Abstract
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. Microsporocyte smears from the treated plants revealed chromosomal aberations that included asynaptic regions, translocations, inversions, and bridges plus fragments or fragments by themselves. It is believed that these abnormalities were due to the physiological effect of HF causing the chromosomes to become sticky and/or to the occurrence of chromatid breakage followed by reunion to form structural changes. These findings indicate that HF is a mutagenic agent.
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No relationship between subchronic fluoride intake and DNA damage in Wistar rats.
Fluoride has been widely used in dentistry because it is an effective caries prophylactic agent. However, excess fluoride may represent a hazard to human health, especially by causing injury on the genetic apparatus. Genotoxicity tests form an important part of cancer research and risk assessment of potential carcinogens. In the
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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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[Modifying effect of nutrition on the mutagenic activity of phosphorus and fluorine compounds].
The test animals were fed with low-grade food during 2-5 months under conditions of acute and chronic action of hydrogen phosphide and hydrogen fluoride induced by inhalation, that resulted in the pronounced impairment of the chromosomal apparatus of the bone marrow cells in the rats. A principal possibility has been
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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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Fluoride in the Central Nervous System and Its Potential Influence on the Development and Invasiveness of Brain Tumours-A Research Hypothesis.
The purpose of this review is to attempt to outline the potential role of fluoride in the pathogenesis of brain tumours, including glioblastoma (GBM). In this paper, we show for the first time that fluoride can potentially affect the generally accepted signalling pathways implicated in the formation and clinical course
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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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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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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 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'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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