Abstract
To investigate whether excitotoxicity is involved in neurotoxicity of fluoride (F) alone and in combination with lead (Pb), the expression levels of the gene and protein N-methyl-D-aspartate receptor 1 (NMDAR1) in the hippocampus of offspring rat pups at postnatal days 14 and 28 exposed to F and/or Pb were determined by quantitative real-time polymerase chain reaction (QRT-PCR) and immunochemistry. During lactation, the pups ingested F and/or Pb via the maternal milk, whose mothers were exposed to sodium fluoride (150 mg/L in drinking water) and/or lead acetate (300 mg/L in drinking water) from the day of delivery. After weaning at postnatal day 21, the pups were exposed to the same treatments as their mother. At day 14 and at day 28, 6 pups (female:male = 1:1) were chosen randomly from each group for further investigation. Results showed that at postnatal days 14 and 28, the expression levels of NMDAR1 gene were increased by 11% and 26%, respectively, in pups exposed to F compared to the controls, and the protein levels were also significantly enhanced. In pups exposed to Pb alone and to Pb plus F, the levels of the NMDAR1 gene and protein were decreased at postnatal day 14 and then increased at postnatal day 28. These results may provide evidence of a relationship between the excitotoxicity and neurotoxicity of F and/or Pb.
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Fluoride-induced neuron apoptosis and expressions of inflammatory factors by activating microglia in rat brain
Excessive exposure to fluoride results in structural and functional damages to the central nervous system (CNS), and neurotoxicity of fluoride may be associated with neurodegenerative changes. Chronic microglial activation appears to cause neuronal damage through producing proinflammatory cytokines and is involved in many neurodegenerative disorders. It is not known about
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Gestational exposure to fluoride impairs cognition in C57 BL/6 J male offspring mice via the p-Creb1-BDNF-TrkB signaling pathway.
Highlights Pregnant mice were exposed to environmentally relevant doses of sodium fluoride from GD1 to GD20. Exposure to sodium fluoride resulted in structural and functional impairments in male offspring mouse hippocampus. The activation of P-Creb1 signaling pathway played a role in sodium fluoride-induced cognitive impairment. We provided new insight
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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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Fluoride enhances the effect of aluminium chloride on interconnections between aggregates of hippocampal neurons
The role of fluoride in aluminium neurotoxicity was studied using an in vitro system of cultured hippocampal neurons from foetal rats. Sodium fluoride (50 microM) and aluminium chloride (12.5 microM) were administered alone or in a specific combination (50 + 12.5 microM) in a 14-day culture in a chemically defined
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Neonatal sevoflurane anesthesia induces long-term memory impairment and decreases hippocampal PSD-95 expression without neuronal loss.
AIM: Volatile anesthetics are widely used in the clinic, and sevoflurane is the most prevalent volatile anesthetic in pediatric anesthesia. Recent findings question the potential risks of volatile anesthetics on brain development. Evidence suggests that sevoflurane may cause neuronal deficiency. This study investigates the long-term effect of sevoflurane in the
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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 78 studies reporting reduced IQ (75 studies with children and 3 studies with adults) and several on the impaired learning/memory in animals. And there are studies which link
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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 Affects Learning & Memory in Animals
An association between elevated fluoride exposure and reduced intelligence has now been observed in 65 IQ studies. Although a link between fluoride and intelligence might initially seem surprising or random, it is actually consistent with a large body of animal research. This animal research includes the following 45 studies (out
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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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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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