Abstract
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 (NaF). Cell morphology, viability, lactate dehydrogenase (LDH) leakage, apoptosis, and expression of inositol-requiring enzyme 1 (IRE1) pathway-related molecules were assessed. Results showed 50 mM of KI, 1 mM of NaF, and 50 mM of KI +1 mM of NaF changed cellular morphology, decreased viability, and increased LDH leakage and apoptosis. Elevated expression of binding protein (BiP), IRE1, and C/EBP homologous protein (CHOP) mRNA and protein, as well as spliced X-box-binding protein-1 (sXBP-1) mRNA, were observed in the 1 mM NaF and 50 mM KI +1 mM NaF groups. Collectively, excessive iodide and/or fluoride is cytotoxic to the human thyroid. Although these data do not manifest iodide could induce the IRE1 pathway, the cytotoxicity followed by exposure to fluoride alone or in combination with iodide may be related to IRE1 pathway-induced apoptosis. Furthermore, exposure to the combination of excessive iodide and fluoride may cause interactive effects on thyroid cytotoxicity.
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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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Role of endoplasmic reticulum stress-induced apoptosis in rat thyroid toxicity caused by excess fluoride and/or iodide
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
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[Effects of endoplasmic reticulum stress-induced apoptosis in thyroid injury caused by fluoride in rat].
Objective: To explore the effects of endoplasmic reticulum stress-induced apoptosis in thyroid injury of rats caused by excessive fluoride intake. Methods: All 40 Wistar rats were randomly divided into four groups, control group, low fluoride group, medium fluoride group and high fluoride group. The rats in control group were fed with
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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's Impact on Thyroid Hormones
Up through the 1950s, doctors in Europe and South America prescribed fluoride for this purpose in patients with hyperthyroidism. (Merck Index 1968). Fluoride was selected as a thyroid suppressant based on findings dating back to the mid-19th century that fluoride is a goitrogen (a substance that can cause goiter). When used as
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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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The Relationship Between Fluoride Exposure & Goitre in South Africa
As a general rule simple goitre, irrespective of the cause, can be very, or fairly, satisfactorily combated by an adequate increase in man's daily iodine intake, except when the enlargement of the gland is due to the ingestion of excessive amounts of fluorine. The only correct solution to fluorine-induced endemic goitre is the removal of this element from the drinking water.
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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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