Abstract
The mechanisms underlying the neurotoxicity of fluorosis still remain obscure. To investigate DNA damage, cell-cycle distribution and expression of nuclear factor kappa B (NF-kappaB) induced by fluoride, the primary rat hippocampal neurons were incubated with various concentrations (20mg/l, 40 mg/l, and 80 mg/l) of sodium fluoride for 24 h in vitro. Our results showed that olive tail moments (OTMs) were significantly elevated in all fluoride-treated groups, while significant increases in the percentage of DNA in the tail were, respectively, observed at 40 mg/l and 80 mg/l levels of fluoride. An increase in the proportion of cells in S-phase was observed in response to the treatment of 40 mg/l and 80 mg/l fluoride. Gene expression of NF-kappaB was also enhanced by fluoride treatment in a dose-dependent manner. The results indicated that fluoride could induce S-phase cell-cycle arrest, up-regulation of NF-kappaB and DNA damage in primary rat hippocampal neurons.
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[Study of the mechanism of neurone apoptosis in rats from the chronic fluorosis].
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
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[Effects of selenium and zinc on the DNA damage caused by fluoride in pallium neural cells of rats].
To investigate the effects of fluoride on DNA damage as well as the effects of selenium and zinc against fluoride respectively or jointly in pallium neural cells of rats, single cell gel electrophoresis was used to detect the DNA damage of neural cells prepared in vitro. The results showed that
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Comet assay of DNA damage in brain cells of adult rats exposed to high fluoride and low iodine.
Thirty-two one-month-old Wistar albino rats were divided randomly into four equal groups of eight (female:male = 3:1). To assess damage to DNA in their brain cells, the first group (1) of rats served as the untreated control, the second group (2) was administered high fluoride (HiF, 100 mg NaF/L in the drinking water), the third group
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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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[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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NRC (2006): Fluoride's Neurotoxicity and Neurobehavioral Effects
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