Abstract
After the establishment of fluorosis animal model, the gene expression of SNAP-25 was detected in order to provide experimental data for nervous system injury induced by fluoride. The results showed that, compared with the de-ionized water group, SNAP-25 mRNA expression was significantly reduced by fluoride.
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[Expression of receptor for advanced glycation endproducts and nuclear factor kB in brain hippocampus of rat with chronic fluorosis].
Objective To investigate the expressions of receptor for advanced glycation endproducts (RAGE) and nuclear factor kB (NF-kB) in brain hippocampus of rat with chronic fluorosis, and to reveal the mechanism of brain damage resulted from chronic fluorosis. Methods Sixty clean grade SD rats were randomly divided to three groups (20 rats
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Fluoride Alteration of [3H]Glucose Uptake in Wistar Rat Brain and Peripheral Tissues.
The present study was designed to investigate the role of postnatal fluoride intake on [3H]glucose uptake and transport in rat brain and peripheral tissues. Sodium fluoride (NaF) in a concentration of 10 or 50 ppm was added to the drinking water of adult Wistar rats. The control group received distilled
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Protective effect of lovastatin on neurotoxicity of excessive fluoride in primary hippocampal neurons
The protective role of lovastatin against neurotoxicity induced by fluorosis was investigated by using primary hippocampal neurons. The cholesterol content, activity of superoxide dismutase (SOD), and content of malondialdehyde (MDA) were measured by biochemical assays. The cell viability was assessed by examining the rate of apoptosis by flow cytometry. The
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Effects of chronic fluorosis on CAMKIIA, C-FOS, BAX, and BCL-2 channel signalling in the hippocampus of rats
In this study, the neurotoxicity of fluoride (F) in the hippocampus of rats exposed to 15, 30, and 60 mg NaF/L in their drinking water for nine months was investigated. Compared with the control (<0.5 mg F/L), significant increases in the expression of calcium/calmodulin-dependent kinase II alpha (CaMKII?) (F=5.228, p<0.05)
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Effects of fluoride on synapse morphology and myelin damage in mouse hippocampus
Highlights Fluoride induced myelin damage in mouse hippocampus. Fluoride shortened the synaptic cleft and thickened the postsynaptic density. Fluoride altered the expressions of CREB, BDNF, and NCAM in hippocampus. To investigate the fluoride-induced neurotoxicity on mice hippocampus, healthy adult mice were exposed to 25, 50, and 100 mg NaF/L for 60 days.
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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 & 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 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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NRC (2006): Fluoride's Neurotoxicity and Neurobehavioral Effects
The NRC's analysis on fluoride and the brain.
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