Abstract
This study investigated the effects of fluoride exposure on the mRNA expression of Cav1.2 calcium signaling pathway and apoptosis regulatory molecules in PC12 cells. The viability of PC12 cell receiving high fluoride (5.0mM) and low fluoride (0.5mM) alone or fluoride combined with L-type calcium channel (LTCC) agonist/inhibitor (5umol/L FPL6417/2umol/L nifedipine) was detected using cell counting kit-8 at different time points (2, 4, 6, 8, 12, 10, and 24h). Changes in the cell configuration were observed after exposing the cells to fluoride for 24h. The expression levels of molecules related to the LTCC were examined, particularly, Cav1.2, c-fos, CAMK II, Bax, and Bcl-2. Fluoride poisoning induced severe cell injuries, such as decreased PC12 cell activity, enhanced cell apoptosis, high c-fos, CAMKII, and Bax mRNA expression levels. Bcl-2 expression level was also reduced. Meanwhile, high fluoride, high fluoride with FPL64176, and low fluoride with FPL64176 enhanced the Cav1.2 expression level. In contrast, low fluoride, high fluoride with nifedipine, and low fluoride with nifedipine reduced the Cav1.2 expression level. Thus, Cav1.2 may be an important molecular target for the fluorosis treatment, and the LTCC inhibitor nifedipine may be an effective drug for fluorosis.
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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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Effects of NaF on the expression of intracellular Ca2+ fluxes and apoptosis and the antagonism of taurine in murine neuron
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
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Alterations of apoptosis and expressions of Bax and Bcl-2 in the cerebral cortices of rats with chronic fluorosis
The aim of the study was to investigate the influence of chronic fluorosis on apoptosis and the expression of Bax and Bcl-2 in the cerebral cortices of rats in an attempt to elucidate molecular mechanisms. Sixty Sprague Dawley (SD) rats were divided randomly into three groups of 20 each: an
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The Effect of Chronic Fluorosis on Calcium Ions and CaMKIIa, and c-fos Expression in the Rat Hippocampus.
This study investigated neurotoxicity of chronic fluorosis in the rat hippocampus. Newly weaning, male, Sprague-Dawley (SD) rats were administered 15, 30, and 60 mg/L sodium fluoride (NaF) solution (fluorine ion concentration 8.25, 16.50, and 33.00 mg/L, respectively), and tap water, for 18 months. The neurotoxicological mechanism was examined with a focus on intracellular
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[Studies on DNA damage and apoptosis in rat brain induced by fluoride].
OBJECTIVE: To explore the DNA damage effects and apoptosis in brain cells of rats induced by sodium fluoride. METHODS: SD rats were divided into two groups, i.e. control group and fluoride treated group, which were injected intraperitoneally with distilled water and sodium fluoride (20 mg.kg(-1).d(-1)) respectively. On the hand, 5
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Fluoride's Direct Effects on Brain: Animal Studies
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