P < 0.001). Urine iodine of thyroid cancer patients with stage III and IV disease was significantly higher than that of patients with stage I and II diseases (P < 0.001). Multivariable analyses showed that, like sand calcification of thyroid nodule and TSH, urine iodine was an independent risk factor for PTC. These data demonstrate a significant association between high urinary iodine and benign and malignant thyroid nodules and PTC aggressiveness, supporting high urinary iodine as a risk factor for thyroid malignancy. Further studies are warranted to confirm these findings.

Rapid urinary iodide test.

Abstract: Assessment of iodine deficiency and monitoring of iodine supplementation programs demand rapid, simple, and cost-effective methods for the determination of urinary iodide concentrations. We propose a semiquantitative rapid test, based on the iodide-catalyzed oxidation of 3,3′,5,5′-tetramethylbenzidine by peracetic acid/H2O2, to yield colored products. The color of the chemical reaction is compared with color categories of a pictogram corresponding to three ranges: 300μ g/L ( 2.36 μmol/L) of iodide concentrations. The test is very easy to perform and does not require any instrumentation or apparatus. Sample preparation is simple and consists of the removal of interfering substances by disposable columns, 65 × 10.5 mm, packed with purified activated charcoal. For comparison with a reference method for measuring urinary iodide, by high-performance liquid chromatography, we determined the iodide concentrations of 370 random (untimed) urine samples from consecutive pat...

The effect of propylthiouracil on the conversion of monoiodotyrosine to diiodotyrosine.

Abstract: The ratio of monoiodotyrosine to diiodot3Tosine (MIT⁄DIT) and triiodothyronine to thyroxine (T3⁄T4) was increased by feeding rats propylthiouracil before the injection of I131. This change occurred even when the uptake of I131 by he thyroid had returned to normal by allowing 24 hours or more to elapse after stopping propylthiouracil or by using small amounts of propylthiouracil. A depletion of total iodine in the gland was not the cause since the MIT⁄DIT remained elevated when total iodine was preserved by adding thyroid to propylthiouracil. A high thyrotropin did not account for the result since the added thyroid would have suppressed this. A high intrathyroidal iodide was not the explanation sincethe addition of KSCN made no difference. Thyroid alone increased MIT⁄DIT probably by inhibiting the thyrotropin essential to the conversion of monoiodotyrosine to diiodotyrosine. The results indicated that the conversion of monoiodotyrosine to diiodotyrosine was more sensitive to propylthiouracil than the iodin...