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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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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Genotoxic effect of an environmental pollutant, sodium fluoride, in mammalian in vivo test system
Genotoxicity of Sodium fluoride was evaluated in mice in vivo with the help of different cytogenetic assays. The frequency of chromosome aberration was dose - and time - dependent but not exactly route-dependent. Fractionated dosing induced less aberration. Incidence of micronucleus and sperm abnormality increased with dose. Relative sensitivity 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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Chromosomal changes in maize induced by hydrogen fluoride gas
Maize seedlings of the genotype A1A2C1Wx were fumigated in growth chambers with hydrogen fluoride (HF) at a concentration of about 3 ug/m3. The experiment was run for 10 days, with the first group of treated plants removed from the chambers after 4 days and then at intervals of 2 days.
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Sodium fluoride promotes morphological transformation of Syrian hamster embryo cells
Sequential treatment of Syrian hamster embryo (SHE) cells with a chemical carcinogen followed by sodium fluoride (NaF) resulted in a higher yield of morphologically transformed cell colonies than treatment of the cells with carcinogen alone. For example, cells treated with benzo[a]pyrene (B[a]P; 3 micrograms/ml) for 3 days, then with NaF
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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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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'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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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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