Excerpt:
An investigation has been carried out on the effects of the intake of small amounts of sodium fluoride on kidney structure and function in rats, with a view to the possibility of establishing some means of testing for the toxic effects of fluorine in human beings, and of demonstrating the existence of a fluorine hazard before such severe intoxication has resulted as to cause disability and obvious skeletal lesions. The effects on kidney function are immediate.
SUMMARY:
Rats given small amounts of NaF in the diet exhibited, in addition to the well-known skeletal and dental lesions, marked polydipsia and polyuria,
… At autopsy the kidneys were dark, shrunken and nodulated.
Demonstration of alkaline phosphatase showed that there were fibrotic lesions in the cortex, where the enzyme was practically absent owing to absence of functional tubular tissue.
The histological examination indicated that in the kidneys there was a vascular, glomerular and more obviously tubular degeneration leading finally to interstitial fibrosis.
The fluoride-fed rats showed diminished growth, and at low body weights there was a marked diminution of fat stores.
Nitrogen metabolism was greater in the fluoride-fed rats than in the controls.
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Author Correction: Sodium fluoride induces nephrotoxicity via oxidative stress-regulated mitochondrial SIRT3 signaling pathway.
Accumulation of mitochondrial reactive oxygen species (mROS) has been implicated in the pathogenesis of fluorosis. As the main mitochondrial deacetylase, SIRT3 is closely associated with oxidative stress. To investigate the role of SIRT3 in response to sodium fluoride (NaF)-induced nephrotoxicity. Our results showed that NaF treatment impaired mitochondrial ultrastructure, decreased
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[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
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Renal tubular site of action of fluoride in Fischer 344 rats
Methoxyflurane is capable of producing high-output renal failure in some patients and animal models, probably through metabolic liberation of free fluoride. The tubular site of action of fluoride was examined in Fischer 344 rats using clearance techniques. Free water reabsorption (TCH2O) and free water excretion (CH2O) were measured during mannitol
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Changes in urinary ion excretion and related renal enzyme activities in fluoride-treated rats
Fluoride (NaF, 50 mg/kg po) administration to rats caused an increased urinary excretion of inorganic phosphate, calcium, magnesium, potassium, and sodium associated with polyuria. The renal enzyme activities of Na+ and K+-stimulated adenosine triphosphatase [(Na+ + K+)-ATPase], Mg2+ and Ca2+-stimulated adenosine triphosphatase [(Mg2+ + Ca2+)-ATPase], acid phosphatase, and alkaline phosphatase
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Effect of sodium fluoride administration on body changes in old rats
The effects of feeding low levels of sodium fluoride from conception until old age were determined in a total of 456 albino rats. Four levels of sodium fluoride (0, 1, 5, and 10 PPM fluorine) were given to 4 groups of animals in their drinking water. In one study half
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