Abstract
Effects of exposure of Swiss albino adult male mice to 17.6 mg NaF/L in their drinking water for up to 30 days on the NADPH diaphorase (NADPH-d) positive neurons in the forebrain were studied. Histochemical study by the method developed by Hope and Vincent for the distribution of NADPH-d positive neuron cell bodies was conducted in the cerebral cortex, hippocampus, amygdala, caudate putamen, and selected nuclei of the hypothalamus. Counting neuronal cell bodies, their dendritic intersections, and varicosities in the brain of the F-exposed mice showed significant increase in the neuron cell bodies. In the cerebral cortex, amygdala, and caudate putamen, the increase in the number of NADPH-d positive neurons and their dendritic intersections was highly significant (p<0.05), but no significant difference was seen in the dendritic branching. A significant increase in the number of varicosities was also observed in the brain of the F-treated mice. These results indicate that excessive F intake caused morphological changes in NADPH-d/NOS (nitric oxide synthase) positive neurons in the brain, thus increasing nitric oxide (NO) synthesis, which is implicated in F-induced neuron cell death. A possible mechanism of F neurotoxicity is thereby suggested.
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Protective role of tert-butylhydroquinone against sodium fluoride-induced oxidative stress and apoptosis in PC12 cells.
The neurotoxicity of fluoride is associated with oxidative stress due to imbalance between production and removal of reactive oxygen species (ROS). In contrast, induction of detoxifying and antioxidant genes through activation of NF-E2-related factor 2 (Nrf2) has been implicated in preventing oxidative stress and apoptosis in neurodegenerative diseases. The present
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Interplay of glia activation and oxidative stress formation in fluoride and aluminium exposure.
BACKGROUND: Oxidative stress formation is pivotal in the action of environmental agents which trigger the activation of glial cells and neuroinflammation to stimulate compensatory mechanisms aimed at restoring homeostasis. AIM: This study sets to demonstrate the interplay of fluoride (F) and aluminium (Al) in brain metabolism. Specifically, it reveals how oxidative
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Sodium fluoride affects zebrafish behaviour and alters mRNA expressions of biomarker genes in the brain: Role of Nrf2/Keap1
Highlights Sodium fluoride (NaF) treatment changed the behaviour of zebrafish. Expression of antioxidant genes was upregulated. Expression of Nrf2 and its related genes were also altered. Results indicated that Nrf2 plays a significant role in NaF induced neurotoxicity. Sodium fluoride (NaF), used as pesticides and for industrial purposes are deposited
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Apoptotic and Degenerative Changes in the Enteric Nervous System Following Exposure to Fluoride During Pre- And Post-natal Periods.
Children born in fluorosis endemic areas usually suffer from gastrointestinal complications and are unable to attain normal growth as per their age group. The enteric nervous system (ENS) controls gut movement and functions. It is highly vulnerable to any ingested toxins. Based on observations, it was hypothesized that fluoride exposure
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JNK and NADPH oxidase involved in fluoride-induced oxidative stress in BV-2 microglia cells.
Abstract Excessive fluoride may cause central nervous system (CNS) dysfunction, and oxidative stress is a recognized mode of action of fluoride toxicity. In CNS, activated microglial cells can release more reactive oxygen species (ROS), and NADPH oxidase (NOX) is the major enzyme for the production of extracellular superoxide in microglia. ROS
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Fluoride & IQ: 74 Studies
• As of May 2022, a total of 83 human studies have investigated the relationship between fluoride and human intelligence. • Of these investigations, 74 studies have reported that elevated fluoride exposure is associated with reduced IQ in humans. • The studies which reported an association of reduced IQ with exposure to
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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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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'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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NRC (2006): Fluoride's Neurotoxicity and Neurobehavioral Effects
The NRC's analysis on fluoride and the brain.
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