Abstract
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- was partially relieved by the addition of glucose to the medium; it was mimicked by sodium oxamate. These data suggest that NaF depresses the endocytosis of colloid and thyroid secretion by inhibiting aerobic glycolysis in the follicular cell. NaF inhibited the activation of colloid droplet accumulation and secretion by N6,O2-dibutyryladenosine 3′,5′-monophosphate (dibutyryl cyclic AMP) and the accumulation of cyclic AMP in thyrotropin-stimulated slices. This suggests an inhibition at the level of both cyclic AMP accumulation and cyclic AMP action. The inhibition by NaF and sodium oxamate of colloid droplet formation and thyroid secretion but not of glucose C-r oxidation in stimulated slices further confirms our conclusion that the latter effect is not merely a consequence of the activation by thyrotropin of colloid endocytosis.
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Comparison of the effects of various agents on thyroidal adenyl cyclase activity with their effects on thyroid hormone release
Intact mouse thyroid glands were used to measure the formation of cyclic [3H]AMP from [3H]adenine, and the release of thyroidal iodine. These two parameters of thyroid activity responded to similar concentrations of thyroid-stimulating hormone (TSH). Both were stimulated by prostaglandin E1, although the response was always very much less than
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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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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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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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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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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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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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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 Aggravates Thyroid Damage Caused by Excess Iodine Intake
Chinese researchers have found that the combination of excess fluoride with excess iodine caused greater reductions in IQ, or greater increases in goitre than either scenario by itself.
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