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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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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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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Chronic AIF3 Administration: II. Selected Historical Observations.
Male Long-Evans rats were divided into four groups based on the concentrations of the AlF3 in the drinking water: 0.5 ppm, 5.0 ppm, 50 ppm, or a control solution of double-distilled, de-ionized water. Water was available ad libitum for 45 weeks. Following the behavioral studies, histological, immunohistochemical, and overall brain
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Protective effect of resveratrol against neuronal damage through oxidative stress in cerebral hemisphere of aluminum and fluoride treated rats.
Aluminum has no defined biological function and it is potentially involved in the pathogenesis of neurodegenerative disorders. Furthermore, the presence of fluoride causes more aluminum to accumulate in the brain, resulting in increased neuronal damage. In recent years, resveratrol through its ameliorative effects was found to be a neuroprotectant. This
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Chronic Fluoride Exposure and the Risk of Autism Spectrum Disorder.
The continuous rise of autism spectrum disorder (ASD) prevalent in the past few decades is causing an increase in public health and socioeconomic concern. A consensus suggests the involvement of both genetic and environmental factors in the ASD etiopathogenesis. Fluoride (F) is rarely recognized among the environmental risk factors of
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