Abstract
In order to reveal mechanisms of the decreased nicotinic acetylcholine receptors (nAChRs) resulted from fluoride toxicity, we treated PC12 cells by different concentrations of fluoride (0.1-100 ppm) for 48 h, and exposed rats to high doses of fluoride (30 and 100 ppm) in their drinking water for 7 months. The expression of nAChRs at mRNA and protein levels, neurotoxicity and oxidative stress were analyzed in the study. The results indicated that there were no significant changes at mRNA level of the nAChR alpha3, alpha7, beta2 subunits in PC12 cells, and alpha4, alpha7, beta2 subunits in rat brains between the groups with fluorosis and controls. A significant decline in 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction, and increased levels of protein oxidation and lipid peroxidation were observe in PC12 cells treated with high doses of fluoride or rat brains with chronic fluorosis. The decreases of nAChR alpha3 and alpha7 subunit proteins in PC12 cells resulted from fluoride toxicity were mostly prevented by a pretreatment with antioxidant. The results suggest that the deficit of nAChRs induced by fluoride toxicity occurs at the level of post-transcription of the receptor gene, in which a mechanism might be involved in the damage by oxidative stress.
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Role of triphala on fluoride neuorotoxicity in the rat
To investigate effects of sodium fluoride (NaF) on the cerebellum cerebral hemisphere brain of rats and its possible amelioration by the popular Ayurvedic herbal health product triphala, adult female Wistar rats (Rattus novergicus) were administered 10 mg NaF/kg bw/day and 30 mg triphala/kg bw/day for 30 days. A significant decline in body and brain
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Protective role of gallic acid on sodium fluoride induced oxidative stress in rat brain
Gallic acid is known as a potent antioxidant active compound of the edible and medicinal plant Peltiphyllum peltatum. The main objective of this study was to evaluate the neuroprotective effects of gallic acid against sodium fluoride induced oxidative stress in rat brain. Gallic acid (10 and 20 mg/kg) and vitamin C
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Protective effects of curcumin against fluoride-induced oxidative stress in the rat brain
We examined effects of a plant polyphenolic compound, curcumin, against fluoride-induced oxidative stress in the rat brain. Five experimental groups of male rats (10 animals each) were compared. Animals of these experimental groups were treated with curcumin (10 and 20 mg/kg body mass), vitamin C (10 mg/kg), and sample solvent
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Silymarin and quercetin abrogates fluoride induced oxidative stress and toxic effects in rats
Flavonoids have been extensively studied and reported to possess widespread biological activities, including antioxidant and chelating properties. They have been proposed to exert beneficial effects in a multitude of diseased states generated due to oxidative stress. Therapeutic efficacy of oral administration of Silymarin and Quercetin after fluoride exposure (50 ppm
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Neuroprotective effects of methyl-3-O-methyl gallate against sodium fluoride-induced oxidative stress in the brain of rats
Methyl-3-O-methyl gallate (M3OMG) is a rare natural product that showed promising in vitro antioxidant activities. In this study, the protective role of synthetic M3OMG against sodium fluoride (NaF)-induced oxidative stress in rat brain was evaluated. Animals were treated with either M3OMG (10 and 20 mg/kg i.p.), vitamin C (10 mg/kg
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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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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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Fluoride Affects Learning & Memory in Animals
An association between elevated fluoride exposure and reduced intelligence has now been observed in 65 IQ studies. Although a link between fluoride and intelligence might initially seem surprising or random, it is actually consistent with a large body of animal research. This animal research includes the following 45 studies (out
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Fluoride Exposure Increases Metabolic Requirement for Calcium & Vitamin D
It is well known that individuals with nutrient deficiencies are more susceptible to fluoride toxicity, including fluoride's bone effects. As discussed in the following studies, fluoride increases the skeleton's need for calcium (and vitamin D) by increasing the amount of unmineralized tissue (osteoid) in the bone. When insufficient calcium and
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Fluoride's Direct Effects on Brain: Animal Studies
The possibility that fluoride ingestion may impair intelligence and other indices of neurological function is supported by a vast body of animal research, including over 40 studies that have investigated fluoride's effects on brain quality in animals. As discussed by the National Research Council, the studies have consistently demonstrated that fluoride, at widely varying concentrations, is toxic to the brain.
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