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Fluoride does not induce DNA breakage in Chinese hamster ovary cells in vitro
Brazilian Oral Research, 2004
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. In the current study, the potential DNA damage associated with exposure to fluoride was assessed by the single cell gel (comet) assay in vitro. Chinese hamster ovary cells were exposed to sodium fluoride (NaF) at final concentration ranging from 7 to 100 µg/ml for 3 h, at 37°C. The results pointed out that NaF in all concentrations tested did not contribute to DNA damage as depicted by the mean tail moment and tail intensity. These findings are clinically important since they represent an important contribution to a correct evaluation of the potential health risk associated with the exposure to dental agents.
Putative mechanisms of genotoxicity induced by fluoride: a comprehensive review
Environmental science and pollution research international, 2017
Genotoxicity is the ability of an agent to produce damage on the DNA molecule. Considering the strong evidence for a relationship between genetic damage and carcinogenesis, to elucidate the putative mechanisms of genotoxicity induced by fluoride are important to measure the degree of risk involved to human populations. The purpose of this article is to provide a comprehensive review on genotoxicity induced by fluoride on the basis of its mechanisms of action. In the last 10 years, all published data showed some evidence related to genotoxicity, which is due to mitochondrial disruption, oxidative stress, and cell cycle disturbances. However, this is an area that still requires a lot of investigation since the published data are not sufficient for clarifying the genotoxicity induced by fluoride. Certainly, the new information will be added to those already established for regulatory purposes as a safe way to promote oral healthcare and prevent oral carcinogenesis.
Biomedicines
Background: Fluorides are an essential component of oral hygiene products used to prevent dental decay. Therefore, a question arises about the potential harms of joint use of fluoridated toothpaste and mouthwashes regarding the increased amount of fluoride in the oral mucosa. Methods: This prospective, double-blinded parallel randomized clinical trial was conducted using a buccal micronucleus cytome assay (BMCyt assay). Forty-one participants were randomly assigned to the two groups. All participants used the same kinds of toothpaste for 12 weeks, designed explicitly for this study (non-fluoride, 1050 ppm F, and 1450 ppm F each for 4 weeks). Simultaneously, during the 3 months of the research, one group used mouthwash with fluoride (450 ppm) and another without fluoride. The buccal mucosal sampling was taken before using the tested products and after 4, 8, and 12 weeks of their use. Results: The frequency of micronuclei and the majority of other scored endpoints from the BMCyt assay...
2015
Fluoride is an essential trace element but also an environmental contaminant with major sources of exposure being drinking water, food and pesticides. Previous studies showed that sodium fluoride (NaF) at 5 mM or more is required to induce apoptosis and chromosome aberrations and proposed that DNA damage and apoptosis play an important role in toxicity of excessive fluoride. The aim of this study is directed to understand the nature of DNA-lesions induced by NaF by allowing its interaction with radiation induced DNAlesions. NaF 5 mM was used after observing inability to induce DNA damages and apoptosis by single exposure with 50 M or 1 mM NaF. Co-exposure to NaF and radiation significantly increased the frequency of aberrant metaphases and exchange aberrations in human lymphocytes and arrested the cells in G1 stage instead of apoptotic death. Flow cytometric analysis, DNA fragmentation and PARP-cleavage analysis clearly indicated that 5 mM NaF together with radiation (1 Gy) induced ...
Fluoride
: In an in vivo genotoxicity investigation of the action of fluoride (F) on bone marrow cells, sodium fluoride (NaF) was administered through the drinking water of 2–3 month old Swiss albino mice for 30 days at lower (7.5, 15, and 30 mg/L) and higher concentrations (100 and 150 mg/L). Mitotic inhibition, chromosomal aberrations, and chromatid breaks were most pronounced in mice that received the relatively low dose of 15 mg NaF/L. The effects became obvious after the first week of treatment and were maximal after 3 months of sustained exposure. Chromosome aberrations induced by one month treatment with 15 mg NaF/L was significantly higher than those found with the 100 and 150 mg NaF/L concentrations. The total number of femur bone marrow cells remained unchanged in all the treatment groups except in the 150 mg NaF/L group, in which it declined significantly. F treatment did not elicit any change in the percentage of viable cells in the bone marrow. Depletion of S-phase fraction of b...
Effect of three fluoride compounds on the growth of oral normal and tumor cells
In vivo (Athens, Greece)
Comparative study of the growth inhibition by different types of fluoride compounds used in dentistry has been limited. We investigated the effects of sodium fluoride (NaF), diammine silver fluoride [Ag(NH3)2F] and 5-fluorouracil (5-FU) on the growth of eleven human normal and tumor cells in total. Viable cell number was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Apoptosis induction was evaluated by caspase-3 activation and DNA fragmentation. Fluoride was determined using a fluoride-specific electrode. All compounds had little or no growth stimulating effect (hormesis) on all cells. Ag(NH3)2F exhibited the highest cytotoxicity towards both normal and tumor cells. 5-FU had the selective cytostatic activity towards oral squamous cell carcinoma cell lines, whereas NaF was selectively cytotoxic towards glioblastoma cell lines. None of the compounds induced internucleosomal DNA fragmentation and only 5-FU induced slight activation of caspase-3...
Mutation Research/Genetic Toxicology and Environmental Mutagenesis, 2013
Fluoride compounds are naturally present in soil, water and food. The objective of this study was to investigate the genotoxic and oxidative damage induced by chronic fluoride exposure on mammalian cells in vivo. For this purpose, the genotoxic potential was investigated in bone marrow cells by the micronucleus test, chromosome aberration assay and comet assay (DNA strand breaks). In addition, DNA damage was evaluated in soft tissues and organs like spleen, liver and kidney cells. The oxidative damage was assessed by selective biochemical parameters by the measurement of lipid peroxidation, reduced glutathione (GSH), glutathione S-transferase (GST) and catalase (CAT) activity in liver. Adult Swiss albino male mice were exposed to sodium fluoride in drinking water at the concentrations of 4, 12 and 20 mg/L for 30 consecutive days. Control groups (vehicle and positive) were also included. Animals were sacrificed; bone marrow and soft tissue samples were collected and subjected to series of assays respectively. We observed that NaF exposure, at the various concentrations tested caused a significant increase in the frequency of micronucleus (MN) in polychromatic erythrocytes (PCEs), structural chromosome aberrations in bone marrow cells. With the exception of the spleen cells, DNA damage was observed in bone marrow cells as well as in kidney and liver cells. We found an increase in lipid peroxidation, and catalase activity as well as decrease in glutathione activity (GSH and GST) in liver of mice respectively which were exposed to sodium fluoride. In conclusion, the data obtained clearly documents that NaF exhibits genotoxic activity and enhanced oxidative damage in mouse model.
Cell Biology and Toxicology, 1996
The mutagenic activity of sodium fluoride at reduced pH was studied in the V79/HGPRT system. Statistical analysis of the results of mutagenicity testing suggests that, despite its high toxicity, sodium fluoride has no mutagenic effects at reduced pH on hamster V79 cells. Short-term treatment of cells with sodium fluoride at reduced pH inhibits growth activity of cells as well as synthesis of pulse-labeled nascent DNA and cumulative RNA synthesis and proteosynthesis. From the results of this study we suggest that an acid environment which supports formation of hydrogen fluoride increases toxic but not mutagenic potencies of sodium fluoride.