Abstract
Excessive fluoride ingestion has been identified as a risk factor for fluorosis and oxidative stress. The oxidative stress results from the loss of equilibrium between oxidative and antioxidative mechanisms that can produce kinase activation, mitochondrial disturbance and DNA fragmentation, resulting in apoptosis. Actually many people are exposed to no-adverted fluoride consumption in acute or chronic way. The aim of this study was to determine the effect of sodium fluoride on first molar germ in relation to its effect on antioxidative enzymes immunoexpression and apoptosis. Thirty first molar germs from 1-day-old Balb/c mice were cultured for 24 h with sodium fluoride (0 mM, 1 mM and 5 mM). Immunoexpression determination of CuZnSod, MnSod, catalase, Bax, Bid, caspase 8, caspase 9, caspase 3 and TUNEL assay were performed. Cellular disorganization in ameloblast and odontoblast-papilla zones was observed. CuZnSod and MnSod immunoexpression decrease in experimental groups. Caspase 8, caspase 3, Bax, Bid increase expression and more TUNEL positive cells in both experimental groups than control, suggest that apoptosis induced by fluoride is related to oxidative stress due to reduction of the enzymatic antioxidant.
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Biphasic Functions of Sodium Fluoride (NaF) in Soft and in Hard Periodontal Tissues.
Sodium fluoride (NaF) is widely used in clinical dentistry. However, the administration of high or low concentrations of NaF has various functions in different tissues. Understanding the mechanisms of the different effects of NaF will help to optimize its use in clinical applications. Studies of NaF and epithelial cells, osteoblasts,
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Protective effect of lycopene on fluoride-induced ameloblasts apoptosis and dental fluorosis through oxidative stress-mediated Caspase pathways
Fluoride is an environmental toxicant and induces dental fluorosis and oxidative stress. Lycopene (LYC) is an effective antioxidant that is reported to attenuate fluoride toxicity. To determine the effects of LYC on sodium fluoride (NaF) -induced teeth and ameloblasts toxicity, rats were treated with NaF (10 mg/kg) and/or LYC (10 mg/kg) by
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Fluorosis caused cellular apoptosis and oxidative stress of rat kidneys
As the strongest electronegative element, fluorine can stimulate the production of superoxide radicals in cells. In view of the important roles of kidneys in bone metabolism, the authors analyzed the quantitative pathomorphological characteristics of renal damage and the potential cellular apoptosis and oxidative stress mechanisms in rats treated with excessive
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Sodium fluoride induces apoptosis in mouse embryonic stem cells through ROS-dependent and caspase- and JNK-mediated pathways
Sodium fluoride (NaF) is used as a source of fluoride ions in diverse applications. Fluoride salt is an effective prophylactic for dental caries and is an essential element required for bone health. However, fluoride is known to cause cytotoxicity in a concentration-dependent manner. Further, no information is available on the
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Fluoride exposure abates pro-inflammatory response and induces in vivo apoptosis rendering zebrafish (Danio rerio) susceptible to bacterial infections.
Highlights Chronic fluoride exposure induces histopathological changes in spleen of zebrafish. Fluoride modulates cyp1a, sod1/2, rad51, gadd45ba, baxa/bcl2a and casp3a expression. Fluoride diminishes pro-inflammatory cytokine response in zebrafish. Fluoride leads to immunosuppression rendering zebrafish susceptible to bacterial infections. The present study describes the immunotoxic effect of chronic fluoride exposure on
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Severe Dental Fluorosis: Perception and Psychological Impact
[caption id="attachment_8879" align="aligncenter" width="550"] Severe fluorosis - Photograph by David Kennedy, DDS[/caption] In its severe forms, dental fluorosis causes highly disfiguring brown and black staining of the teeth, which can cause chronic embarrassment and social anxiety for the impacted child. In 1984, a panel from the National Institute of Mental Health (NIMH) warned
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Nutrient Deficiencies Enhance Fluoride Toxicity
It has been known since the 1930s that poor nutrition enhances the toxicity of fluoride. As discussed below, nutrient deficiencies have been specifically linked to increased susceptibility to fluoride-induced tooth damage (dental fluorosis), bone damage (osteomalacia), neurotoxicity (reduced intelligence), and mutagenicity. The nutrients of primary importance appear to be calcium,
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Dental Fluorosis Is a "Hypo-mineralization" of Enamel
Teeth with fluorosis have an increase in porosity in the subsurface enamel ("hypomineralization"). The increased porosity of enamel found in fluorosis is a result of a fluoride-induced impairment in the clearance of proteins (amelogenins) from the developing teeth. Despite over 50 years of research, the exact mechanism by which fluoride impairs amelogin
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Dental Fluorosis in the U.S. 1950-2004
Before the widespread use of fluoride in dentistry, dental fluorosis was rarely found in western countries. Today, with virtually every toothpaste now containing fluoride, and most U.S. water supplies containing fluoride chemicals, dental fluorosis rates have reached unprecedented levels. In the 1950s, it was estimated that only 10% of children in
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Fluoride & Oxidative Stress
A vast body of research demonstrates that fluoride exposure increases oxidative stress. Based on this research, it is believed that fluoride-induced oxidative stress is a key mechanism underlying the various toxic effects associated with fluoride exposure. It is also well established that fluoride's toxic effects can be ameliorated by exposure
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