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.

• Related Studies :

  • Fluoride-induced histopathology and synthesis of stress protein in liver and kidney of mice

    Selective low (15 mg sodium fluoride (NaF)/L) and relatively high (150 mg NaF/L) doses of in vivo fluoride (F) treatment to Swiss albino mice through drinking water elicited organ-specific toxicological response. All the F-exposed groups showed severe alterations in both liver and kidney architectures, but there was no significant change

  • Nephrotoxicity of chlorofluoroacetic acid in rats.

    Dichloroacetic acid (DCA), chlorofluoroacetic acid (CFA), and difluoroacetic acid (DFA) are inhibitors of pyruvate dehydrogenase kinase. DCA is used for the clinical management of congenital lactic acidosis. Glutathione transferase zeta (GSTZ1-1) catalyzes the biotransformation of DCA and CFA, and DCA is a mechanism-based inactivator of GSTZ1-1. In rodents, DCA causes

  • Effects of selenium intervention on chronic fluorosis-induced renal cell apoptosis in rats

    This study aims to explore the effect of selenium in fluoride-induced renal cell apoptosis in rats and determine the optimal level of selenium in drinking water to prevent fluorosis. Experimental animals were divided into a control group, a sodium fluoride-treated group (NaF, 50 mg/L), three sodium selenite-treated groups (Na2SeO3, 0.375, 0.75,

  • Histological and histochemical appearance of livers and kidneys of rats after long-term treatment with different concentrations of sodium fluoride in drinking water

    After a review of the controversies in the literature, a histologic and histochemical study of the livers and kidneys of 48 albino rats was performed. The animals were placed on a diet containing 1 ppm NaF in demineralized drinking water, or 1, 10 or 100 ppm NaF in tap water

  • 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

• Related FAN Content :

  • 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

  • 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

  • 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.

  • 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

  • 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