Topic
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.
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TL;DR: Seven per cent of individual urine samples indicated severe iodine deficiency without this being present in the group studied, and Dispersion was reduced by 24% when using estimated 24 h urinary iodine excretion rather than urinary iodine concentration.
Abstract: Objective: The iodine intake level in a population is determined in cross-sectional studies. A fraction of samples with iodine content below a certain level, e.g. 25 mg/l, may suggest iodine deficiency in part of the population. However, urinary iodine varies considerably from day to day and the fraction of low samples caused by dispersion remains unsettled. Design: A longitudinal study of 16 healthy men living in an area of mild to moderate iodine deficiency. Methods: We measured urinary iodine and creatinine concentrations, and serum TSH, total thyroxine (T4), free T4 index and total tri-iodothyronine (T3) in samples collected monthly for 1 year. Results: Average urinary iodine excretion was 57.0 mg/l (49.1 mg/24 h (corrected for creatinine excretion)) and varied from 29 to 81 mg/l (28 to 81 mg/24 h) between participants. Individual samples varied between 10 and 260 mg/l, and the variation around the mean was 2.4 times larger when calculated for the 180 individual samples compared with the 15 average annual values (1.7 times larger for estimated 24 h iodine excretion values). The fraction of individual samples below 25 mg/l was 6.7% (7.2% ,25 mg/24 h), whereas none of the participants had average iodine excretion below 25 mg/l or 25 mg/24 h. Participants with average annual iodine excretion below 50 mg/24 h had a negative correlation between iodine excretion and TSH, whereas a positive correlation was observed when average annual iodine excretion was above this level. Conclusions: Seven per cent of individual urine samples indicated severe iodine deficiency without this being present in the group studied. Dispersion was reduced by 24% when using estimated 24 h urinary iodine excretion rather than urinary iodine concentration. Participants with moderate iodine deficiency (average annual urinary iodine excretion 25‐50 mg/24 h) showed clear signs of substrate deficiency for thyroid hormone synthesis while participants with mild iodine deficiency (50‐100 mg/ 24 h) did not.
98 citations
98 citations
TL;DR: It was found that the gradieni, remained constant when doses up to 100 ng.
Abstract: The thyroid gland of an animal chronically treated with a thiouracillike drug, although unable to manufacture thyroid hormone, manifests a remarkable ability to collect and concentrate the iodide ion (Vanderlaan and Vanderlaan, 1947; Taurog, Chaikoff, and Feller, 1947). About one hour after the subcutaneous administration of iodide in rats the thyroid exhibits an average concentration gradient of 250 over the serum. Taurog, Chaikoff, and Feller (1947) noted this ratio to be unchanged when 2 μg. or 100 μg. of iodide were given to adult rats. Vanderlaan and Vanderlaan (1947) found that the gradieni, remained constant when doses up to 100 ng. of potassium iodide were administered in young rats, but that when larger quantities were given it diminished progressively. However, even when 10,000 μg. were given the. gradient was not abolished completely, a concentration of 3 fold persisting in favor of the gland.
98 citations
TL;DR: Of the variables tested, sea surface temperature is the strongest predictor of iodide concentration, but chlorophyll-a was not, and Nitrate was also strongly inversely associated with iodide concentrations, but chlorine was not.
Abstract: Recent studies have highlighted the impact of sea surface iodide concentrations on the deposition of ozone to the sea surface and the sea to air flux of reactive iodine. The use of models to predict this flux demands accurate, spatially distributed sea surface iodide concentrations, but to date, the observational data required to support this is sparse and mostly arises from independent studies conducted on small geographical and temporal scales. We have compiled the available measurements of sea surface iodide to produce a data set spanning latitudes from 69°S to 66°N, which reveals a coherent, large scale distribution pattern, with highest concentrations observed in tropical waters. Relationships between iodide concentration and more readily available parameters (chlorophyll, nitrate, sea surface temperature, salinity, mixed layer depth) are evaluated as tools to predict iodide concentration. Of the variables tested, sea surface temperature is the strongest predictor of iodide concentration. Nitrate was also strongly inversely associated with iodide concentration, but chlorophyll-a was not.
98 citations
TL;DR: Selenium deficiency coupled to iodine deficiency increased necrosis, induced fibrosis and impeded compensatory epithelial cell proliferation, compatible with histological and functional description of thyroid tissue from myxoedematous cretins.
Abstract: It has been suggested that selenium deficiency is a co-factor to iodine deficiency in the pathogenesis of myxoedematous cretinism. The mechanism proposed is that the generation of hydrogen peroxide is greatly increased in iodine-deficient thyroid glands, and that selenium is involved in the control of hydrogen peroxide and its derived free radicals. This study was carried out to investigate the effect of the possibly impaired cellular defence mechanism associated with selenium deficiency on thyroid necrosis and tissue repair. For this purpose, we studied thyroid tissue from selenium- (SE-) and/or iodine-deficient (I-) rats before and after an acute toxic iodine overload. In I- thyroids, necrotic cells were numerous. Acute iodine administration increased this effect. Necrosis was associated with transient infiltration of inflammatory cells. In I-SE+ thyroids the tissue resumed its normal appearance. In I-SE- thyroid glands, the iodide toxicity was stronger, with greater necrosis and inflammatory reaction. The inflammation resolved but was replaced by fibrotic tissue. Fifteen days after the toxic overload, the connective tissue volume was twice the control value. Before iodide overload, the proportion of dividing cells was equal in I-SE+ and I-SE- thyroids. Three days after the iodide overload, this proportion was increased in I-SE+ thyroids but reduced in the I-SE- thyroids. Overall, the I-SE- thyroids had four times fewer dividing cells than the I-SE+ thyroids. In summary, selenium deficiency coupled to iodine deficiency increased necrosis, induced fibrosis and impeded compensatory epithelial cell proliferation. These results are compatible with histological and functional description of thyroid tissue from myxoedematous cretins.
98 citations