Abstract
To investigate the effects of fluoride exposure on the microglialmorphology and the expression of inflammatory cytokines in the cerebral cortex of mice, thirty-six ICR male mice were randomly divided into groups and given different doses of sodium fluoride (0, 25, and 50 mg/L NaF). After 50 days, the microglialmorphology and the expression of interleukin-6 (IL-6), interleukin-1B (IL-1B),transforming growth factor-B (TGF-B), and tumor necrosis factor-a (TNF-a) were detected using immunohistochemistry (IHC) and enzyme-linked immunosorbent assay (ELISA). In our results, the degeneration of pyramidal cells and glial cells was one of the most obvious pathological changes in the fluoride-exposed brains. Compared to the control group, the number of ramified, intermediate, and amoeboid microglia was significantly elevated in the NaF treatment groups. Additionally, the ELISA results showed that 50 mg/L NaF dramatically increased the expression of IL-6, IL-1B, TGF-B,and TNF-a when compared to the control group. These findings suggest that NaF can promote morphological changes of activated microglia and the release of inflammatory factors in the cortex, which may be one of the mechanisms of fluoride-induced nerve damage.
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Weakened interaction of ATG14 and the SNARE complex blocks autophagosome-lysosome fusion contributes to fluoride-induced developmental neurotoxicity.
Highlights NaF induced autophagosome-lysosome fusion blockage. NaF weakened the interaction of ATG14 and SNARE complex. ATG14 regulates the SNARE complex in NaF-induced developmental neurotoxicity. ATG14 upregulation restored autophagosome-lysosome fusion and autophagic flux. ATG14 upregulation protects against developmental fluoride neurotoxicity. Fluoride is capable of inducing developmental neurotoxicity, but the mechanisms involved remain
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Protective effect of resveratrol on sodium fluoride-induced oxidative stress, hepatotoxicity and neurotoxicity in rats
Protective effect of resveratrol on sodium fluoride-induced oxidative stress, hepatotoxicity and neurotoxicity were studied in rats. A total of 28 Wistar albino male rats were used. Four study groups were randomly formed with seven animals in each. The groups were treated for 21 days with distilled water (control group), with
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Fluoride exposure disrupts the cytoskeletal arrangement and ATP synthesis of HT-22 cell by activating the RhoA/ROCK signaling pathway
Highlights Fluoride exposure impaired cytoskeleton of HT-22 cell by activating the RhoA/ROCK/LIMK/Cofilin signaling pathway. Fluoride exposure induced mitochondrial damage and abnormal expression of GLUTs in HT-22 cell thus disrupted the ATP synthesis. Fluoride affects neural structure and function because of disorderly actin homeostasis. Background Fluoride, an environmental contaminant, is ubiquitously present in
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Effects of long-term fluoride exposure on cognitive ability and the underlying mechanisms: Role of autophagy and its association with apoptosis.
Highlights Autophagy suppression contributes to fluoride neurotoxicity in addition to apoptosis. Fluoride suppresses autophagy via mTOR/p70S6K pathway in vivo and in vitro. Rapamycin-activated autophagy inhibits apoptosis and promotes cell survival. Circulating autophagy markers are positively related to children's IQ scores. Autophagy and apoptosis are two important cellular processes that are
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DNA methylation and fluoride exposure in school-age children: Epigenome-wide screening and population-based validation.
Highlights Long-term fluoride exposure affects the genomic DNA methylation pattern in children. The methylation status of NNAT and CALCA are susceptible to long-term F exposure. NNAT gene methylation is negatively correlated with fluoride exposure. CALCA gene methylation and fluoride exposure are positively associated. Excessive fluoride exposure and epigenetic change can
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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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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 & 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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