Abstract
SUMMARY: Adult female Wistar rats were treated daily for 60 days with sodium fluoride (500 ppm NaF = 226 ppm fluoride ion) in drinking water, alone or in combination with vitamin D (200 IU/kg by oral intubation). Throughout the period, food intake was measured daily. Body weight gain, exploratory motor activity (EMA) rota-rod motor coordination, dental structure, brain acetylcholinesterase (AchE) activity, and serum fluoride and serum calcium concentration were determined 24 hr after the last treatment. Serum fluoride concentration increased markedly in the NaF-treated animals and was accompanied by decreased food intake, reduced body weight gain, impairment of EMA and motor coordination, dental lesions, inhibition of brain AchE activity, and hypocalcemia. Administration of vitamin D along with NaF prevented hypocalcemia. However, the toxic action fluoride on motor coordination, brain AchE activity, and the teeth was not prevented in these animals, probably because vitamin D is not able to decrease the level of fluoride in the serum. Therefore, vitamin D has only limited value as a protective dietary factor against chronic toxic effects of fluoride.
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Modulation of fluoride toxicity in rats by calcium carbonate and by withdrawal of fluoride exposure.
In order to assess the effect of calcium on the toxic effects of fluoride, adult female Wistar rats were treated with sodium fluoride (NaF, 500 ppm in drinking water) alone or in combination with calcium carbonate (CaCO3, 50 mg/kg by oral intubation) daily for 60 days. Food, water and fluoride
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Renal osteodystrophy in patients on long-term hemodialysis with fluoridated water
Serum and bone fluoride concentrations of ten patients maintained on long-term hemodialysis with fluoridated water (1 ppm, i.e., 50uM) were correlated with duration of treatment and the occurrence of clinical, radiological, and histological manifestations of bone disease. Two patients had symptomatic renal osteodystrophy when accepted on the program, whereas six
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The association of fluoride in drinking water with serum calcium, vitamin D and parathyroid hormone in pregnant women and newborn infants.
Background: Chronic exposure to fluoride in drinking water causes an increase in plasma fluoride levels that is related to a reduction in calcium transport across the renal tubule endoplasmic reticulum and plasma membrane. In the present study, it was hypothesised that varying levels of fluoride present in drinking
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Non-Endemic Skeletal Fluorosis: Causes And Associated Secondary Hyperparathyroidism (Case Report and Literature Review).
Highlights Fluorocarbon “huffing” is an under-appreciated cause of skeletal fluorosis (SF) We present a SF case with hyperparathyroidism, osteosclerosis, and osteomalacia SF may go undetected due to variation in symptoms, radiology, and biochemistry Dietary calcium, prior bone health, and skeletal F exposure influence SF features SF is common in
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Environmental Fluoride 1977 by Rose & Marier
The Associate Committee on Scientific Criteria for Environmental Quality was established by the National Research Council of Canada in response to a mandate provided by the Federal Government to develop scientific guidelines for defining the quality of the environment. The concern of the NRC Associate Committee is strictly with scientific
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Nutrient Deficiencies Enhance Fluoride Toxicity
It has been known since the 1930s that poor nutrition enhances the toxicity of fluoride. As discussed below, nutrient deficiencies have been specifically linked to increased susceptibility to fluoride-induced tooth damage (dental fluorosis), bone damage (osteomalacia), neurotoxicity (reduced intelligence), and mutagenicity. The nutrients of primary importance appear to be calcium,
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Fluoride's Effect on Fetal Brain
The human placenta does not prevent the passage of fluoride from a pregnant mother's bloodstream to the fetus. As a result, a fetus can be harmed by fluoride ingested pregnancy. Based on research from China, the fetal brain is one of the organs susceptible to fluoride poisoning. As highlighted by the excerpts
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Fluoride Exposure Increases Metabolic Requirement for Magnesium
Fluoride's toxicity is significantly enhanced in the presence of nutritional deficiencies. Similarly, fluoride exposure increases the body's requirement for certain nutrients. An individual with a high intake of fluoride, for example, will need a proportional increase in calcium to avoid the mineralization defects (e.g., osteomalacia) that fluoride causes to bone
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Mayo Clinic: Fluoridation & Bone Disease in Renal Patients
The available evidence suggests that some patients wtih long-term renal failure are being affected by drinking water with as little as 2 ppm fluoride. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers and if fluoride is indeed the cause. It would seem prudent, therefore, to monitor the fluoride intake of patients with renal failure living in high fluoride areas.
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Fluoride Is Not an Essential Nutrient
In the 1950s, dentists believed that fluoride was a “nutrient.” A nutrient is a vitamin or mineral that is necessary for good health. Dentists believed that fluoride ingestion during childhood was necessary for strong, healthy teeth. A “fluoride deficiency” was thus believed to cause cavities, just like a deficiency of calcium can
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