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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Chronic exposure to environmentally relevant concentration of fluoride alters Ogg1 and Rad51 expressions in mice: Involvement of epigenetic regulation.
Highlights Almost 200 million people all over the world are facing dreadful effects of fluoride. Mice were treated orally with environmentally relevant concentration of fluoride for 8 months. Fluoride treatment resulted into histopathology, oxidative stress response and transcriptional alterations of Ogg1 and Rad51. DNA fragmentations and apoptosis induction was
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Impaired V-ATPase leads to increased lysosomal pH, results in disrupted lysosomal degradation and autophagic flux blockage, contributes to fluoride-induced developmental neurotoxicity.
Highlights NaF exposure caused developmental neurotoxicity. NaF-induced neuronal apoptosis results from autophagic flux blockage. Raised lysosomal pH disrupting lysosomal degradation caused autophagic flux blockage. V-ATPase is a crucial factor regulating neuronal lysosomal pH. Upregulation of V-ATPase alleviate NaF-induced developmental neurotoxicity. Fluoride is capable of inducing developmental neurotoxicity, yet its mechanisms
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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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Fluoride Stimulates Anxiety- and Depression-like Behaviors Associated with SIK2-CRTC1 Signaling Dysfunction.
Using Sprague-Dawley rats and rat PC12 cells treated with sodium fluoride (NaF), we investigated the effects of SIK2-CRTC1 signaling on the neurobehavioral toxicity induced by fluoride. The in vivo results demonstrated that NaF treatment induced anxiety- and depression-like behaviors in juvenile rats, resulting in histological and ultrastructural abnormalities in the
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[The effects of fluorine on antioxidant system and apoptosis of brain tissue in carp (cyprinus carpio L. )].
The physiological toxicity of sodium fluoride on antioxidant system, organizational structure and apoptosis of brain tissue in Cyprinus carpio Linnaeus were studied. Results showed that along with the increasing concentration of sodium fluoride, the superoxide dismutase (SOD) and glutathione (GSH) activities increased firstly and then were inhibited after 30 days
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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'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'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 & IQ: 76 Studies
Note: See the Updated list of fluoride IQ studies at https://fluoridealert.org/researchers/fluoride-iq-studies/the-fluoride-iq-studies/ • As of July 18, 2022, a total of 85 human studies have investigated the relationship between fluoride and human intelligence. • Of these investigations, 76 studies have reported that elevated fluoride exposure is associated with reduced IQ in humans. • The studies
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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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