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.
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Sodium fluoride-induced chromosome aberrations in different stages of the cell cycle: a proposed mechanism
In an attempt to clarify the controversy about sodium fluoride (NaF) clastogenicity, the induction of chromosome aberrations in Chinese hamster ovary cells (CHO) by NaF was investigated. Following a protocol used for screening chemicals for clastogenic activity, significant increases of aberrant cells were observed when cells were exposed to NaF
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Investigation of the genotoxic effects of fluoride on a bone tissue model .
Fluorides are thought to be a major cause of osteocarcinogenesis, due to their widespread industrial use, ability to accumulate in bone tissue, and genotoxic and probable carcinogenic properties. In vitro experiments investigating the genotoxic potential of fluorides in bone tissue models can provide valuable indirect information on their involvement in
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Mutual interactions among ingredients of betel quid in inducing genotoxicity on Chinese hamster ovary cells
The purpose of this study is to explore the mutual interactions among the chemical ingredients of betel quid including arecoline, sodium fluoride, catechin and glycyrrhizin in producing genotoxicity on Chinese hamster ovary (CHO) cells using the micronucleus method. Our results show that arecoline at a rather low concentration of 0.2-2
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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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Leukocyte response in young mice chronically exposed to fluoride
A light and fluorescent microscopy study of sternal and femoral bone marrow, taken from young Swiss mice exposed for up to 280 days to elevated levels of NaF in drinking water, revealed morphologic abnormalities in cell structure and mitotic figure formation in immature leukocytes. Alterations in the content and distribution
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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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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: 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.
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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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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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