Abstract
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 microM which could be in the oral cavity during betel quid chewing and NaF(0.8-2.4 mM) significant elevated the number of micronucleated cells in a concentration-dependent manner. In addition, significant prolongation of cell cycles was observed by treatment with arecoline (> or = 2.0 microM) or NaF (2.4 nM) in CHO cells. Both catechin and glycyrrhizin could antagonize not only the increased micronucleated cells induced by arecoline and NaF but also the prolonged cell cycle induced by arecoline in CHO cells. This find implies that the adjuvant ingredients, catechu and liquorice root extract provide not only a flavor but also an antagonist against the genotoxicity of arecoline and fluoride containing betel quid.
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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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Induction of micronuclei by sodium fluoride
More than 500 million people live in communities with artificially or naturally fluoridated drinking water that has been treated with 1 ppm or more of fluoride. Workers in aluminum plants, phosphate fertilizer plants and other fluoride-related factories are also exposed to high concentrations of fluoride. It is reported that workers
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[Modifying effect of nutrition on the mutagenic activity of phosphorus and fluorine compounds].
The test animals were fed with low-grade food during 2-5 months under conditions of acute and chronic action of hydrogen phosphide and hydrogen fluoride induced by inhalation, that resulted in the pronounced impairment of the chromosomal apparatus of the bone marrow cells in the rats. A principal possibility has been
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Genotoxic evaluation of sodium fluoride in the Somatic Mutation and Recombination Test (SMART)
In this study, genotoxic effect of sodium fluoride (NaF) was investigated in Drosophila melanogaster Somatic Mutation and Recombination Test. Third-instar larvae trans-heterozygous for two genetic markers mwh and flr, were treated at different concentrations (2.5 microg/ml, 5 microg/ml and 10 microg/ml) of the test compounds. After the treatment the observed
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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
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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: 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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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/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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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.
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