Previous behavioural studies shows that excessive exposure of fluoride caused diminished intelligent quotient in children compared to the normal children (Wang et al., 2004) and sodium fluoride intoxicated rat exerted loss of memory and learning disability (Yaning et al., 2005). In the present study postnatal rats aged day 21 and day 30 demonstrated loss of memory, learning inability and there was a considerable increase in the goal achieve latency period in NaF treated group when compared to the control pups. The concomitant administration of NaF and quercetin received pups showed better memory, learning ability and there was a significant decrease in the goal achieve latency period compared to the sodium fluoride treated rat pups.
The present study indicates the evidence on mitigation of NaF induced oxidative damage, behavioural and learning impairment, and alternations in levels of pro and antioxidants neurotransmitters and histological changes on concomitant administration of quercetin in developing rat brain. Quercetin restored the levels of antioxidants enzymes (SOD, catalase and Glutathione), monoamines (epinephrine and norepinephrine) levels, as well as ameliorated behavioural and histopathological alterations when compared to the sodium fluoride treated rat pups. The administration of quercetin ameliorated the neuron morphology, nucleus shrinkage and neuronal degeneration in the cerebral cortex of developing rat brain.
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Alterations in the memory of rat offspring exposed to low levels of fluoride during gestation and lactation: Involvement of the a7 nicotinic receptor and oxidative stress.
Daily exposure to fluoride (F) depends mainly on the intake of this element with drinking water. When administered during gestation and lactation, F has been associated with cognitive deficits in the offspring. However, the mechanisms underlying the neurotoxicity of F remain obscure. In the current study, we investigated the effects
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A correlation between serum vitamin, acetylcholinesterase activity and IQ in children with excessive endemic fluoride exposure in Rajasthan, India
Fluoride is widely distributed in nature and a direct source of adverse health effects in human populations. Fluoride poisoning attributed by long-term exposure to high levels of fluoride [is] called fluorosis. The present study was carried out among 9-14 years old school children of Dausa district, Rajasthan India. The subjects
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Sirt3-mediated mitochondrial dysfunction is involved in fluoride-induced cognitive deficits.
Highlights Fluoride induces cognitive deficits in mice. Fluoride exposure results in neural/synaptic injury in the hippocampus of mice. Mitochondrial dysfunction contributes to neural/synaptic alternations. Inhibition of Sirt3 is involved in the fluoride-evoked mitochondrial abnormalities. Abstract Excessive fluoride is capable of inducing cognitive deficits, but the mechanisms remain elusive. This study aimed
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Integrated transcriptomic and proteomic analysis indicated that neurotoxicity of rats with chronic fluorosis may be in mechanism involved in the changed cholinergic pathway and oxidative stress.
Highlights Chronic fluorosis decreased learning and memory of rats and induced neurotoxicity. Thirteen corresponding DEGs and DAPs (cor-DEGs-DAPs) were identified. Most of cor-DEGs-DAPs were related to neurodegenerative changes and oxidative stress response The neurotoxicity by high fluoride involved in the changes in cholinergic pathway and oxidative stress. Background To reveal the
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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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Nutrient Deficiencies Enhance Fluoride Toxicity
It has been known since the 1930s that poor nutrition enhances the toxicity of fluoride. As discussed below, nutrient deficiencies have been specifically linked to increased susceptibility to fluoride-induced tooth damage (dental fluorosis), bone damage (osteomalacia), neurotoxicity (reduced intelligence), and mutagenicity. The nutrients of primary importance appear to be calcium,
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Fluoride & IQ: 76 Studies
Note: See the Updated list of fluoride IQ studies at https://fluoridealert.org/researchers/fluoride-iq-studies/the-fluoride-iq-studies/ • As of July 18, 2022, a total of 85 human studies have investigated the relationship between fluoride and human intelligence. • Of these investigations, 76 studies have reported that elevated fluoride exposure is associated with reduced IQ in humans. • The studies
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Fluoride's Effect on Fetal Brain
The human placenta does not prevent the passage of fluoride from a pregnant mother's bloodstream to the fetus. As a result, a fetus can be harmed by fluoride ingested pregnancy. Based on research from China, the fetal brain is one of the organs susceptible to fluoride poisoning. As highlighted by the excerpts
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Fluoride & Oxidative Stress
A vast body of research demonstrates that fluoride exposure increases oxidative stress. Based on this research, it is believed that fluoride-induced oxidative stress is a key mechanism underlying the various toxic effects associated with fluoride exposure. It is also well established that fluoride's toxic effects can be ameliorated by exposure
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Fluoride's Direct Effects on Brain: Animal Studies
The possibility that fluoride ingestion may impair intelligence and other indices of neurological function is supported by a vast body of animal research, including over 40 studies that have investigated fluoride's effects on brain quality in animals. As discussed by the National Research Council, the studies have consistently demonstrated that fluoride, at widely varying concentrations, is toxic to the brain.
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