Abstract
Mineral balance studies were performed to clarify the mechanism of the development of renal calcification and its prevention by dietary fluoride (0.1% as NaF) in KK mice fed a low magnesium (0.04% ) diet. Upon feeding the diet, the product of urinary calcium and phosphorus concentrations showed a 10-fold increase which was due to a marked rise of the urinary phosphorus concentration. The same phenomenon was also observed in ICR mice which did not develop renal calcification. Therefore, the inherited high susceptibility to renal calcification of KK mice was explicable by a lowered threshold level of the product in the crystal formation of calcium phosphate salt. Supplemental fluoride inhibited the rise of the concentration product, which may partly be responsible for the prevention of the development of renal calcification. The action of fluoride was based on a depressed urinary phosphorus excretion and also a dilution of the excreted calcium and phosphorus by a fluoride-induced polyuria. The diuretic action of fluoride was evidenced by an increased urinary volume, sodium excretion and a decreased osmolality. Feeding the low magnesium diet caused a hyperpotassemia without changes in heart potassium. The hyperpotassemia was prevented by a smaller amount of fluoride than that required for the prevention of renal calcification.
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Effects of melatonin and epiphyseal proteins on fluoride-induced adverse changes in antioxidant status of heart, liver, and kidney of rats
Several experimental and clinical reports indicated the oxidative stress-mediated adverse changes in vital organs of human and animal in fluoride (F) toxicity. Therefore, the present study was undertaken to evaluate the therapeutic effect of buffalo (Bubalus bubalis) epiphyseal (pineal) proteins (BEP) and melatonin (MEL) against F-induced oxidative stress in heart,
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Sodium fluoride induces apoptosis in the kidney of rats through caspase-mediated pathways and DNA damage
Long-term excessive sodium fluoride (NaF) intake can cause many bone diseases and nonskeletal fluorosis. The kidneys are the primary organs involved in the excretion and retention of NaF. The objective of the present study was to determine the effects of NaF treatment on renal cell apoptosis, DNA damage, and the
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The mitochondrial pathway is involved in sodium fluoride (NaF)-induced renal apoptosis in mice.
The objective of the present study was to explore the molecular mechanism of apoptosis induced by sodium fluoride (NaF) in the mouse kidney by using the methods of flow cytometry, quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, and experimental pathology. 240 four-week-old ICR mice were randomly divided into 4
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The Influence of fluoride on chronic kidney disease of uncertain aetiology (CKDu) in Sri Lanka.
Fluoride is an element that is widely distributed in the environment. The involvement of fluoride in pathogenesis of Chronic Kidney Disease of uncertain aetiology (CKDu) in Sri Lanka is a much-debated topic. This study aimed to investigate the fluoride concentration in drinking water in CKDu affected areas in Sri Lanka
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Medical aspects of excessive fluoride in a water supply
A 10-year study of 116 persons in Bartlett and 121 in Cameron, Tex., was conducted to determine if prolonged exposure to fluoride in the water supply of Bartlett had produced detectable physiological effects. Bartlett's water contained about 8 p.p.m. F until 1952, when an experimental defluoridation unit was installed, reducing the
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Fluoridation of drinking water and chronic kidney disease: Absence of evidence is not evidence of absence
A fairly substantial body of research indicates that patients with chronic renal insufficiency are at an increased risk of chronic fluoride toxicity. Patients with reduced glomerular filtration rates have a decreased ability to excrete fluoride in the urine. These patients may develop skeletal fluorosis even at 1 ppm fluoride in the drinking water.
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Fluoride Gels & Kidney Function
Scientists have found that the application of "Fluoride Gels" at the dental office causes very high spikes in the blood fluoride level. The high spikes in blood fluoride levels are a result of three factors: the high concentration of fluoride in the gel (= 12.3 mg of fluoride in each
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Fluoride as a Cause of Kidney Disease in Humans
Because the kidney is exposed to higher concentrations of fluoride than all other soft tissues (with the exception of the pineal gland), there is concern that excess fluoride exposure may contribute to kidney disease - thus initiating a "vicious cycle" where the damaged kidneys increase the accumulation of fluoride, causing
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Kidney: A potential target for fluoride toxicity
The kidneys are the organ responsible for clearing fluoride from the body. In the process of doing so, the kidneys are exposed to concentrations of fluoride that exceed, by a factor of 50, the concentration of fluoride in human blood. As such, the kidney have long been considered a potential
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Fluoride & Kidney Stones
It has long been suspected that fluoride may contribute to the formation of kidney stones. This suspicion has recently gained support from a study of an American man with skeletal fluorosis. According to the authors: "A new, important, medical problem (that seemed temporally related to cessation of fluoride exposure and subsequent negative calcium
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