The contamination of ground water by fluoride has been reported worldwide. Most fluoride (approximately 70%) is filtered by the kidneys; humans or experimental animals with renal damage therefore may be more affected by fluoride exposure than those with normal kidney function. Tubulointerstitial fibrosis, which involves macrophage-promoted extracellular matrix production and myofibroblast migration, can be induced in rats by unilateral ureteral obstruction (UUO). We examined the effects of fluoride exposure on tubulointerstitial fibrosis in the obstructed kidney of UUO rats. The left ureters of 6-week-old male rats were ligated using silk sutures. Fluoride was then administered for 2 weeks at doses of 0, 75, and 150 ppm in the drinking water. Real-time polymerase chain reaction was performed to analyze transforming growth factor beta 1 (TGF-?1) transcription; histological and immunohistochemical staining were used to identify positive areas within the renal cortex and staining-positive cells by image analysis. Significant increases were observed in the obstructed kidneys of UUO rats exposed to 150 ppm fluoride (compared to 0 ppm) for areas or number of cells that stained with Masson trichrome or with antibodies against collagen type I, alpha-smooth muscle actin (?-SMA, a myofibroblast marker), ED1, ED2, and ED3 (macrophage markers), and TGF-?1. Taken together, these observations suggested that fluoride exacerbates tuburointerstitial nephropathy resulting from UUO, and that this effect occurs via activation of the M2 macrophage-TGF-?1-fibroblast/myofibroblast-collagen synthesis pathway.
Hemodialyzability of ionizable fluoride in hemodialysis session
The fluoride ion content in serum and in dialysate medium was determined by means of a fluoride ion-selective electrode in 29 patients undergoing hemodialysis treatment. Abnormally high serum fluoride of 65.9 +/- 28.3 microg l(-1) at the beginning and 46.5 +/- 26.7 microg l(-1) at the completion of the hemodialysis
Toxic effects of fluoride on the rat kidney. II. Chronic effects
1. The 30-day LC50 of sodium fluoride administered in the drinking water was 205 ppm fluoride in the weanling rat. Death generally occurred between the third and fifth day after administration was begun. When levels of 150–250 ppm fluoride were administered in the water, 30–40% of the surviving rats showed
Chronic toxicity of dietary sodium monofluorophosphate in growing rats, with special reference to kidney changes.
MATERIAL AND METHODS: Male white rats weighing about 100 grams at the start of the experiments were used in the study. They were raised in a standardized way by the Anticimex Co., Stockholm on pellets containing about 28 ppm fluoride and tap water containing about 0.1 ppm fluoride. In a four-week
Fluoride aggravation of oxidative stress in patients with chronic renal failure.
Based on evidence that fluoride ion (F) increases the production of reactive oxygen species, inhibits antioxidant enzyme activity, and enhances lipid peroxidation, a study of these effects was conducted on 52 patients with chronic renal failure (CRF), of whom 33 were under going chronic haemodialysis (HD) with the use of polysulphone membrane dialysers, while 19 with
Alterations in drug metabolising enzymes and lipid peroxidation in different rat tissues by fluoride.
Sodium fluoride at a dose level of 5.0 mg/kg enhanced aminopyrine N-demethylase and NADPH cytochrome c reductase activities and cytochrome P450 and cytochrome b5 levels in rat liver, kidney, lung, intestine and testis, whereas acetanilide hydroxylase activity remained unchanged in kidney and lung and was increased in liver, intestine and
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