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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Ameliorative effects of oleanolic acid on fluoride induced metabolic and oxidative dysfunctions in rat brain: experimental and biochemical studies
Beneficial effects of oleanolic acid on fluoride-induced oxidative stress and certain metabolic dysfunctions were studied in four regions of rat brain. Male Wistar rats were treated with sodium fluoride at a dose of 20 mg/kg b.w./day (orally) for 30 days . Results indicate marked reduction in acidic, basic and neutral
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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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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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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 & Rickets
One of fluoride's most well-defined effects on bone tissue is it's ability to increase the osteoid (unmineralized bone) content of bone. When bones have too much osteoid, they become soft and prone to fracture -- a condition known as osteomalacia. When osteomalacia develops during childhood, it is called "rickets." The potential for fluoride
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Fluoride Is Not an Essential Nutrient
In the 1950s, dentists believed that fluoride was a “nutrient.” A nutrient is a vitamin or mineral that is necessary for good health. Dentists believed that fluoride ingestion during childhood was necessary for strong, healthy teeth. A “fluoride deficiency” was thus believed to cause cavities, just like a deficiency of calcium can
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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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