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.
-
-
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
-
The mutagenicity of sodium fluoride to L5178Y [wild-type and TK+/- (3.7.2c)] mouse lymphoma cells
L5178Y wild-type and TK+/- (3.7.2c) cells were treated with sodium fluoride over a range of concentrations (10-500 micrograms ml-1) and treatment times (4, 16 and 48 h) covering less than 10-100% survival. The mutant frequency at five genetic loci (resistance to ouabain, 6-thioguanine, excess thymidine, methotrexate and 1-beta-D-arabinofuranosyl cytosine) was
-
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
-
Micronucleus and sister chromatid exchange frequency in endemic fluorosis
Inhabitants of the Hohhot Region in Inner Mongolia who drink high-fluoride (4-15 mg/L) water were compared for their micronucleus (MN) rate and sister chromatid exchange (SCE) frequency in their peripheral blood lymphocytes. In persons with fluorosis as well as those considered "healthy", the MN rafe and SCE frequency were significantly
-
Induction of chromosomal aberrations in male mouse germ cells by uranyl fluoride containing enriched uranium
Cytogenetic damage induced by a wide range of concentrations of uranyl fluoride injected into mouse testes was evaluated by determining the frequencies of chromosomal aberrations in spermatogonia and primary spermatocytes. Breaks, gaps and polyploids were observed in spermatogonia. The frequencies of the significant type of aberration, breaks, were induced according
Related Studies :
-
-
-
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.
-
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.
-
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
-
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).
-
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.
Related FAN Content :
-