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 :

  • Evaluation of the toxicity of fluorine in Antarctic krill on soft tissues of Wistar rats

    Antarctic krill are a potential food source for humans and animals, but krill are known to contain high levels of fluorine (F). In this study, we investigated the toxicity of F in Antarctic krill using Wistar rats. There were three experimental groups: The control group were fed a basal diet,

  • Diagnosis of fluorosis and recovery through easy to practise interventions.

    The objectives of the present study were to highlight (i) how to diagnose fluorosis, due to fluoride ion (F) toxicity, in out-patient departments, by retrieving the history and through tests and (ii) the interventions available for recovery. In patients suspected of fluorosis, the F levels were investigated in samples of

  • In Vivo Comparison of the Phenotypic Aspects and Molecular Mechanisms of Two Nephrotoxic Agents, Sodium Fluoride and Uranyl Nitrate.

    Because of their nephrotoxicity and presence in the environment, uranium (U) and fluoride (F) represent risks to the global population. There is a general lack of knowledge regarding the mechanisms of U and F nephrotoxicity and the underlying molecular pathways. The present study aims to compare the threshold of the

  • 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,

  • [Study on the relationship between renal apoptosis and expression of caspase protein in fluoride induced rat].

    OBJECTIVE:  To study the relationship between death receptor pathway, mitochondrion pathway and fluoride-induced apoptosis of renal cell. METHODS:  Male Sprague-Dawley rats were divided randomly into four groups (control, low-fluoride, medium-fluoride,and high-fluoride) and administered 0, 50, 100, and 200 mg/L of sodium fluoride, respectively, via drinking water for 120 days. The incidence

• Related FAN Content :

  • 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

  • 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 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 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