Abstract
Silymarin is a well-known potent antioxidant agent. Numerous reports highlighted that antioxidant consumption can mitigate sodium fluoride induced neuronal damage. The present study aimed to examine the ameliorative potential of silymarin on sodium fluoride-induced oxidative stress using the rat brain as model. Silymarin (10 and 20 mg/kg) and vitamin C (10 mg/kg) were intraperitoneally administrated for seven days followed by one week of sodium fluoride (600 ppm) treatment through drinking water. Antioxidant enzyme activities – superoxide dismutase and catalase – the levels of reduced glutathione and lipid peroxidation were evaluated in brain homogenates. The levels of lipid peroxidation were significantly increased in the sodium fluoride treated group (42.0 ± 2.1 nmol MDA eq/g tissue) compared to the control group (36.0 ± 1.1 nmol MDA eq/g tissue). Silymarin at 20 mg/kg showed significant a reduction in the levels of lipid peroxidation (36.0 ± 1.2 nmol MDA eq/g tissue). Treatment of rats with sodium fluoride significantly reduced the activities of the antioxidant enzymes and the levels of reduced glutathione in brain homogenates. Pre-treatment with silymarin prevented the deleterious effects of sodium fluoride intoxication in a dose dependent response. In conclusion, sodium fluoride induced oxidative stress in rat brain which can be prevented with silymarin administration.
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Ameliorative effects of quercetin on sodium fluoride-induced oxidative stress in rat's kidney
OBJECTIVE: The in vivo nephroprotective effect of quercetin against sodium fluoride (NaF)-induced damage was studied. METHODS: Renal injury was induced by daily administration of NaF (600 ppm) through drinking water for 1 week. The levels of reduced glutathione (GSH), lipid peroxidation as well as superoxide dismutase and catalase activity of
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Reversal of fluoride induced cell injury through elimination of fluoride and consumption of diet rich in essential nutrients and antioxidants
The objective of the present communication is to address the issues concerning reversal of fluoride induced cell injury and disease (i.e. fluorosis) through the elimination of fluoride and consumption of a diet containing essential nutrients and antioxidants. Humans afflicted with fluorosis, as a result of consuming fluoride contaminated water or
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Endogenous and exogenous antioxidants status in seminal plasma of skeletal fluorotic patients
Fluoride contamination in water (>1.5ppm) is the global problem for health in general. Fluoride has been reported to be a causative factor for male infertility. However, limited scientific literature is available on this aspect. The objective of the present study was to examine the fluoride induced oxidative burden and its
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Cytoprotective effects of curcumin on sodium fluoride-induced intoxication in rat erythrocytes
Curcumin is well known for its potent antioxidant activity. The result of numerous studies showed that antioxidants can protect against fluoride-induced toxicity. In the present study, protective effects of curcumin against sodium fluoride-induced toxicity in rat erythrocytes were evaluated. Curcumin (10 and 20 mg/kg) and vitamin C (10 mg/kg) were
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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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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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Mayo Clinic: Fluoridation & Bone Disease in Renal Patients
The available evidence suggests that some patients wtih long-term renal failure are being affected by drinking water with as little as 2 ppm fluoride. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers and if fluoride is indeed the cause. It would seem prudent, therefore, to monitor the fluoride intake of patients with renal failure living in high fluoride areas.
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Factors which increase the risk for skeletal fluorosis
The risk for developing skeletal fluorosis, and the course the disease will take, is not solely dependent on the dose of fluoride ingested. Indeed, people exposed to similar doses of fluoride may experience markedly different effects. While the wide range in individual response to fluoride is not yet fully understood, the following are some of the factors that are believed to play a role.
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Skeletal Fluorosis & Individual Variability
One of the common fallacies in the research on skeletal fluorosis is the notion that there is a uniform level of fluoride that is safe for everyone in the population. These "safety thresholds" have been expressed in terms of (a) bone fluoride content, (b) daily dose, (c) water fluoride level, (d) urinary fluoride level, and (e) blood fluoride level. The central fallacy with each of these alleged safety thresholds, however, is that they ignore the wide range of individual susceptibility in how people respond to toxic substances, including fluoride.
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