Abstract
OBJECTIVE: To investigate the pathogenesis of brain damage by fluoride intoxication, phospholipid content, and fatty acid composition in rat brain with fluorosis were annlysed.
METHODS: Wistar rats were fed with NaF in various amounts and time periods to produce the animal model with chronic fluorosis. Phospholipid content and fatty acids composition were analysed using high performance liquid chromatography and gas chromatography, respectively.
RESULTS: All animals fed with high amount of fluoride suffered from chronic fluorosis. The total brain phospholipid content was lower in the rat treated with fluoride, which mainly influenced phosphatidylethanolamine, phosphatidylcholin, and phosphatidylserine. No modifications were detected in fatty acid and aldehyde compositions of individual phospholipid classes.
CONCLUSION: The metabolism of brain phospholipid might be interfered by fluoride accumulated in brain tissue, which is related with the degeneration of neuron. The changes of brain phospholipid could be involved in the pathogenesis of chronic fluorosis.
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Effects of fluoride on DNA damage, S-phase cell-cycle arrest and the expression of NF-kappaB in primary cultured rat hippocampal neurons.
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
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MiR-132, miR-204 and BDNF-TrkB signaling pathway may be involved in spatial learning and memory.
Highlights Spatial learning and memory of offspring rats were impaired after exposure to fluorine combined with aluminium(FA). Hippocampal miR-132 and miR-204 were increased after FA exposure. Hippocampal BDNF-TrkB signaling pathway was down-regulated after FA exposure. There were antagonistic effects between F and Al, with Al reducing the toxicity of F. Fluorine
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Effect of olfactory bulbectomy on adenylyl cyclase activity in the limbic system.
Monoaminergic neurotransmission is a key element in the physiopathology of depressive disorders, but information is still sparse on animal models of this disease. Here, we used the olfactory bulbectomy (OBX) model of depression to characterize cAMP-second messenger signaling pathways, i.e., adenylyl cyclase activity (basal, sodium fluoride (NaF)- and forskolin-stimulated conditions)
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Fluoride-induced developmental disorders and iodine deficiency disorders as examples of developmental disorders due to disturbed thyroid hormone metabolism.
Both exposure to fluoride and iodine deficiency during early development can lead to disturbed thyroid hormone metabolism and produce the same spectrum of developmental disorders including short stature, bone deformities, cognitive impairment, delayed dental eruption, and dental fluorosis. The levels of creatinine-adjusted urinary fluoride experienced by pregnant women in areas
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Neuroprotective effects of methyl-3-O-methyl gallate against sodium fluoride-induced oxidative stress in the brain of rats
Methyl-3-O-methyl gallate (M3OMG) is a rare natural product that showed promising in vitro antioxidant activities. In this study, the protective role of synthetic M3OMG against sodium fluoride (NaF)-induced oxidative stress in rat brain was evaluated. Animals were treated with either M3OMG (10 and 20 mg/kg i.p.), vitamin C (10 mg/kg
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