Abstract
Conflicting evidence has been reported concerning the mutagenicity of sodium fluoride (NaF), especially clastogenicity at concentrations of more than 1 mM. NaF is known to induce chromosome aberrations at these concentrations in human cells, but not in most rodent cells. We considered that such species-specific difference in chromosomal sensitivity would be derived from the phylogenetic distance between rodents and man. To clarify the role of interspecies differences, we investigated the chromosomal sensitivity to NaF in cell lines from various primates, which diverged into many species, including rodent-like prosimians and human-like great apes. The results showed that the clastogenicity of NaF was limited to human and great ape cells.
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DNA damage induced by fluoride in rat kidney cells.
DNA damage by fluoride to newborn rat kidney cells isolated by enzymic digestion is reported. The cells were exposed for 24 hr to sodium fluoride at NaF concentrations of 0, 0.2, 0.4, 0.8, and 1.0 mM. Damage to DNA was determined by single cell gel electrophoresis assay (Comet assay). Significant breakage of DNA strands
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Sister chromatid exchange frequency and chromosome aberrations in residents of fluoride endemic regions of South Gujarat
Peripheral blood lymphocytes of residents of three villages and one nearby township in South Gujarat with fluoride concentrations in the drinking water of 1.56 - 3.46 and 0.6 - 0.8 ppm, respectively, were examined for their frequency of sister chromatid exchanges (SCE) and chromosome aberra-tions. The rates of SCEs and
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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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Genotoxic evaluation of sodium fluoride and sodium perborate in mouse bone marrow cells
The LD50 was obtained as the geometric mean of the determined experimental data on mice lethality. The value for sodium fluoride was 32 mg/kg and for sodium perborate the result was 775 mg/kg. The results concerning the SCE rate induced by sodium fluoride are shown in Table 1. Although no
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Mutual interactions among ingredients of betel quid in inducing genotoxicity on Chinese hamster ovary cells
The purpose of this study is to explore the mutual interactions among the chemical ingredients of betel quid including arecoline, sodium fluoride, catechin and glycyrrhizin in producing genotoxicity on Chinese hamster ovary (CHO) cells using the micronucleus method. Our results show that arecoline at a rather low concentration of 0.2-2
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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 & 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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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 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: The "Oral Health Research Institute's" Studies
Although many in vitro and in vivo studies have detected mutagenic effects from fluoride exposure, the Oral Health Research Institute at Indiana University's School of Dentistry has repeatedly failed to find any such effect in multiple studies on the subject.
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