Abstract
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 exposure. The SOD and GSH activities decreased after 60 and 90 days exposure. The content of lipid peroxides (MDA) increased during the whole test period. After 90 days exposure, histopathological changes of brain tissue were observed. It was found that thrombosis and structural changes in the cell layers were resulted from the exposure of sodium fluoride. The biological investigation results showed that there was a positive correlation between the cell apoptosis rate and the MDA levels (r = 0. 9968), but with dosage increasing, Bcl-2 protein concentration decreased, which was positive correlated with SOD and GSH activities (r =0. 9198 and 0. 9889, respectively).
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Rutin attenuates neurobehavioral deficits, oxidative stress, neuro-inflammation and apoptosis in fluoride treated rats.
Highlights The influence of rutin on fluoride – induced neurotoxicity in rat was studied. Rutin reversed the fluoride – induced neurobehavioral deficits in rats. Rutin reversed the fluoride – induced inhibition of acetylcholinesterase activity in rat cerebrum and striatum. Rutin enhanced antioxidant status and inhibited neuro-inflammation and apoptosis in fluoride
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Effects of sodium fluoride on lipid peroxidation and PARP, XBP-1 expression in PC12 cell
This study aims to clarify the molecular mechanism of fluorine exposure that leads to nerve injury. PC12 cells were treated with fluorine at different concentrations (0.5, 1.0, 1.5, and 2.0 mM). Cytoactivity was detected at different time points (2, 4, 6, 8, 12, 24, and 48 h). After 2 h, DCF was used
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Protective role of tert-butylhydroquinone against sodium fluoride-induced oxidative stress and apoptosis in PC12 cells.
The neurotoxicity of fluoride is associated with oxidative stress due to imbalance between production and removal of reactive oxygen species (ROS). In contrast, induction of detoxifying and antioxidant genes through activation of NF-E2-related factor 2 (Nrf2) has been implicated in preventing oxidative stress and apoptosis in neurodegenerative diseases. The present
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Apoptotic and Degenerative Changes in the Enteric Nervous System Following Exposure to Fluoride During Pre- And Post-natal Periods.
Children born in fluorosis endemic areas usually suffer from gastrointestinal complications and are unable to attain normal growth as per their age group. The enteric nervous system (ENS) controls gut movement and functions. It is highly vulnerable to any ingested toxins. Based on observations, it was hypothesized that fluoride exposure
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Protective role of maize purple plant pigment against oxidative stress in fluorosis rat brain.
Excerpts 1 Introduction Given the widespread presence of fluorine in the natural environment, individuals are exposed to fluoride via food intake, inhalation, and dermal contact. Drinking water represents the largest exposure source. In particular, in highly fluoridated regions and in some developed areas that fluoridate the public water supply to reduce dental
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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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Nutrient Deficiencies Enhance Fluoride Toxicity
It has been known since the 1930s that poor nutrition enhances the toxicity of fluoride. As discussed below, nutrient deficiencies have been specifically linked to increased susceptibility to fluoride-induced tooth damage (dental fluorosis), bone damage (osteomalacia), neurotoxicity (reduced intelligence), and mutagenicity. The nutrients of primary importance appear to be calcium,
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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 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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NRC (2006): Fluoride's Neurotoxicity and Neurobehavioral Effects
The NRC's analysis on fluoride and the brain.
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