Abstract
Sodium fluoride (NaF) is widely used for the prevention of dental caries at various concentrations. The clastogenic effect of NaF has been tested by the use of several cytogenetic assay systems, but the findings on its genotoxicity are not consistent. In this study, the effects of NaF on chromosomes, unscheduled DNA synthesis (UDS) and sister-chromatid exchanges (SCEs) were investigated using cultured human lymphocytes. For clastogenicity testing, cells were treated for 24 h in various concentrations of NaF. At least two donors were tested for each concentration and more than 10,000 cells were totally observed. The frequencies of chromosome aberrations were 0.78 + 0.72, 0.88 + 0.56, 0.77 + 0.45, 5.95 + 5.35, 57.76 + 31.46, 108.00 + 59.40, 80.00 + 53.70 and 40.00 + 5.66 per 100 cells for concentrations of 0, 0.25, 0.5, 1.0, 2.0, 4.0, 6.0 and 8.0 mM, respectively. Considerable differences among individuals were observed, but there was no significant difference between sexes. Sodium fluoride treatment had remarkable effects on the induction of isochromatid gaps and chromosome breaks (NUpds). At various concentrations of NaF ranging from 1.0 to 4.0 mM, no increase in UDS and SCE was observed.
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The lack of genotoxicity of sodium fluoride in a battery of cellular tests
In a comprehensive assessment of genotoxicity, sodium fluoride was evaluated in a battery of cellular tests providing different genetic end points and biotransformation capabilities. The tests included the following: rat hepatocyte primary culture/DNA repair assay, Salmonella typhimurium histidine locus reversion assay, adult rat liver epithelial cell/hypoxanthine guanine phosphoribosyl transferase mutation
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Curcumin supplementation protects from genotoxic effects of arsenic and fluoride
The present study was aimed to evaluate curcumin as a potential natural antioxidant to mitigate the genotoxic effects of arsenic (As) and fluoride (F) in human peripheral blood lymphocytes. The study was divided into nine groups consisting of negative control, positive control treated with ethyl methane sulphonate (EMS; 1.93 mM)
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DNA damage, apoptosis and cell cycle changes induced by fluoride in rat oral mucosal cells and hepatocytes
AIM: To study the effect of fluoride on oxidative stress, DNA damage and apoptosis as well as cell cycle of rat oral mucosal cells and hepatocytes. METHODS: Ten male SD rats weighing 80-120 g were randomly divided into control group and fluoride group, 5 animals each group. The animals in
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Cytogenetic studies of sodium fluoride in mice
The cytogenetic effects of sodium fluoride (NaF) were measured in mice following administration in the drinking water for 6 weeks. Bone fluoride levels were determined and showed a dose-related incorporation of fluoride. Micronuclei were measured in peripheral blood erythrocytes following 1 and 6 weeks of NaF administration. Bone marrow cell
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Chromosomal aberrations and sister-chromatid exchanges in Lithuanian populations: effects of occupational and environmental exposures
Cytogenetic analysis of chromosomal aberrations (CA) in 175,229 cells from 1113 individuals, both unexposed and occupationally or environmentally exposed to heavy metals (mercury and lead), organic (styrene, formaldehyde, phenol and benzo(a)pyrene) and inorganic (sulfur and nitrogen oxides, hydrogen and ammonium fluorides) volatile substances and/or ionizing radiation was performed. In addition,
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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'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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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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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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