Abstract
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 iodide. Cell viability, lactate dehydrogenase (LDH) leakage, reactive oxygen species (ROS) formation, apoptosis, and the expression levels of inositol-requiring enzyme 1 (IRE1) pathway-related molecules were detected. Fluoride and/or iodide decreased cell viability and increased LDH leakage and apoptosis. ROS, the expression levels of glucose-regulated protein 78 (GRP78), IRE1, C/EBP homologous protein (CHOP), and spliced X-box-binding protein-1 (sXBP-1) were enhanced by fluoride or the combination of the two elements. Collectively, excessive fluoride and excessive iodide have detrimental influences on human thyroid cells. Furthermore, an antagonistic interaction between fluoride and excessive iodide exists, and cytotoxicity may be related to IRE1 pathway-induced apoptosis.
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DNA damage in thyroid gland cells of rats exposed to long-term intake of high fluoride and low iodine.
Thirty-two one-month-old Wistar albino rats were divided randomly into four equal groups of eight (female:male = 3:1). To assess damage to DNA in their thyroid gland cells, the first group (1) of rats served as the untreated control, the second group (2) was administered a high concentraiton of fluoride (HiF,
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Synergistic action of iodine-deficiency and fluorine-intoxication on rat thyroid.
212 Wistar rats were divided randomly into five groups, each of which was fed on one of the following regimes: (1) Normal iodine and fluorine; (2) normal iodine, 10 ppm fluorine; (3) normal iodine, 30 ppm fluorine; (4) now iodine, normal fluorine; (5) low iodine, 10 ppm fluorine. The experiment
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Epigallocatechin gallate potentially attenuates fluoride induced oxidative stress mediated cardiotoxicity and dyslipidemia in rats
The present study was undertaken to evaluate the cardioprotective role of (-)-epigallocatechin-gallate (EGCG) against Fluoride (F) induced oxidative stress mediated cardiotoxicity in rats. The animals exposed to F as sodium Fluoride (NaF) (25mg/kg BW) for 4 weeks exhibited a significant increase in the levels of cardiac troponins T and I
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Long-term effects of various iodine and fluorine doses on the thyroid and fluorosis in mice
OBJECTIVE: To elucidate the participation of the independent and combined long term effect of various concentrations of iodine and fluorine on the pathogenesis of goiter and fluorosis in mice. METHODS: Nine drinking water supplies with different iodine and fluorine content were prepared by combination of potassium iodate and sodium fluoride solutions in bidistilled
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NADPH oxidase participates in the oxidative damage caused by fluoride in rat spermatozoa. Protective role of a-tocopherol
Fluorosis, caused by drinking water contaminated with inorganic fluoride, is a public health problem in many areas around the world. The aim of this study was to evaluate oxidative stress in spermatozoa caused by fluoride and NADPH oxidase in relationship to fluoride. Four experimental groups of male Wistar rats were
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Fluoride, Water Hardness, and Endemic Goitre
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Fluoride & Oxidative Stress
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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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