Abstract
Objective To establish the rat model of cognitive dysfunction induced by chronic fluorosis and to investigate the underlying mechanism.
Methods Animal model of chronic fluorosis was established by feeding Wistar rats on distillated water containing different concentrations of sodium fluoride (0, 50, 100, and 150 mg/L) for six months; Y-maze and open field test were used to evaluate the changes in cognitive ethology of rats; the morphological changes of rat hippocampus were observed using H-E staining.
Results The learning and memory abilities were lower in chronic fluorosis groups, particularly in medium and high fluorosis groups (P <0.05 or P <0.01) than in the normal group. Compared with the normal group, marked morphological changes were observed in the hippocampal cells in high fluorosis group.
Conclusion The rat model has a strong resemblance in cognitive dysfunction caused by chronic fluorosis to that in population of high fluorosis areas, which is available to serve as an animal model to study the cognitive impairment caused by chronic fluorosis.
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Proteomic analysis of hippocampus in offspring male mice exposed to fluoride and lead
Fluoride and lead are two common pollutants in the environment. Previous investigations have found that high fluoride exposure can increase the lead burden. In this experiment, in order to study on the molecular mechanisms of central neural system injury induced by the above two elements, differently expressed protein spots in
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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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Effect of fluoride exposure on synaptic structure of brain areas related to learning-memory in mice.
SUMMARY: Learning-memory behavior was tested in mice on a Y-maze after they drank water containing different concentrations of sodium fluoride. Impairment of the structure of the Gray I synaptic interface in the CA3 area of the hippocampus was analyzed quantitatively by electron microscopy and a computer imaging processor. The main
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Excessive ER stress and the resulting autophagic flux dysfunction contribute to fluoride-induced neurotoxicity.
Highlights Excessive ER stress plays an important role in NaF-induced neurotoxicity. NaF-induced neuronal death is caused by ER stress-elicited apoptosis and the impaired autophagic flux. Impaired autophagic flux was mediated by excessive ER stress in NaF-induced neurotoxicity. Fluoride is capable of inducing neurotoxicity, but its mechanisms remain elusive. This study
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Fluoride exposure decreased learning ability and the expressions of the insulin receptor in male mouse hippocampus and olfactory bulb.
Fluoride is one of the common environmental pollutants. Internal exposure to fluoride is related to the lowered cognitive function and intelligence, particularly for children. Determination of protein content in brain tissue is a means to reflect the functional development of the central nervous system. Insulin and insulin receptor (IR) signaling
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NRC (2006): Fluoride's Neurotoxicity and Neurobehavioral Effects
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Fluoride's Direct Effects on Brain: Animal Studies
The possibility that fluoride ingestion may impair intelligence and other indices of neurological function is supported by a vast body of animal research, including over 40 studies that have investigated fluoride's effects on brain quality in animals. As discussed by the National Research Council, the studies have consistently demonstrated that fluoride, at widely varying concentrations, is toxic to the brain.
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Fluoride Affects Learning & Memory in Animals
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Fluoride & IQ: 68 Studies
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