Abstract
Inbred mice, fed a low-fluoride diet, 0.263 + 028 ppm F, were given drinking water containing 0, 1, 5, 10, 50, 100, or 200 ppm F for 3 to 6 weeks. Cytological studies on bone marrow cell chromosomes and spermatocytes showed that 1-200 ppm F (as sodium fluoride) was able to induce chromosomal changes in a dose-dependent manner. The frequency of the induced chromosomal damage was significantly higher in each treatment than in the controls. The observed abnormalities included translocations, dicentrics, ring chromosomes, and bridges plus fragments, or fragments by themselves. There was a significant correlation between the amount of fluoride in the body ash and the frequency of the chromosomal abnormalities.
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[Dependence of lethality and incidence of chromosome aberrations induced by treatment of synchronized human diploid fibroblasts with sodium fluoride on different periods of the cell cycle].
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
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Long-term exposure to fluoride in drinking water and sister chromatid exchange frequency in human blood lymphocytes
The genetic toxicity of fluoride has been investigated extensively by various test systems. However, results obtained have been inconsistent. Fluoride has been reported to be non-genotoxic, genotoxic, and synergistic or antagonistic with certain mutagens. To date, there are no published human studies on the genotoxicity of fluoride. The purpose of
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Sister-chromatid exchanges in lymphocytes of workers at a phosphate fertilizer factory
The frequencies of sister-chromatid exchange (SCE) in peripheral blood lymphocytes of 40 workers at a phosphate fertilizer factory in North China were studied. HF and SiF4 are main air pollutants in the factory, there is also some dust containing fluoride, phosphate fog, NH3 and SO2. It was shown that the
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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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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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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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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'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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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 vitro Studies
According to the National Toxicology Program, "the preponderance of evidence" from laboratory "in vitro" studies indicate that fluoride is a mutagenic compound. Many substances which are mutagens, are also carcinogens (i.e. they can cause cancer). As is typical for in vitro studies, the concentrations of fluoride that have generally been tested
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