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.

• Related Studies :

  • Clastogenic activity of sodium fluoride in great ape cells

    Conflicting evidence has been reported concerning the mutagenicity of sodium fluoride (NaF), especially clastogenicity at concentrations of more than 1 mM. NaF is known to induce chromosome aberrations at these concentrations in human cells, but not in most rodent cells. We considered that such species-specific difference in chromosomal sensitivity would

  • DNA damage, apoptosis and cell cycle changes induced by fluoride in rat oral mucosal cells and hepatocytes

    AIM:  To study the effect of fluoride on oxidative stress, DNA damage and apoptosis as well as cell cycle of rat oral mucosal cells and hepatocytes. METHODS:  Ten male SD rats weighing 80-120 g were randomly divided into control group and fluoride group, 5 animals each group. The animals in

  • 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

  • Genotoxic damage in oral epithelial cells induced by fluoride in drinking-water on students of Tula de Allende, Hidalgo, Mexico

    Fluoride (F-) compounds are present on the earth’s surface, water, volcanoes and are also a product of petrochemical and cement industries. Little amounts of F- are required for the formation of bones and enamel, however, according to World Health Organization (WHO), ingestion of over 1.5 mg/L of F- may be

  • Effect of static magnetic field on the induction of micronuclei by some mutagens

    OBJECTIVES:  It is important to assess the risk of static magnetic fields (SMFs) on human health, because epidemiological studies have indicated that SMFs play a role in the development of diseases such as leukemia and brain tumor. In our environment, we have numerous chances to be exposed to not only

• Related FAN Content :

  • 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'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

  • 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/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).

  • 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.