Abstract
Fluoride and aluminium have been reported to cause severe alterations in the brain. However, their exact mechanisms of neurotoxic activities remain unknown.
AIM: This study was designed to investigate the role of fluoride and aluminium in neuronal transport, lysosomal, cell cycle protein and acetylcholinesterase activities.
METHOD: Adult Wistar rats were given low and high doses of fluoride, aluminium and a combination of both with the control group receiving distilled water for 30 days. Blood sera and brain homogenates were quantified for alkaline phosphatase (biomarker for neuronal transport) activities. Brain sections were stained with cresyl fast violet to detect neuronal cell damage. Histochemical demonstration of acetylcholinesterase (AChE) activity and the immunohistochemical detection of cell cycle protein (anti-cyclin D) and lysosomal protein (anti-cathepsin D) were done using the antigen retrieval method.
RESULT: Results showed severe histomorphologic alterations, dysregulation of membrane transport activities, inhibition of AChE activities and increased expression of lysosomal and cell cycle proteins.
CONCLUSION: These findings confirm that excessive fluoride and aluminium intake induces the progression of cell death which inhibit AChE activities and trigger the release of lysosomal and cell cycle proteins.
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Effects of high fluoride and arsenic on brain biochemical indexes and learning-memory in rats
Nine-six Wistar rats were randomly divided into four groups of 24 rats in each group (female:male = 1:1). Over a period up to 90 days, with one untreated group as controls, the other three groups were administered, respectively, high fluoride (100 mg NaF/L), high arsenic (50 mg As2O3/L), or both
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Interplay of glia activation and oxidative stress formation in fluoride and aluminium exposure.
BACKGROUND: Oxidative stress formation is pivotal in the action of environmental agents which trigger the activation of glial cells and neuroinflammation to stimulate compensatory mechanisms aimed at restoring homeostasis. AIM: This study sets to demonstrate the interplay of fluoride (F) and aluminium (Al) in brain metabolism. Specifically, it reveals how oxidative
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Fluoride enhances the effect of aluminium chloride on interconnections between aggregates of hippocampal neurons
The role of fluoride in aluminium neurotoxicity was studied using an in vitro system of cultured hippocampal neurons from foetal rats. Sodium fluoride (50 microM) and aluminium chloride (12.5 microM) were administered alone or in a specific combination (50 + 12.5 microM) in a 14-day culture in a chemically defined
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Confirmation of and explanations for elevated blood lead and other disorders in children exposed to water disinfection and fluoridation chemicals
Silicofluorides (SiFs), fluosilicic acid (FSA) and sodium fluosilicate (NaFSA), are used to fluoridate over 90% of US fluoridated municipal water supplies. Living in communities with silicofluoride treated water (SiFW) is associated with two neurotoxic effects: (1) Prevalence of children with elevated blood lead (PbB>10microg/dL) is about double that in non-fluoridated
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Buffalo (Bubalus bubalis) epiphyseal proteins give protection from arsenic and fluoride-induced adverse changes in acetylcholinesterase activity in rats
The objective of this study was to determine the effect of fluoride (F) and arsenic (As) on the activity of acetylcholinesterase (AChE), a critically important nervous system enzyme, and to test the protective role of buffalo epiphyseal (pineal) proteins (BEP) in rats. Arsenic (20 mg/kg BW, intraperitoneally) and F (150
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NRC (2006): Fluoride's Neurotoxicity and Neurobehavioral Effects
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