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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Fluoride exposure decreased learning ability and the expressions of the insulin receptor in male mouse hippocampus and olfactory bulb.
Fluoride is one of the common environmental pollutants. Internal exposure to fluoride is related to the lowered cognitive function and intelligence, particularly for children. Determination of protein content in brain tissue is a means to reflect the functional development of the central nervous system. Insulin and insulin receptor (IR) signaling
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Cognitive Decline of Rats with Chronic Fluorosis Is Associated with Alterations in Hippocampal Calpain Signaling.
The study was designed to evaluate an influence of excessive fluoride (F-) intake on cognitive capacities of adult rats and on proteins of memory-related calpain signaling in hippocampus. Control animals were given water with natural F- content of 0.4 ppm; rats from other groups consumed the same water supplemented with 5,
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Vitamin A deficiency: An oxidative stress marker in sodium fluoride (NaF) induced oxidative damage in developing rat brain
Fluoride induced oxidative stress through depletion in levels of various anti-oxidants such as glutathione, superoxide dismutase (SOD), fat soluble vitamins (D and E) with increased levels of lipid peroxidation (LPO) and fluoride aggravate the damage in rodents as well as in humans. Vitamins A, a fat soluble vitamin possess antioxidant
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SIRT1-dependent mitochondrial biogenesis supports therapeutic effects of resveratrol against neurodevelopment damage by fluoride.
Rationale: Potential adverse effects of fluoride on neurodevelopment has been extensively explored and mitochondria have been recognized as critical targets. Mitochondrial biogenesis serves a crucial role in maintaining mitochondrial homeostasis and salubrious properties of resveratrol (RSV) has been well-defined. However, the molecular mechanisms governing mitochondrial biogenesis in developmental fluoride neurotoxicity
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Effects of fluoride on learning and memory and cholinesterase activity in rat brains.
Objective: To study the role of fluorosis on learning and memory in rat and its possible mechanisms; to explore the correlation between cholinesterase activity and the level of intelligence. Methods: SD rats divides into 3 group of stochastically according to the sex and the body weight, control group treated with
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Fluoride Affects Learning & Memory in Animals
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NRC (2006): Fluoride's Neurotoxicity and Neurobehavioral Effects
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Fluoride: Developmental Neurotoxicity.
Developmental Neurotoxicity There has been a tremendous amount of research done on the association of exposure to fluoride with developmental neurotoxicity. There are over 60 studies reporting reduced IQ in children and several on the impaired learning/memory in animals. And there are studies which link fluoride to Attention Deficit Hyperactivity Disorder. Teaching
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