Abstract
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 inhibition, chromosomal aberrations, and chromatid breaks were most pronounced in mice that received the relatively low dose of 15 mg NaF/L. The effects became obvious after the first week of treatment and were maximal after 3 months of sustained exposure. Chromosome aberrations induced by one month treatment with 15 mg NaF/L was significantly higher than those found with the 100 and 150 mg NaF/L concentrations. The total number of femur bone marrow cells remained unchanged in all the treatment groups except in the 150 mg NaF/L group, in which it declined significantly. F treatment did not elicit any change in the percentage of viable cells in the bone marrow. Depletion of S-phase fraction of bone marrow cells occurred in the mice receiving 150 mg NaF/ L for 30 days, whereas treatment with 15 mg NaF/L for 90 days elevated the sub-G1 fraction, suggesting inhibition of DNA synthesis and up-regulation of apoptosis, respectively. These results indicate that the action of F in vivo is actually more genotoxic at certain lower concentrations than at higher concentrations.
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Cytogenetic effects of hydrogen fluoride on plants
Studies on the effects of HF on meiotic chromosomes of tomatoes indicated a trend toward a higher frequency of chromosomal aberrations with an increase in the fumigation period. It was indicated that HF was capable of inducing paracentric inversions with the possibility of the induction of deficiencies, duplications or even
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Lack of DNA damage induced by fluoride on mouse lymphoma and human fibroblast cells by single cell gel (comet) assay
Fluoride has widely been used in Dentistry because it is a specific and effective caries prophylactic agent. However, excess fluoride may represent a hazard to human health, especially by causing injury on genetic apparatus. Genotoxicity tests constitute an important part of cancer research for risk assessment of potential carcinogens. In
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Sister chromatid exchanges: a study in fluorotic individuals of North Gujurat
The purpose of this preliminary investigation was to compare the genotoxic effect of fluoride in human individuals directly exposed to high concentrations of drinking water fluoride (1.95 to 2.2 ppm) with those in individuals exposed to concentrations (0.6 to 1.0 ppm) within the WHO permissible limit. Sister chromatid exchanges (SCE)
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Chromosome aberrations in cultured rat bone marrow cells treated with inorganic fluorides
The genotoxic effects of inorganic fluorides were investigated by treating cultured rat bone marrow cells with varying concentrations (0.1-100 microM) of potassium fluoride (KF) and sodium fluoride (NaF) for different durations (12, 24 and 36 h) and measuring the incidence of cells with aberrations and number of breaks per cell.
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Genotoxic effect and rat hepatocyte death occurred after oxidative stress induction and antioxidant gene downregulation caused by long term fluoride exposure
Studies focusing on possible genotoxic effects of excess fluoride are contradictory and inconclusive. Currently, studies have reported a probable link to oxidative stress, DNA damage and apoptosis induced by fluoride in rat hepatocytes. We developed an in vivostudy administering three doses of fluoride by gavage given to rats for 60 day.
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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/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 & 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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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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