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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[Study of the mechanism of neurone apoptosis in rats from the chronic fluorosis].
Objective: Study the mechanism of action chronic fluorosis in neurones. Methods: Terminal deoxyribo-nucleotide transferase-mediated dUTP-biotin nick end labeling (TUNEL) and flow cytometry (FCM) were used to observe changes of apoptosis in cerebral cells in chronic fluorosis in rats. Results: TUNEL results show non-random expression of DAB positive stain apoptosis cells which appear
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Silymarin and quercetin abrogates fluoride induced oxidative stress and toxic effects in rats
Flavonoids have been extensively studied and reported to possess widespread biological activities, including antioxidant and chelating properties. They have been proposed to exert beneficial effects in a multitude of diseased states generated due to oxidative stress. Therapeutic efficacy of oral administration of Silymarin and Quercetin after fluoride exposure (50 ppm
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Effect of dexmedetomidine on sevoflurane-induced neurodegeneration in neonatal rats.
Background: Structural brain abnormalities in newborn animals after prolonged exposure to all routinely used general anaesthetics have raised substantial concerns for similar effects occurring in millions of children undergoing surgeries annually. Combining a general anaesthetic with non-injurious sedatives may provide a safer anaesthetic technique. We tested dexmedetomidine as a mitigating
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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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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 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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Fluoride & Oxidative Stress
A vast body of research demonstrates that fluoride exposure increases oxidative stress. Based on this research, it is believed that fluoride-induced oxidative stress is a key mechanism underlying the various toxic effects associated with fluoride exposure. It is also well established that fluoride's toxic effects can be ameliorated by exposure
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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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NRC (2006): Fluoride's Neurotoxicity and Neurobehavioral Effects
The NRC's analysis on fluoride and the brain.
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