Abstract
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 of taurine in intervention, the toxic effects of NaF on neurons, is also investigated. The primary mouse hippocampal neurons were incubated with 5.0, 10.0, 15.0, 20.0, and 40.0?mg NaF/L in vitro and Kunming mice were exposed to 0.7, 2.8, and 11.2?mg NaF/kg and 7.5 and 15.0?mg taurine/kg in vivo. Intracellular Ca(2+) fluxes and apoptosis were assayed. Compared with the control, the significant differences of intracellular Ca(2+) concentration and apoptotic peaks were found in 5.0-40.0?mg NaF/L groups in vitro (p?<?0.01) and in the groups of 0.7-11.2?mg NaF/kg in vivo (p?<?0.01). Instantaneously, taurine can minimize F-induced neurotoxicity significantly at doses of 7.5 and 15.0?mg/kg (p?<?0.01). The present study herein suggested that NaF could increase intercellular Ca(2+) concentration leading to apoptosis. Meanwhile, taurine could minimize neurotoxicity caused by fluoride through decreasing intercellular Ca(2+) concentration and cell apoptosis.
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Neuroprotective effect of ascorbic acid and ginkgo biloba against fluoride caused neurotoxicity
Excessive consumption of fluoride through drinking water or other sources lead to skeletal and dental fluorosis. According to the world health organization 23 nations are facing the problem of fluorosis. In the recent past researchers describe the non-skeletal fluorosis where soft tissues and major organs are the victims of fluoride
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Ameliorative effects of oleanolic acid on fluoride induced metabolic and oxidative dysfunctions in rat brain: experimental and biochemical studies
Beneficial effects of oleanolic acid on fluoride-induced oxidative stress and certain metabolic dysfunctions were studied in four regions of rat brain. Male Wistar rats were treated with sodium fluoride at a dose of 20 mg/kg b.w./day (orally) for 30 days . Results indicate marked reduction in acidic, basic and neutral
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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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Mitigating role of quercetin against sodium fluoride-induced oxidative stress in the rat brain
CONTEXT: Quercetin is a well known aglycone flavonoid that is widely found in different food sources. OBJECTIVE: In this study, the in vivo neuroprotective potential of quercetin against sodium fluoride-induced oxidative stress was evaluated. MATERIALS AND METHODS: Wistar rats were divided into five treatment groups and then subjected to daily
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Roles of mitochondrial fission inhibition in developmental fluoride neurotoxicity: mechanisms of action in vitro and associations with cognition in rats and children.
Fluoride neurotoxicity is associated with mitochondrial disruption. Mitochondrial fission/fusion dynamics is crucial to maintain functional mitochondria, yet little is known about how fluoride perturbs this dynamics and whether such perturbation contributes to impaired neurodevelopment. Here in human neuroblastoma SH-SY5Y cells treated with sodium fluoride (NaF, 20, 40 and 60 mg/L), mitochondrial
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Fluoride's Effect on Fetal Brain
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Fluoride Exposure Increases Metabolic Requirement for Magnesium
Fluoride's toxicity is significantly enhanced in the presence of nutritional deficiencies. Similarly, fluoride exposure increases the body's requirement for certain nutrients. An individual with a high intake of fluoride, for example, will need a proportional increase in calcium to avoid the mineralization defects (e.g., osteomalacia) that fluoride causes to bone
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NRC (2006): Fluoride's Neurotoxicity and Neurobehavioral Effects
The NRC's analysis on fluoride and 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 Exposure Increases Metabolic Requirement for Calcium & Vitamin D
It is well known that individuals with nutrient deficiencies are more susceptible to fluoride toxicity, including fluoride's bone effects. As discussed in the following studies, fluoride increases the skeleton's need for calcium (and vitamin D) by increasing the amount of unmineralized tissue (osteoid) in the bone. When insufficient calcium and
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