Abstract

In Drosophila melanogaster the frequency of adults with melanotic tumors increases both when .larvae from genetically normal and genetically melanotic tum0r strains are exposed to nutrient containing silver nitrate. Larval nutrient containing sodium fluoride also has this effect on genetically normal individuals. The present work was performed to test simultaneously the melanotic tumorigenic
capacity of sodium fluoride in two different genetic lines in which such tumors normally occur or do not occur with appreciable frJ1quency.

. . . .

In D. Melanogaster, when larvae are grown in nutrient containing different concentrations of NaF, the tu-soj strain, which normally has a relatively strong genetic predisposition for the formation of melanotic tumors, demonstrates a significantly higher rate of induced melanotic tumors in the adult stage than does the wild·type Oregon R strain, which normally has a relatively weak genetic predisposition in this respect.

• Related Studies :

  • In vivo suppression by fluoride of chromosome aberrations induced by mitomycin-C in mouse bone marrow cells.

    In vivo clastogenic effects of mitomycin-C (MMC) in bone marrow cells of four groups of young male Swiss albino mice exposed to 0, 7.5, 15, and 30 mg NaF/L in their drinking water for 30 days were investigated. The percentages of aberrant metaphases and chromosome aberrations in all F-treated mice

  • The lack of genotoxicity of sodium fluoride in a battery of cellular tests

    In a comprehensive assessment of genotoxicity, sodium fluoride was evaluated in a battery of cellular tests providing different genetic end points and biotransformation capabilities. The tests included the following: rat hepatocyte primary culture/DNA repair assay, Salmonella typhimurium histidine locus reversion assay, adult rat liver epithelial cell/hypoxanthine guanine phosphoribosyl transferase mutation

  • [Dependence of lethality and incidence of chromosome aberrations induced by treatment of synchronized human diploid fibroblasts with sodium fluoride on different periods of the cell cycle].

    The cytotoxic and clastogenic effects of sodium fluoride during various phases of cell cycle of human cultured diploid fibroblasts were examined. The cells in confluence were synchronized at G1/G0 phase by a period of growth in medium containing 1% serum (low serum medium). To obtain the cells in S phase

  • Cell cycle dependence of cytotoxicity and clastogenicity induced by treatment of synchronized human diploid fibroblasts with sodium fluoride

    To study the cell cycle dependence of cytotoxicity and clastogenicity of sodium fluoride (NaF), synchronized human diploid fibroblasts were treated with NaF during different phases of the cell cycle and analyzed. Exponentially growing cells were synchronized by the following two procedures. (1) The cells were synchronized at G0/G1 phase by

  • A stable and sensitive testing system for potential carcinogens based on DNA damage-induced gene expression in human HepG2 cell

    In order to analyze potential carcinogenic and genotoxic responses caused by exposure to pollutants existing in environment, a screening method has been established in our laboratory that uses a stably transfected HepG2 cell lines containing gadd153 promoter regions which drive a luciferase reporter gene. Activation of the exogenous gadd153 promoter

• Related FAN Content :

  • 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.

  • 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: The "Oral Health Research Institute's" Studies

    Although many in vitro and in vivo studies have detected mutagenic effects from fluoride exposure, the Oral Health Research Institute at Indiana University's School of Dentistry has repeatedly failed to find any such effect in multiple studies on the subject.

  • 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.

  • 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