Abstract
Sprague Dawley albino rats were treated with 30, 45, and 75 mg NaF/kg body weight/day respectively for 20 days and 35 days to study neurotoxic effect of fluoride. The control rats were injected with double distilled water 1cc/kg body weight/day. The animals were sacrificed and the cerebrum was analysed for neurodegenerative anomalies. The adenomatous foci were formed in the cerebral cortex containing degenerating glial cells. The glial cells became vacuolated and showed hyperchromatization of nuclei in brain of rats treated with 30 mg NaF/kg body weight/day. The chain formation of the disintegrated glial cells, senile plaque and large globose shaped neurofibillary tangle inside the perikaryon in cerebral cortex were observed in rats treated with 45 mg NaF/kg body weight/day. An elongated highly chromatolytic region with large number of vacuolated cells was visible. In some neurons, neuroplasm become hyperchromatic, fragmentation and apoptosis of nuclei was prominent. Pleomorphic, irregular glial cells showed necrosis, the cerebral cortex exhibited diffused haemorrhages in rats of 75 mg NaF dose group. The results of present study revealed a fairly consistent pattern of adverse effects by fluoride on cerebral neuropathology, which may be a cause of neurological sequelae and abnormal neuro-behavioural patterns in fluorosis.
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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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Oxidative stress might be a mechanism connected with the decreased alpha 7 nicotinic receptor influenced by high-concentration of fluoride in SH-SY5Y neuroblastoma cells
The possible mechanism concerning decreased alpha 7 nicotinic acetylcholine receptor (nAChR) influenced by fluorosis was investigated. SH-SY5Y cells were exposed to fluoride within the range of 0.05-5 mM [corrected] or ferrous iron (1-100 mM) [corrected] a free radical inducer. The levels of alpha 7 nAChR expression, lipid peroxidation and protein
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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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Cytochemical response of kidney, liver and nervous system of fluoride ions in drinking water
Morphological and cytochemical studies on the squirrel monkey have been made after maintaining the sujects on pure distilled water and fluoridated distilled water for 18 months with the objective of determining the effect of fluoride on the activity of some hydrolytic and oxidative enzymes in the kidney, liver and nervous
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Effects of fluoride on the expression of NCAM, oxidative stress, and apoptosis in primary cultured hippocampal neurons.
The mechanisms underlying the neurotoxicity of endemic fluorosis still remain unknown. To investigate the expression level of neural cell adhesion molecules (NCAM), oxidative stress, and apoptosis induced by fluoride, the primary rat hippocampal neurons were incubated with 20, 40, and 80 mg/l sodium fluoride for 24 h in vitro. The
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Fluoride's Direct Effects on Brain: Animal Studies
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