Abstract
Don Chinese-hamster cells were treated with 25, 50, or 75 micrograms/milliliter (microg/ml) of sodium-fluoride (7681494) to determine the chromosomal effects of fluoride exposure on these cells. Cultures were assayed at 12, 24, and 36 hours after initiation of treatment. Chromosomal aberrations were recorded for all the concentrations used. Maximum effect at all concentrations was observed after 24 hours of treatment. Several kinds of abnormalities were revealed with the main ones being bridges, double bridges, sidearm bridges, bridges with fragments, tripolar and multipolar anaphases with and without bridges, fragments, and laggards. “Y” and “X” configurations were also noted at metaphase. No significant differences were noted for different concentrations of sodium-fluoride, while the difference between treated and control cultures was significant at the 5 percent probability level. The authors suggest that bridges scored in anaphase/telophase may result from stickiness of chromosomes or from exchanges between chromosomes or chromatids. Fluoride may be responsible for disruption of microtubules causing “Y” and “X” type configurations to occur in metaphase, since sodium-fluoride affects the rate of protein synthesis and since the mitotic spindle fibers are composed of proteins. The authors conclude that sodium-fluoride may be considered to be clastogenic in these cells.
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Toxicity assessment of sodium fluoride in Drosophila melanogaster after chronic sub-lethal exposure
Sodium fluoride (NaF), one of the most frequently used fluoride compound is composed of Na+ and F-. Apart from its use in water fluoridation, NaF also acts as a major component for different dental products like toothpastes, gels and mouth rinses etc. The present study was carried out to explore the toxic impact of chronic
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Sodium fluoride and chromosome damage (in vitro human lymphocyte and in vivo micronucleus assays)
The clastogenic potential of sodium fluoride was determined both in vitro (using cultured human lymphocytes) and in vivo (using the rat bone-marrow micronucleus test). The incidence of chromosome aberrations in human lymphocyte cultures exposed to 20 or 40 micrograms/ml sodium fluoride (3 and 9% respectively) was significantly increased compared with
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Chromosomal aberrations and sister-chromatid exchanges in Lithuanian populations: effects of occupational and environmental exposures
Cytogenetic analysis of chromosomal aberrations (CA) in 175,229 cells from 1113 individuals, both unexposed and occupationally or environmentally exposed to heavy metals (mercury and lead), organic (styrene, formaldehyde, phenol and benzo(a)pyrene) and inorganic (sulfur and nitrogen oxides, hydrogen and ammonium fluorides) volatile substances and/or ionizing radiation was performed. In addition,
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Fluoride-induced genotoxicity in mouse bone marrow cells: effect of buthionine sulfoximine and N-acetyl-l-cysteine.
A significant level of reactive oxygen species generation was observed in sodium fluoride (NaF) treated mouse bone marrow cells (BMCs). Reduced glutathione (GSH) as a free radical scavenger could be an important determining factor in F-induced genotoxicity. We therefore attempted to monitor GSH to understand the mechanism of NaF-induced genotoxicity.
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Sodium fluoride induced chromosome aberrations and sister chromatid exchange in cultured human lymphocytes
Experimental sodium fluoride (NaF) up 10 30 times the level recommended In drinking waler (1 ppm) was compared with an inorganic salt for its ability to induce chromosome aberrations and sister chromatid exchange (SCE) in cultured human lymphocytes. An increase in the frequencies of chromosome aberrations but not of SCE
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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 & 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/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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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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