Abstract
Co-existing as environmental pollutants in certain areas of China where lead (Pb) is mined, fluoride (F) and Pb pose serious risks to the human central nervous system (CNS). Calcium/calmodulin-dependent protein kinase II (CaMKII) expression, which is involved in the process of learning and memory, has an important role in CNS functioning. Here, in order to verify whether F and/or Pb affect CaMKII expression, we determined the CaMKII expression level in the hippocampus of rats administered 150 mg sodium fluoride/L and/or 300 mg lead acetate/L in their drinking water for 30 days. Through quantitative positioning analysis by western blotting and immunofluorescence, respectively, CaMKII expression levels in the F, Pb, and F plus Pb groups were found to be significantly depressed compared with controls. Interestingly, the western blotting technique, but not the immunofluorescence results indicated greater depression in the Pb group than in either the F or the F+Pb group. Overall, these findings may be helpful to gain a better understanding of the mechanism underlying F and Pb combined neurotoxicity.
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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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Decreased learning ability and low hippocampus glutamate in offspring rats exposed to fluoride and lead.
Fluoride (F) and lead (Pb) are two common environmental pollutants which are linked to the lowered intelligence, especially for children. Glutamate, a major excitatory neurotransmitter in the central nervous system, plays an important role in the process of learning and memory. However, the impact of F and Pb alone or
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MiR-132, miR-204 and BDNF-TrkB signaling pathway may be involved in spatial learning and memory.
Highlights Spatial learning and memory of offspring rats were impaired after exposure to fluorine combined with aluminium(FA). Hippocampal miR-132 and miR-204 were increased after FA exposure. Hippocampal BDNF-TrkB signaling pathway was down-regulated after FA exposure. There were antagonistic effects between F and Al, with Al reducing the toxicity of F. Fluorine
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Fluoride enhances the effect of aluminium chloride on interconnections between aggregates of hippocampal neurons
The role of fluoride in aluminium neurotoxicity was studied using an in vitro system of cultured hippocampal neurons from foetal rats. Sodium fluoride (50 microM) and aluminium chloride (12.5 microM) were administered alone or in a specific combination (50 + 12.5 microM) in a 14-day culture in a chemically defined
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Fisetin prevents fluoride- and dexamethasone-induced oxidative damage in osteoblast and hippocampal cells
Fluoride intoxication and dexamethasone treatment produce deleterious effects in bone and brain. The aim of this study was to evaluate the effect of fluoride (F) and dexamethasone (Dex) co-exposure on oxidative stress and apoptosis in osteoblast-like MC3T3-E1 and hippocampal HT22 cell lines. Co-exposure to F and Dex resulted in a
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