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.
Sodium fluoride induces apoptosis in the kidney of rats through caspase-mediated pathways and DNA damage
Long-term excessive sodium fluoride (NaF) intake can cause many bone diseases and nonskeletal fluorosis. The kidneys are the primary organs involved in the excretion and retention of NaF. The objective of the present study was to determine the effects of NaF treatment on renal cell apoptosis, DNA damage, and the
Fluoridation and bone disease in renal patients
About the Authors: William J Johnson, director of the Mayo Artificial Kidney Center and professor of medicine with the Division of Nephrology at the Mayo Clinic, has been involved in the study of calcium and phosphorus metabolism and renal osteodystrophy, potassium metabolism, and uremic neuropathy. He is past chairman of the Minnesota
Effect of aging on animal response to chronic fluoride exposure
This study was conducted to test the hypothesis that physiological changes which occur during aging increase the biological impact of fluoride and reduce the threshold of safe fluoride exposure. Four groups of rats were fed a low-fluoride diet (< 1.2 ppm) ad libitum and received 0, 5, 15, or 50
Study on changes of clinical indicators and key proteins from fluoride exposure
Few studies have evaluated the biomarker changes of fluoride exposure. In order to explore early and sensitive indicators, animal experiment was designed. Ninety-six healthy SD rats (48 males and 48 females) weighing approximately 60 g were randomly divided into six groups of 16 animals each by gender average. Control animals
[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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