Abstract
Sodium fluoride (NaF) has been shown to be cytotoxic and produces inflammatory responses in humans. However, the cellular mechanisms underlying the neurotoxicity of fluoride are unclear. The present study aims to define a possible mechanism of NaF-induced neurotoxicity with respect to apoptosis and intracellular Ca(2+) fluxes. Meanwhile, the cytoprotective role of taurine in intervention, the toxic effects of NaF on neurons, is also investigated. The primary mouse hippocampal neurons were incubated with 5.0, 10.0, 15.0, 20.0, and 40.0?mg NaF/L in vitro and Kunming mice were exposed to 0.7, 2.8, and 11.2?mg NaF/kg and 7.5 and 15.0?mg taurine/kg in vivo. Intracellular Ca(2+) fluxes and apoptosis were assayed. Compared with the control, the significant differences of intracellular Ca(2+) concentration and apoptotic peaks were found in 5.0-40.0?mg NaF/L groups in vitro (p?<?0.01) and in the groups of 0.7-11.2?mg NaF/kg in vivo (p?<?0.01). Instantaneously, taurine can minimize F-induced neurotoxicity significantly at doses of 7.5 and 15.0?mg/kg (p?<?0.01). The present study herein suggested that NaF could increase intercellular Ca(2+) concentration leading to apoptosis. Meanwhile, taurine could minimize neurotoxicity caused by fluoride through decreasing intercellular Ca(2+) concentration and cell apoptosis.
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Molecular mechanism of brain impairment caused by drinking-acquired fluorosis and selenium intervention
This study investigated the molecular mechanism of brain impairment induced by drinking fluoridated water and selenium intervention. Results showed that the learning and memory of rats in NaF group significantly decreased. Moreover, the number of apoptotic cells, the expression levels of Cytc mRNA and protein, and the expression levels of
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Protective effects of blackberry and quercetin on sodium fluoride-induced oxidative stress and histological changes in the hepatic, renal, testis and brain tissue of male rat
BACKGROUND: Sodium fluoride (NaF) intoxication is associated with oxidative stress and altered antioxidant defense mechanism. The present study was carried out to evaluate the potential protective role of blackberry and quercetin (Q) against NaF-induced oxidative stress and histological changes in liver, kidney, testis and brain tissues of rats. METHODS: The rats
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Changed expressions of N-methyl-D-aspartate receptors in the brains of rats and primary neurons exposed to high level of fluoride
Expressions of N-methyl-d-aspartic acid receptors (NMDARs) in the brains of rats and primary neurons exposed to high fluoride were investigated. Sprague-Dawley rats were divided randomly into a fluorosis group (50 ppm fluoride in the drinking water for 6 months) and controls (<0.5ppm fluoride) and the offspring from these rats sacrificed
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Fluoride-induced neuron apoptosis and expressions of inflammatory factors by activating microglia in rat brain
Excessive exposure to fluoride results in structural and functional damages to the central nervous system (CNS), and neurotoxicity of fluoride may be associated with neurodegenerative changes. Chronic microglial activation appears to cause neuronal damage through producing proinflammatory cytokines and is involved in many neurodegenerative disorders. It is not known about
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Neuroprotective influence of taurine on fluoride-induced biochemical and behavioral deficits in rats
Epidemiological and experimental studies have demonstrated that excessive exposure to fluoride induced neurodevelopmental toxicity both in humans and animals. Taurine is a free intracellular B-amino acid with antioxidant and neuroprotective properties. The present study investigated the neuroprotective mechanism of taurine by evaluating the biochemical and behavioral characteristics in rats exposed
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Fluoride & IQ: 67 Studies
As of May 2020, a total of 75 studies have investigated the relationship between fluoride and human intelligence. Of these investigations, 67 studies have found that elevated fluoride exposure is associated with reduced IQ in humans, while over 60 animal studies have found that fluoride exposure impairs the learning and/or
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Fluoride's Effect on Fetal Brain
The human placenta does not prevent the passage of fluoride from a pregnant mother's bloodstream to the fetus. As a result, a fetus can be harmed by fluoride ingested pregnancy. Based on research from China, the fetal brain is one of the organs susceptible to fluoride poisoning. As highlighted by the excerpts
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Fluoride: Developmental Neurotoxicity.
Developmental Neurotoxicity There has been a tremendous amount of research done on the association of exposure to fluoride with developmental neurotoxicity. There are over 60 studies reporting reduced IQ in children and several on the impaired learning/memory in animals. And there are studies which link fluoride to Attention Deficit Hyperactivity Disorder. Teaching
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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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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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