Abstract
To determine the carcinogenic potential of sodium fluoride (NaF), we fed Sprague-Dawley rats a diet containing NaF for up to 99 weeks. Rats receiving NaF at a dose of 4, 10, or 25 mg/kg per day added to a low-fluoride diet were compared with controls receiving either a low-fluoride diet or laboratory chow. Each treatment group consisted of 70 rats of each sex. A 30% decrement in weight gain occurred at an NaF dose of 25 mg/kg per day. Evidence of fluoride toxicity was seen in the teeth, bones, and stomach, and the incidence and severity of these changes were related to the dose of NaF and the duration of exposure. Despite clear evidence of toxicity, NaF did not alter the incidence of preneoplastic and neoplastic lesions at any site in rats of either sex. Results from this study indicate that NaF is not carcinogenic in Sprague-Dawley rats.
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Fluorosilicic acid induces DNA damage and oxidative stress in bone marrow mesenchymal stem cells.
Highlights Fluorosilicic acid is the most used additive for water fluoridation. Dental fluorosis can be caused by fluorosilicic acid present in drinking water. DNA damage was caused by fluorosilicic acid in mesenchymal stem cells. Fluorosilicic acid altered bone mineralization in mesenchymal stem cells. DNA damage caused by fluorosilicic acid
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The effects of sodium fluoride and iodacetamide on mutation induction by x-irradiation in mature spermatoza of drosophila
The effect of two inhibitors of glycolysis, NaF and iodacetamide on the production of recessive lethal mutations by X-rays in mature Drosophila sperm has been investigated. Pre-treatment with NaF resulted in a consistent and highly significant increase of the mutation frequency. This effect is thought to result from interference with
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Fluoride in drinking water and cancer mortality in Taiwan
The possibility that cancer risk is associated with naturally fluoridated water in Taiwan is examined. The 1982-1991 age-adjusted mortality rates for cancer for 10 municipalities whose water supplies contained the highest naturally occurring fluoride concentrations in Taiwan were compared to those rates for 10 matched municipalities with unfluoridated water. The
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Effects of melatonin and amla antioxidants on fluoride-induced genotoxicity in human peripheral blood lymphocyte cells
This investigation reports genotoxic effects of sodium fluoride (NaF) at 17, 34, and 51 ?M for 72 hr and induction of sister chromatid exchanges (SCEs) and related changes, together with ameliorative effects by melatonin and amla, in human peripheral blood lymphocyte cell cultures. The cell cycle proliferative index (CCPI) significantly
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Effects of different concentrations of fluoride in oral mucosal cells in albino rats
INTRODUCTION: Fluoride has been described to be physiologically essential for the normal development and growth of human beings. However, it is well known that excessive fluoride causes skeletal, nonskeletal and dental complications. Therefore, outlining the cytogenetic effects induced by fluorosis is necessary. OBJECTIVES: To evaluate the cytomorphology of exfoliated oral mucosal
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Fluoride & Osteosarcoma: A Timeline
Several human epidemiological studies have found an association between fluoride in drinking water and the occurrence of osteosarcoma (bone cancer) in young males. These studies are consistent with the National Toxicology Program's (NTP) cancer bioassay which found that fluoride-treated male rats had an dose-dependent increase in osteosarcoma. Although a number of studies have failed to detect an association between fluoride and osteosarcoma, none of these studies have measured the risk of fluoride at specific windows in time, which based on recent results, is the critical question with respect to fluoride and osteosarcoma.
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Fluoride/Osteosarcoma Link Is Biologically Plausible
The "biological plausiblility" of a fluoride-osteosarcoma link is widely acknowledged in the scientific literature. The biological plausibility centers around three facts: 1) Bone is the principal site of fluoride accumulation, particularly during the growth spurts of childhood; 2) Fluoride is a mutagen when present at sufficient concentrations, and 3) Fluoride can stimulate the proliferation of osteoblasts (bone-forming cells).
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Fluoride's Mutagenicity: In vivo Studies
Consistent with dozens of in vitro studies, a number of in vivo studies, in both humans and animals, have found evidence of fluoride-induced genetic damage. In particular, research on humans exposed to high levels of fluoride have found increased levels of "sister chromatid exchange" (SCE). As noted in one study: "In
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NTP Bioassay on Fluoride/Cancer (1990)
In 1977, the U.S. Congress requested that animal studies be conducted to determine if fluoride can cause cancer. The result of the Congressional request was an extensive animal study conducted in the 1980s by the National Toxicology Program (NTP) and published in 1990. The main finding of NTP's study was a dose-dependent increase in osteosarcoma (bone cancer) among the fluoride-treated male rats.
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Fluoride & Liver Cancers in NTP Bioassay
On October 28, 1988, Battelle Columbus Laboratories submitted its Final Report to the NTP concerning the results of the Mouse study. The principal finding of Battelle's report was that a dose-dependent increase of a rare liver cancer (hepatocholangiocarcinoma) had occurred in the fluoride-treated male and female mice.
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