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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Clastogenic activity of sodium fluoride to rat vertebral body-derived cells in culture
The US National Toxicology Program has shown equivocal evidence of carcinogenic activity of sodium fluoride (NaF) in male F344/N rats based on the occurrence of five osteosarcomas in treated animals. In the study the osteosarcomas developed mainly in the rat vertebrae. To provide a possible mechanistic basis for the observed
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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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Is fluoride a mutagen?
Recent studies suggest that fluoride may be genotoxic. While the concentration of fluoride in artificially fluoridated water (1 mg Fl-1) is generally considered to be "safe", levels of fluoride present in a number of widely used dental health products, such as fluoride-containing toothpaste, appear to be potentially mutagenic. Since fluoride
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Leukocyte response in young mice chronically exposed to fluoride
A light and fluorescent microscopy study of sternal and femoral bone marrow, taken from young Swiss mice exposed for up to 280 days to elevated levels of NaF in drinking water, revealed morphologic abnormalities in cell structure and mitotic figure formation in immature leukocytes. Alterations in the content and distribution
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Fluoride-induced genotoxicity in mouse bone marrow cells: effect of buthionine sulfoximine and N-acetyl-l-cysteine.
A significant level of reactive oxygen species generation was observed in sodium fluoride (NaF) treated mouse bone marrow cells (BMCs). Reduced glutathione (GSH) as a free radical scavenger could be an important determining factor in F-induced genotoxicity. We therefore attempted to monitor GSH to understand the mechanism of NaF-induced genotoxicity.
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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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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/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 & 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'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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