Abstract
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 (0.5 ml) for a week prior to sodium fluoride intoxication. After treatment, rats of the experimental groups, except for the normal control group, were intoxicated with sodium fluoride (600 ppm through drinking water) for a week. Then, brains were collected and homogenized, and activities of superoxide dismutase and catalase and levels of reduced glutathione and lipid peroxidation final products were evaluated in the brain tissue homogenates. Treatment with curcumin prior to fluoride intoxication significantly normalized the above biochemical parameters; the intensity of protective effects of 20 mg/kg curcumin was close to that of vitamin C.
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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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Mitigating role of quercetin against sodium fluoride-induced oxidative stress in the rat brain
CONTEXT: Quercetin is a well known aglycone flavonoid that is widely found in different food sources. OBJECTIVE: In this study, the in vivo neuroprotective potential of quercetin against sodium fluoride-induced oxidative stress was evaluated. MATERIALS AND METHODS: Wistar rats were divided into five treatment groups and then subjected to daily
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Neuroprotective effect of ascorbic acid and ginkgo biloba against fluoride caused neurotoxicity
Excessive consumption of fluoride through drinking water or other sources lead to skeletal and dental fluorosis. According to the world health organization 23 nations are facing the problem of fluorosis. In the recent past researchers describe the non-skeletal fluorosis where soft tissues and major organs are the victims of fluoride
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Fluoride-induced neuronal oxidative stress amelioration by antioxidants in developing rats
Premated 3-month-old albino rats received 200-ppm fluoride ion (F) in their drinking water; the pups born to them were separately administered, in groups of six, daily doses of clinoptilolite, zinc, selenium, vitamin C, vitamin D, and propolis. On post-partum day 45, the pups were sacrificed, brain regions separated, and oxidative
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Oxidative stress might be a mechanism connected with the decreased alpha 7 nicotinic receptor influenced by high-concentration of fluoride in SH-SY5Y neuroblastoma cells
The possible mechanism concerning decreased alpha 7 nicotinic acetylcholine receptor (nAChR) influenced by fluorosis was investigated. SH-SY5Y cells were exposed to fluoride within the range of 0.05-5 mM [corrected] or ferrous iron (1-100 mM) [corrected] a free radical inducer. The levels of alpha 7 nAChR expression, lipid peroxidation and protein
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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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Fluoridation, Dialysis & Osteomalacia
In the 1960s and 1970s, doctors discovered that patients receiving kidney dialysis were accumulating very high levels of fluoride in their bones and blood, and that this exposure was associated with severe forms of osteomalacia, a bone-softening disease that leads to weak bones and often excruciating bone pain. Based on
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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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Fluoride Exposure Increases Metabolic Requirement for Magnesium
Fluoride's toxicity is significantly enhanced in the presence of nutritional deficiencies. Similarly, fluoride exposure increases the body's requirement for certain nutrients. An individual with a high intake of fluoride, for example, will need a proportional increase in calcium to avoid the mineralization defects (e.g., osteomalacia) that fluoride causes to bone
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