Abstract
Axonal and dendrictic degenerations were observed in non-skeleton fluorosis as the neurological manifestations. Microtubules, composed of the assembled tubulin dimers, are the essential cytoskeleton of axon and dendron. However, the effect of fluoride (F) on microtubules status and tubulin dimer expression in central nerves system remains largely unknown. In this study, the ultrastructure of microtubules and expression of TubB1a and TubB2a were detected in hippocampus of mice orally administrated with 25, 50, or 100mgL(-1) NaF for 60d. Results showed that in F treatment groups, microtubules were broken into discrete fragments and bended, which were no longer stretched and went along the axon well. In addition, the expression of TubB1a and TubB2a on both gene and protein levels were significantly reduced in high F group. The visual results of immunocytochemistry also confirmed the decreased protein expressions of TubB1a and TubB2a. These findings suggested that microtubule lesions could be an important cause for neurodegeneration observed in fluorosis, and F may threaten the microtubule stability by affecting the expression of tubulin dimers.
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Evaluation of fluoride-induced oxidative stress in rat brain: a multigeneration study.
Multigenerational evaluation was made in rats on exposure to high fluoride (100 and 200 ppm) to assess neurotoxic potential of fluoride in discrete areas of the brain in terms of lipid peroxidation and the activity of antioxidant enzyme system. The rats were given fluoride through drinking water (100 and 200 ppm) and
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Effects of fluoride and lead on N-methyl-D-aspartate receptor 1 expression in the hippocampus of offspring rat pups
To investigate whether excitotoxicity is involved in neurotoxicity of fluoride (F) alone and in combination with lead (Pb), the expression levels of the gene and protein N-methyl-D-aspartate receptor 1 (NMDAR1) in the hippocampus of offspring rat pups at postnatal days 14 and 28 exposed to F and/or Pb were determined by quantitative real-time polymerase
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[Expression of receptor for advanced glycation endproducts and nuclear factor kB in brain hippocampus of rat with chronic fluorosis].
Objective To investigate the expressions of receptor for advanced glycation endproducts (RAGE) and nuclear factor kB (NF-kB) in brain hippocampus of rat with chronic fluorosis, and to reveal the mechanism of brain damage resulted from chronic fluorosis. Methods Sixty clean grade SD rats were randomly divided to three groups (20 rats
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Effects of fluoride on synaptic membrane fluidity and PSD-95 expression level in rat hippocampus.
The objective of this study is to investigate the neurotoxicity of drinking water fluorosis on rat hippocampus. Just weaning male Sprague-Dawley rats were randomly divided into four groups and given 15, 30, and 60 mg/L NaF solution and distilled water, respectively, for 9 months. The fluidity of brain synaptic membrane
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Protective effect of lovastatin on neurotoxicity of excessive fluoride in primary hippocampal neurons
The protective role of lovastatin against neurotoxicity induced by fluorosis was investigated by using primary hippocampal neurons. The cholesterol content, activity of superoxide dismutase (SOD), and content of malondialdehyde (MDA) were measured by biochemical assays. The cell viability was assessed by examining the rate of apoptosis by flow cytometry. The
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