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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Fluoride does not induce DNA breakage in Chinese hamster ovary cells in vitro
Fluoride has been widely used in dentistry because it is a specific and effective caries prophylactic agent. However, excess fluoride may represent a hazard to human health, especially by causing injury to genetic material. Genotoxicity tests represent an important part of cancer research to assess the risk of potential carcinogens.
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Health Effects of Ingested Fluoride
Excerpts: INTRODUCTION Fluoridation of drinking water has been a subject of controversy for decades. Over the past 50 years, the incidence of dental caries (cavities) has declined considerably in the United States, an important health advance that most scientists attribute principally to increased access to fluoridated water and dental products. According to
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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
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Ameliorative effects of N-acetylcysteine on fluoride-induced oxidative stress and DNA damage in male rats' testis
This study was to elucidate DNA damage in rats treated with sodium fluoride (NaF) by performing 8-Hydroxy-2-deoxyguanosine (8-OHdG) immunohistochemical staining assays on seminiferous tubules of rats' testis, and also to evaluate the protective effects of N-acetylcysteine (NAC) on spermatogenesis. Male Sprague Dawley (SD) rats were exposed to a single dose
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Genotoxic evaluation of chronic fluoride exposure: micronucleus and sperm morphology studies
The purpose of this study was to investigate the genotoxic effects of chronic fluoride exposure on mammalian cells in vivo by use of the mouse bone-marrow micronucleus test and the sperm morphology methodology. Mice of genotype B6C3F1 were obtained at weaning and maintained on a low-fluoride diet (less than 0.2
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Fluoride's Effect on Male Reproductive System - Human Studies
Consistent with in vitro and animal research, studies of human populations have reported associations between fluoride exposure and damage to the male reproductive system. Most notably, a scientist at the Food & Drug Administration reported in 1994 that populations in the United States with more than 3 ppm fluoride in their water had lower "total fertility rates" than populations with lower fluoride levels.
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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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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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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 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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