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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[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
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Cytogenetic analysis of human lymphocytes of fluorosis-affected men from the endemic fluorosis region in Nalgonda district of Andhra Pradesh, India
Cytogenetic analysis was carried out on human lymphocytes of 73 fluorosis-affected men from the endemic fluorosis region in Nalgonda district of Andhra Pradesh, India, who were drinking water with a mean concentration of fluoride (F) of 4.13± 0.55 mg/L, range 1.56–8. 36 mg/L. Eighty healthy men, of a similar age
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The effects of sodium fluoride and iodacetamide on mutation induction by x-irradiation in mature spermatoza of drosophila
The effect of two inhibitors of glycolysis, NaF and iodacetamide on the production of recessive lethal mutations by X-rays in mature Drosophila sperm has been investigated. Pre-treatment with NaF resulted in a consistent and highly significant increase of the mutation frequency. This effect is thought to result from interference with
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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
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Effect of sodium fluoride on tumor growth
Recently a report (1) from this laboratory indicated that NaBr in relatively low concentrations accelerated the growth of mouse and egg cultivated tumor tissue. This result occurred when the drug was introduced by way of the drinking water in mice, by injection over the embryonic membranes of eggs inoculated with
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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: 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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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 & 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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