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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Cognitive Decline of Rats with Chronic Fluorosis Is Associated with Alterations in Hippocampal Calpain Signaling.
The study was designed to evaluate an influence of excessive fluoride (F-) intake on cognitive capacities of adult rats and on proteins of memory-related calpain signaling in hippocampus. Control animals were given water with natural F- content of 0.4 ppm; rats from other groups consumed the same water supplemented with 5,
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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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Gut microbiota perturbations and neurodevelopmental impacts in offspring rats concurrently exposure to inorganic arsenic and fluoride.
Many “hot spot” geographic areas across the world with drinking water co-contaminated with inorganic arsenic (iAs) and fluoride (F-), two of the most common natural contaminants in drinking water. Both iAs and F- are known neurotoxins and affect neurodevelopment of children. However, very few studies have investigated the neurodevelopmental effects
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Gestational exposure to fluoride impairs cognition in C57 BL/6 J male offspring mice via the p-Creb1-BDNF-TrkB signaling pathway.
Highlights Pregnant mice were exposed to environmentally relevant doses of sodium fluoride from GD1 to GD20. Exposure to sodium fluoride resulted in structural and functional impairments in male offspring mouse hippocampus. The activation of P-Creb1 signaling pathway played a role in sodium fluoride-induced cognitive impairment. We provided new insight
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Fluoride & IQ: 76 Studies
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