Abstract
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 only in the hippocampus CA4 region. FCM results show that the percentage of DNA fragmentation increased markedly in the cerebral neurones of rats with chronic fluorosis but not in different cerebral regions.
Conclusions: There is a tendency for neurone apoptosis in chronic fluorosis in rats. It is most evident with changes in pathology. It is not likely that only one form of neurone damage exist in the process of chronic fluorosis. There are recessive changes and apoptosis in the process at the same time.
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[Studies on DNA damage and apoptosis in rat brain induced by fluoride].
OBJECTIVE: To explore the DNA damage effects and apoptosis in brain cells of rats induced by sodium fluoride. METHODS: SD rats were divided into two groups, i.e. control group and fluoride treated group, which were injected intraperitoneally with distilled water and sodium fluoride (20 mg.kg(-1).d(-1)) respectively. On the hand, 5
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Effects of chronic fluorosis on the brain.
Highlights Reviewing the mechanism of brain injury caused by chronic fluorosis is of great significance for protecting residents in fluorosis endemic areas. Abstract This article reviews the effects of chronic fluorosis on the brain and possible mechanisms. We used PubMed, Medline and Cochraine databases to collect data on fluorosis, brain injury,
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Co-exposure to arsenic and fluoride on oxidative stress, glutathione linked enzymes, biogenic amines and DNA damage in mouse brain.
We studied the effects of combined exposure to arsenic and fluoride on (i) brain biogenic amines, oxidative stress and its correlation with glutathione and linked enzymes; (ii) alterations in the structural integrity of DNA; and (iii) brain and blood arsenic and fluoride levels. Efficacy of alpha-tocopherol in reducing these changes
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Fluoride-induced neuron apoptosis and expressions of inflammatory factors by activating microglia in rat brain
Excessive exposure to fluoride results in structural and functional damages to the central nervous system (CNS), and neurotoxicity of fluoride may be associated with neurodegenerative changes. Chronic microglial activation appears to cause neuronal damage through producing proinflammatory cytokines and is involved in many neurodegenerative disorders. It is not known about
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Changed expressions of N-methyl-D-aspartate receptors in the brains of rats and primary neurons exposed to high level of fluoride
Expressions of N-methyl-d-aspartic acid receptors (NMDARs) in the brains of rats and primary neurons exposed to high fluoride were investigated. Sprague-Dawley rats were divided randomly into a fluorosis group (50 ppm fluoride in the drinking water for 6 months) and controls (<0.5ppm fluoride) and the offspring from these rats sacrificed
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