Abstract
The renal clearance of fluoride (CF) was studied in pentobarbital-anesthetized rats. Urine flow rate and chloride clearance, previously thought to be the main determinants of CF, were readily dissociated from CF. Neither the clearance of sodium nor the excretion of potassium correlated consistently with CF. In experiments designed to manipulate urinary pH, viz., the administration of NaHCO3 or NH4Cl, acetazolamide, and mannitol, CF correlated closely with urinary pH. At a urinary pH of 5.0-k96, CF/GFR averaged less than 5%, while at a urinary pH of approximately 7.6, mean CF/GFR exceeded 65%. The data suggest that 35-45% of the filtered fluoride is reabsorbed in the proximal tubule, regardless of the final urinary pH, while in acidosis the majority of fluoride reabsorption occurs in the distal nephron. The results suggest that the tubular reabsorption of fluoride is inversely related to tubular fluid pH. Fluoride reabsorption seems to occur by nonionic diffusion, apparently as hydrogen fluoride. Depending on local pH gradients, it may occur along the entire nephron.
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Environmental and physiological factors affecting dental fluorosis
In addition to differences in fluoride intake and possibly to calcium deficiency or malnutrition, there are several factors which may account for individual differences in the occurrence of dental fluorosis. Disorders in acid-base balance affect the renal handling of fluoride such that, in acidosis, the excretion rate is diminished and,
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Plasma and developing enamel fluoride concentrations during chronic acid-base disturbances
Mild acid-base disturbances were induced in rats for 30 days. These disturbances did not affect % ash of maxillary incisors or % P of the developing enamel from mandibular incisors. Total fluoride intake (food and water) among groups drinking fluoride-free water was constant. Nevertheless, average plasma and developing enamel fluroide
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Intake and metabolism of fluoride
The purpose of this paper is to discuss the major factors that determine the body burden of inorganic fluoride. Fluoride intake 25 or more years ago was determined mainly by measurement of the concentration of the ion in the drinking water supply. This is not necessarily true today because of
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Fluoride metabolism
Knowledge of all aspects of fluoride metabolism is essential for comprehending the biological effects of this ion in humans as well as to drive the prevention (and treatment) of fluoride toxicity. Several aspects of fluoride metabolism - including gastric absorption, distribution and renal excretion - are pH-dependent because the coefficient
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Fluoride pharmacokinetics during acid-base balance changes in man
Five healthy subjects were each given fluoride 3.0 mg (F) as sodium fluoride tablets on two occasions - during production of acid urine, induced by giving NH4Cl, and during production of alkaline urine obtained by giving NaHCO3. Frequent plasma and urine samples were taken up to 12 h and were
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Fluoride Exposure Aggravates the Impact of Iodine Deficiency
A consistent body of animal and human research shows that fluoride exposure worsens the impact of an iodine deficiency. Iodine is the basic building block of the T3 and T4 hormones and thus an adequate iodine intake is essential for the proper functioning of the thyroid gland. When iodine intake is inadequate during infancy and
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Skeletal Fluorosis & Individual Variability
One of the common fallacies in the research on skeletal fluorosis is the notion that there is a uniform level of fluoride that is safe for everyone in the population. These "safety thresholds" have been expressed in terms of (a) bone fluoride content, (b) daily dose, (c) water fluoride level, (d) urinary fluoride level, and (e) blood fluoride level. The central fallacy with each of these alleged safety thresholds, however, is that they ignore the wide range of individual susceptibility in how people respond to toxic substances, including fluoride.
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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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Unheeded Warnings: Government Health Authorities Ignore Fluoride Risk for Kidney Patients
Despite the well known fact that individuals with kidney disease are at much higher risk of fluoride toxicity than the general population, there has yet to be any attempt in the United States, or any other country that practices mass-scale water fluoridation to determine the prevalence of fluoride-related effects (e.g.,
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Factors which increase the risk for skeletal fluorosis
The risk for developing skeletal fluorosis, and the course the disease will take, is not solely dependent on the dose of fluoride ingested. Indeed, people exposed to similar doses of fluoride may experience markedly different effects. While the wide range in individual response to fluoride is not yet fully understood, the following are some of the factors that are believed to play a role.
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