Abstract
Fluoride has been widely used in dentistry because it is an effective caries prophylactic agent. However, excess fluoride may represent a hazard to human health, especially by causing injury on the genetic apparatus. Genotoxicity tests form an important part of cancer research and risk assessment of potential carcinogens. In the current study, the potential DNA damage associated with exposure to fluoride was assessed by the single cell gel (comet) assay in peripheral blood, oral mucosa and brain cells in vivo. Male Wistar rats were exposed to sodium fluoride (NaF) at a 0, 7 and 100 ppm dose for drinking water during 6 weeks. The results pointed out that NaF did not contribute to the DNA damage in all cellular types evaluated as depicted by the mean tail moment and tail intensity. These findings are clinically important since they represent an important contribution to the correct evaluation of the potential health risk associated with dental agents exposure.
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Mutagenic effect of hydrogen fluoride on animals
The mutagenic effect of hydrogen fluoride in concentration 1.0 mg/m-3 was studied in rats and mice. Prolonged inhalation of this compound increased the frequency of cells with chromosome abnormalities in the bone marrow of albino rats. The mutagenic effect was higher in older animals. No dominant-lethal effect was observed in
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Genetic toxicity of fluoride
F- is not mutagenic in standard bacterial systems, but produces chromosome aberrations and gene mutations in cultured mammalian cells. Although there is disagreement in the literature concerning the ability of F- to induce chromosome aberrations in cultured human and rodent cells, the weight of the evidence leads to the conclusion
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Sodium fluoride-induced chromosome aberrations in different stages of the cell cycle: a proposed mechanism
In an attempt to clarify the controversy about sodium fluoride (NaF) clastogenicity, the induction of chromosome aberrations in Chinese hamster ovary cells (CHO) by NaF was investigated. Following a protocol used for screening chemicals for clastogenic activity, significant increases of aberrant cells were observed when cells were exposed to NaF
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Chronic fluoride exposure does not cause detrimental, extraskeletal effects in nutritionally deficient rats
On the basis of observations that endemic fluorosis occurs more often in malnourished populations, a series of studies tested the hypothesis that deficient dietary intake of calcium, protein or energy affects fluoride metabolism so that the margin of safe fluoride exposure may be reduced. The objective of the investigation was
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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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A Critique of Gelberg's Study on Fluoride/Osteosarcoma in New York
The case-control study by Gelberg, published first as a PhD dissertation and then later in two peer-reviewed journals, may represent the most substantive study on fluoride/osteosarcoma previous to Bassin’s 2001 analysis. In assessing Gelberg’s data, we were at first struck by the existence of several notable errors in both the thesis and papers. While these errors do raise questions about the study, our primary concern with Gelberg’s work relates to the methods she used to analyze her data.
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Micronucleus and Sister Chromatid Exchange Frequency in Endemic Fluorosis
The rise of sister chromatid exchange (SCE) and micronucleus (MN) in the peripheral blood lymphocytes of the fluorine-intoxicated patients indicates that fluorine is a mutagenic agent which can cause DNA and chromosomal damage.
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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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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'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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