Abstract
Excess fluoride and iodide coexist in drinking water in many regions, but few studies have investigated the single or interactive effects on thyroid in vivo. In our study, Wistar rats were exposed to excess fluoride and/or iodide through drinking water for 2 or 8 months. The structure and function of the thyroid, cells apoptosis and the expression of inositol-requiring enzyme 1 (IRE1) pathway-related factors were analyzed. Results demonstrated that excess fluoride and/or iodide could change thyroid follicular morphology and alter thyroid hormone levels in rats. After 8 months treatment, both single and co-exposure of the two microelements could raise the thyroid cells apoptosis. However, the expressions of IRE1-related factors were only increased in fluoride-alone and the combined groups. In conclusion, thyroid structure and thyroid function were both affected by excess fluoride and/or iodide. IRE1-induced apoptosis were involved in this cytotoxic process caused by fluoride or the combination of two microelements.
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The role of the IRE1 pathway in excessive iodide- and/or fluoride-induced apoptosis in Nthy-ori 3-1 cells in vitro
Excessive iodide and fluoride coexist in the groundwater in many regions, causing a potential risk to the human thyroid. To investigate the mechanism of iodide- and fluoride-induced thyroid cytotoxicity, human thyroid follicular epithelial cells (Nthy-ori 3-1) were treated with different concentrations of potassium iodide (KI), with or without sodium fluoride
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Fluoride-induced thyroid cell apoptosis
In addition to causing skeletal and dental fluorosis, fluoride (F) in drinking water may damage other organs including the thyroid. The objective of this study was to explore the toxicity of F on immortalized human normal thyroid cells (Nthy-ori 3-1) exposed to 0, 0.1, 1, and 3 mmol/L of sodium
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The effects and underlying mechanism of excessive iodide on excessive fluoride-induced thyroid cytotoxicity
In many regions, excessive fluoride and excessive iodide coexist in groundwater, which may lead to biphasic hazards to human thyroid. To explore fluoride-induced thyroid cytotoxicity and the mechanism underlying the effects of excessive iodide on fluoride-induced cytotoxicity, a thyroid cell line (Nthy-ori 3-1) was exposed to excessive fluoride and/or excessive
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Effects of fluoride on the ultrastructure of glandular epithelial cells of human fetuses.
Objective Ultrastructural changes in epithelial cells of livers, adrenal glands, and thyroid glands of human fetuses from a fluorosis-endemic area were observed to provide an experimental basis for investigating the mechanism by which fluoride causes cellular damage. Methods 10 human fetuses in a fluorosis-endemic area were collected, whose mothers all had
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Inhibition of thyroid secretion by sodium fluoride in vitro
NaF mimicked the activation by thyrotropin of iodide binding to proteins and of glucose C-r oxidation but not the accumulation of intracellular colloid droplets or the stimulation of secretion in dog thyroid slices in vitro. On the contrary, NaF inhibited the two latter thyrotropin effects. The inhibitory action of F-
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Fluoride, Water Hardness, and Endemic Goitre
Variations in goitre prevalence were found to correlate closely with the fluoride content (p=0-74; P<0-01) and with the hardness (p=0.77; P<0-01) of the water in each village. The effects of fluoride and water hardness seem to be independent.
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Fluorine in the Aetiology of Endemic Goitre
The distribution of endemic goitre in the Punjab and in England is related to the geological distribution of fluorine and to the distribution of human dental fluorosis (mottled enamel). Inquiry showed the presence of dental fluorosis among school-children in two areas of Somerset where two previous observers had recorded a high incidence of goitre, and the absence of dental fluorosis in an adjoining area selected as control where endemic goitre was absent.
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Is fluoride-induced hyperthyroidism a cause of psychosis among East African immigrants to Scandinavia?
When people with a compensated fluoride-induced hypothyroidism move to a low-fluoride area, the fluoride-induced inhibition of the production of thyroid hormones ceases. In Scandinavia, the dietary intake of iodine is usually quite high due to iodized table salt and easy access to marine fish. Under these conditions, the elevated capacity for production of thyroid hormones may result in hyperthyroidism.
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Fluoride Exposure Aggravates the Impact of Iodine Deficiency
A consistent body of animal and human research shows that fluoride exposure worsens the impact of an iodine deficiency. Iodine is the basic building block of the T3 and T4 hormones and thus an adequate iodine intake is essential for the proper functioning of the thyroid gland. When iodine intake is inadequate during infancy and
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Mikhailets (1996): Functional state of thyroid under extended exposure to fluorides
Abnormalities in the thyroid function characterized by a decreased iodine absorption function of the thyroid, a low level T3 syndrome, and a slight increase of the TSH level are observed in cases of chronic fluorine intoxication in the industrial workers.
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