Abstract
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 protein expression levels of cytosolic cytochrome C (Cyt C) and cleaved caspases 9, 8, and 3 in vivo. 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 NaF, respectively, via drinking water for 120 days. Histopathological changes in the kidneys were visualized using hematoxylin and eosin staining. Renal cell apoptosis was examined using flow cytometry, and renal cell DNA damage was detected using the comet assay. Cytosolic Cyt C and cleaved caspases 9, 8, and 3 protein expression levels were visualized using immunohistochemistry and Western blotting. The results showed that NaF treatment increased apoptosis and DNA damage. In addition, NaF treatment increased the protein expression levels of cytosolic Cyt C and cleaved caspases 9, 8, and 3. These results indicated that NaF induces apoptosis in the kidney of rats through caspase-mediated pathway, and DNA damage may be involved in this process.
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Exocyclic DNA adducts in sheep with skeletal fluorosis resident in the proximity to the Portoscuso-Portovesme industrial estate on Sardinia Island, Italy
The mechanisms by which fluoride produces its toxic effects are still not clear. Therefore, we conducted a cross-sectional study to evaluate the fluoride-induced toxicity on randomly selected sheep with skeletal fluorosis resident near the large non-ferrous metallurgy Portoscuso-Portovesme industrial estate and the Carbonia and Gonnessa towns (control district) in respect
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Studies on the DNA and RNA contents of heart, liver and kidney of rats with chronic fluorosis
17 rats with chronic fluorosis induced by prolonged drinking of water containing 50 ppm fluorine and 17 rats drinking low-fluorine water served as control were used to study the DNA and RNA contents of heart, liver and kidney. The findings suggest that excessive accumulation of fluorine can suppress the synthesis
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Effects of fluoride on lipid peroxidation, DNA damage and apoptosis in human embryo hepatocytes
OBJECTIVE: To investigate the effects of fluoride on lipid peroxidation, DNA damage and apoptosis in human embryo hepatocyte L-02 cells. METHODS: Lipid peroxide (LPO) level, reduced glutathione (GSH) content, DNA damage, apoptosis, and cell cycle analysis were measured after in vitro cultured L-02 cells were exposed to sodium fluoride at different
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Induction of apoptosis in human gingival epithelial cells by sodium fluoride.
Fluoride (F) causes not only chronic but also short-term toxic effects, such as apoptosis, in several kinds of human cells. Although human gingival epithelial cells (HGECs) are frequently exposed to topical applications of F to teeth, the apoptosis effects of F on HGECs does not appear to have been assessed.
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Effect of fluoride intoxication on endometrial apoptosis and lipid peroxidation in rats: role of vitamins E and C.
Fluoride is a strong, hard anion and cumulative toxic agent. The effect of fluoride intoxication on lipid peroxidation in endometrial tissue and the protective effects of combinations of vitamins E and C in rats were studied. Additionally, the apoptotic changes in endometrial tissue were examined. Experimental groups were as follows:
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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.
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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
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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
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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
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Fluoride & Kidney Stones
It has long been suspected that fluoride may contribute to the formation of kidney stones. This suspicion has recently gained support from a study of an American man with skeletal fluorosis. According to the authors: "A new, important, medical problem (that seemed temporally related to cessation of fluoride exposure and subsequent negative calcium
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