Abstract
The cytotoxic and clastogenic effects of sodium fluoride during various phases of cell cycle of human cultured diploid fibroblasts were examined. The cells in confluence were synchronized at G1/G0 phase by a period of growth in medium containing 1% serum (low serum medium). To obtain the cells in S phase and G2 phase, exponentially growing cells were cultured in low serum medium with a subsequent blockage of the cells at the G1/S boundary by hydroxyurea. Synchronized cells were treated with sodium fluoride for 3 hr during the G1 phase or G2 phase, and for each of three 3-hr periods during the S phase which lasted 9 hr. The cytotoxicity, as determined by a decrease in colony-forming ability, was dependent upon the phase of cell cycle during which treatment was administered. The highest lethality was observed for treatment in early to middle S phase, whereas scare lethality was observed in G1 phase. Inducibility of chromosome aberrations of the cells following treatment with sodium fluoride was also dependent upon the phase of cell cycle. Significant increase in the incidence of chromosome aberrations was observed only in cultures treated during early and/or middle S phases of the cell cycle. These results indicate that cytotoxicity and clastogenicity of sodium fluoride to cultured human diploid fibroblasts are cell phase dependent, and that the cells in early and middle S phases are more sensitive to these effects.
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Ameliorative effects of N-acetylcysteine on fluoride-induced oxidative stress and DNA damage in male rats' testis
This study was to elucidate DNA damage in rats treated with sodium fluoride (NaF) by performing 8-Hydroxy-2-deoxyguanosine (8-OHdG) immunohistochemical staining assays on seminiferous tubules of rats' testis, and also to evaluate the protective effects of N-acetylcysteine (NAC) on spermatogenesis. Male Sprague Dawley (SD) rats were exposed to a single dose
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Genotoxic effect of an environmental pollutant, sodium fluoride, in mammalian in vivo test system
Genotoxicity of Sodium fluoride was evaluated in mice in vivo with the help of different cytogenetic assays. The frequency of chromosome aberration was dose - and time - dependent but not exactly route-dependent. Fractionated dosing induced less aberration. Incidence of micronucleus and sperm abnormality increased with dose. Relative sensitivity of
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Toxicity assessment of sodium fluoride in Drosophila melanogaster after chronic sub-lethal exposure
Sodium fluoride (NaF), one of the most frequently used fluoride compound is composed of Na+ and F-. Apart from its use in water fluoridation, NaF also acts as a major component for different dental products like toothpastes, gels and mouth rinses etc. The present study was carried out to explore the toxic impact of chronic
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Sodium fluoride is a less efficient human cell mutagen at low concentrations
Sodium fluoride was found to induce gene-locus mutations at the thymidine kinase (tk) and hypoxanthine guanine phosphoribosyl transferase (hgprt) loci in human lymphoblastoid cells. A single, 28 hr exposure to up to 600 micrograms/ml sodium fluoride induced a concentration-dependent increase in mutant fraction at both gene loci and reduced cell
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Morphological transformation and effect on gap junction intercellular communication in Syrian hamster embryo cells as screening tests for carcinogens devoid of mutagenic activity
A large fraction of chemicals observed to cause cancer in experimental animals is devoid of mutagenic activity. It is therefore of importance to develop methods that can be used to detect and study environmental carcinogenic agents that do not interact directly with DNA. Previous studies have indicated that induction of
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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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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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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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