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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Role of Some Natural Antioxidants in the Modulation of Some Proteins Expressions against Sodium Fluoride-Induced Renal Injury.
Background: The aim of the present work is to find the effects of N-acetylcysteine (NAC) and/or thymoquinone (THQ) in the protection against acute renal injury induced by sodium fluoride (NaF). Method: Rats were distributed into five groups: G1 was normal (control), G2 was intoxicated with 10mg/kg NaF i.p., G3 was treated
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Changes of acute harmful effects and fluoride kinetics after single intravenous injection of sub-toxic hydrofluoric acid in rats-Renal dysfunction, abnormal serum electrolytes, metabolic acidosis and fluoride kinetics.
Hydrofluoric acid (HFA) is used widely in many industrial processes. There have been many reports on the acute lethal effects of HFA in relation to occupational accidents. This study was designed to investigate the time-dependent harmful effects after exposure of sub-toxic doses. The serum fluoride ion (F) kinetics is also
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Ameliorative effects of quercetin on sodium fluoride-induced oxidative stress in rat's kidney
OBJECTIVE: The in vivo nephroprotective effect of quercetin against sodium fluoride (NaF)-induced damage was studied. METHODS: Renal injury was induced by daily administration of NaF (600 ppm) through drinking water for 1 week. The levels of reduced glutathione (GSH), lipid peroxidation as well as superoxide dismutase and catalase activity of
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Fluoride in drinking water exacerbates glomerulonephritis and induces liver damage in ICR-derived glomerulonephritis mice
To evaluate the effects of fluoride on the kidney and the liver of ICR-derived glomerulonephritis (ICGN) mice by using laboratory tests and pathological examinations, fluoride was administered to the ICGN mice at 0, 25, 50, 100, and 150 ppm in drinking water for 4 weeks and to the ICR mice,
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Changed cellular membrane lipid composition and lipid peroxidation of kidney in rats with chronic fluorosis
An animal model of chronic fluorosis was produced by subjecting Wistar rats to high doses of fluoride in drinking water for a prolonged period. Phospholipid and neutral lipid contents in rat kidney were then analyzed by high-performance liquid chromatography (HPLC), and fatty acid compositions from individual phospholipids were measured by
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Fluoride as a Cause of Kidney Disease in Animals
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 in
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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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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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