Abstract
Objective: Explore the active mechanisms of growth inhibitors (somatostatin, SS) participating in learning and memory obstacles from brick tea fluoride and aluminum poisoning of rats. Method: Based on the tea-drinking habits of herders, a rat chronic brick tea fluoride and aluminum poisoning animal model was established, and randomly divided into control groups and model groups. After the model was established for one year, an eight-arm maze test was performed to observe the differences in the spatial learning and memory capabilities of the two rat groups, and immunochemistry was used to test the changes in the rat hippocampus growth inhibitor expression one year after the model was established. Results: Compared with the control group, there was a significant difference (P<0.01) in the rat eight-arm maze learning and memory capabilities one year after the model was established, and the rat hippocampus SS expression fell (P<0.01) one year after the model was established. Conclusion: Brick tea fluoride and aluminum poisoning of rats obstructs learning and memory and brain tissue SS expression decreases.
(Translated by Alta Language Services in February 2014, courtesy of Fluoride Action Network)
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Neurotoxicity of fluoride: neurodegeneration in hippocampus of female mice
Light microscopic study of hippocampal sub-regions demonstrated significant number of degenerated nerve cell bodies in the CA3, CA4 and dentate gyrus(Dg) areas of sodium fluoride administered adult female mice. Ultrastructural studies revealed neurodegenrative characteristics like involution of cell membranes, swelling of mitochondria, clumping of chromatin material etc, can be observed in cell
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Influence of chronic fluorosis on expression of phospho-Elk-1 in rat brains.
Objective: To investigate the expression and distribution of the downstream substrate of extracellular regulated protein kinase(ERK1/2) pathway, ternary complex factor phospho-Elk-1, in rat brains with chronic fluorosis, and reveal the mechanism of the impaired learning and memory ability caused by chronic fluorosis. Methods: Seventy-two SD rats, weighing 100 - 120 g,
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Excessive ER stress and the resulting autophagic flux dysfunction contribute to fluoride-induced neurotoxicity.
Highlights Excessive ER stress plays an important role in NaF-induced neurotoxicity. NaF-induced neuronal death is caused by ER stress-elicited apoptosis and the impaired autophagic flux. Impaired autophagic flux was mediated by excessive ER stress in NaF-induced neurotoxicity. Fluoride is capable of inducing neurotoxicity, but its mechanisms remain elusive. This study
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Acetylcholinesterase activity in fluorosis adversely affects mental well-being: an experimental study in rural Rajasthan
Fluoride toxicity is a burgeoning problem worldwide and also in Rajasthan in India. In the state of Rajasthan, almost all districts have high fluoride (up to 18.0 ppm) in their drinking/ground water sources and about 11 million of the population [is] at risk. Several clinical and experimental studies have reported
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Association between fluoride exposure in drinking water and cognitive deficits in children: A pilot study.
Highlights Cognitive ability was assessed in children exposed to a range of fluoride levels in drinking water. The study successfully implemented the CANTAB test to children residing in rural Ethiopia. Water fluoride levels were negatively associated with children's drawing skills, and CANTAB's memory and learning tests. Children exposed to high
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