Abstract
Standard cytochemical methods were used to investigate the ameliorative effect of melatonin (0.2 mM) on chromosomal aberrations in human lymphocyte cultures induced by arsenic (As2O3, 1.4 ?M) and/or fluoride (NaF, 34 ?M). As2O3 and/or NaF generated a significant increase in the incidence of chromosomal aberrations as compared to control levels. Combined treatment with As2O3 and NaF induced more chromosomal aberrations and aneuploidy than either reagent individually. Melatonin supplements brought about a significant decrease in the number of aberrations, with the percentage of amelioration varying between 53% and 88%. This reduction by melatonin of genotoxic effects exerted by As and/or F is probably attributable to its protective antioxidant action.
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A possible mechanism for combined arsenic and fluoride induced cellular and DNA damage in mice
Arsenic and fluoride are major contaminants of drinking water. Mechanisms of toxicity following individual exposure to arsenic or fluoride are well known. However, it is not explicit how combined exposure to arsenic and fluoride leads to cellular and/or DNA damage. The present study was planned to assess (i) oxidative stress
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Curcumin supplementation protects from genotoxic effects of arsenic and fluoride
The present study was aimed to evaluate curcumin as a potential natural antioxidant to mitigate the genotoxic effects of arsenic (As) and fluoride (F) in human peripheral blood lymphocytes. The study was divided into nine groups consisting of negative control, positive control treated with ethyl methane sulphonate (EMS; 1.93 mM)
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Evaluation of in vitro anti-genotoxic potential of melatonin against arsenic and fluoride in human blood cultures
Melatonin has been for its anti-oxidant potential but not much studied for the anti-genotoxic potential. The current study elucidate the role of melatonin against in vitro genotoxicity by arsenic (As) and fluoride (F). Human peripheral blood cultures were exposed to As (1.4 microM) and F (34 microM), alone and in
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[A clinical study on the syndrome of arsenism and fluorosis].
A clinical study was made on 65 cases with the syndrome of arsenism and fluorosis (SAD) from March 1982 to August 1989. All the cases with this syndrome had drunk a well water containing arsenic 0.6 mg/L and fluorine 3.45 mg/L for a long period. The patients all had the
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Lack of effect of prior treatment with fluoride on genotoxicity of two chemical agents in vitro
The goal of this study was to investigate the ability of fluoride to modulate the genotoxic effects induced by the oxidative agent hydrogen peroxide (H2O2) and the alkylating agent methyl methanesulfonate (MMS) in vitro by the single-cell gel (comet) assay. Chinese hamster ovary cells were exposed in culture for 1
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Luke (2001): Fluoride Deposition in the Aged Human Pineal Gland
This study has added new knowledge on the fate and distribution of fluoride in the body. It has shown for the first time that fluoride readily accumulates in the human pineal gland although there was considerable inter-individual variation
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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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A Critique of Gelberg's Study on Fluoride/Osteosarcoma in New York
The case-control study by Gelberg, published first as a PhD dissertation and then later in two peer-reviewed journals, may represent the most substantive study on fluoride/osteosarcoma previous to Bassin’s 2001 analysis. In assessing Gelberg’s data, we were at first struck by the existence of several notable errors in both the thesis and papers. While these errors do raise questions about the study, our primary concern with Gelberg’s work relates to the methods she used to analyze her data.
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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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