Abstract
In vivo clastogenic effects of mitomycin-C (MMC) in bone marrow cells of four groups of young male Swiss albino mice exposed to 0, 7.5, 15, and 30 mg NaF/L in their drinking water for 30 days were investigated. The percentages of aberrant metaphases and chromosome aberrations in all F-treated mice were significantly increased. In another experiment, NaF pretreatment was followed by intraperitoneal administration of 4 mg MMC/kg bw. Results indicated that the two chemicals did not have a synergistic effect; instead, a notable suppression of the clastogenic effect of MMC occurred. As expected, mitotic indices (MI) in the bone marrow cells of the MMC-treated mice were significantly lower than in the controls. However, in the mice pretreated with 30 mg NaF/L, the percent of MI was greater than in the MMC-treated group without NaF exposure. Moreover, the percentages of aberrant metaphases and chromatid breaks were significantly higher in all the F groups than in the controls. NaF exposure of the mice for 30 days evidently also helped prevent MMC-induced damage, although the effect was not statistically significant. In the mice pre-exposed to 30 mg NaF/L in their drinking water without treatment with MMC, a 10% decrease in chromatid breaks was observed. Thus these in vivo findings corroborate earlier reports of clastogenic effects of NaF treatment in vitro.
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A possible mechanism for combined arsenic and fluoride induced cellular and DNA damage in mice
Arsenic and fluoride are major contaminants of drinking water. Mechanisms of toxicity following individual exposure to arsenic or fluoride are well known. However, it is not explicit how combined exposure to arsenic and fluoride leads to cellular and/or DNA damage. The present study was planned to assess (i) oxidative stress
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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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Differential in vivo genotoxic effects of lower and higher concentrations of fluoride in mouse bone marrow cells.
In an in vivo genotoxicity investigation of the action of fluoride (F) on bone marrow cells, sodium fluoride (NaF) was administered through the drinking water of 2–3 month old Swiss albino mice for 30 days at lower (7.5, 15, and 30 mg/L) and higher concentrations (100 and 150 mg/L). Mitotic
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Micronucleus and sister chromatid exchange frequency in endemic fluorosis
Inhabitants of the Hohhot Region in Inner Mongolia who drink high-fluoride (4-15 mg/L) water were compared for their micronucleus (MN) rate and sister chromatid exchange (SCE) frequency in their peripheral blood lymphocytes. In persons with fluorosis as well as those considered "healthy", the MN rafe and SCE frequency were significantly
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Induction of unscheduled DNA synthesis in cultured human oral keratinocytes by sodium fluoride
The effect of treatment of cultured human oral keratinocytes with sodium fluoride (NaF) has been investigated with respect to induction of unscheduled DNA synthesis (UDS). Oral keratinocytes were isolated from excised buccal mucosa of normal individuals by trypsinization at 4 degrees C overnight, followed by separation of the epithelium of
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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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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 & 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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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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