Inorganic fluoride and functions of brain

Agalakova, Natalia I.; Nadei, Olga V

doi:10.1080/10408444.2020.1722061

Cited by 37 publications

(8 citation statements)

References 134 publications

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“…Fluoride can enter the brain through the blood–brain barrier, and long-term intake of excessive fluoride can lead to fluoride accumulation in the brain, which affects the normal physiological function of brain cells ( 16 ). Fluoride accumulation can damage the nervous system, which includes neuropathological changes, cholinergic nervous system abnormalities, nerve cell membrane structure changes, neurotransmitter receptor changes, neurocyte apoptosis, and decreased intelligence ( 17 ). The change in the intelligence of children in endemic fluorosis areas was confirmed in several countries ( 18 ).…”

Section: Introductionmentioning

confidence: 99%

Exploration of the SIRT1-mediated BDNF–TrkB signaling pathway in the mechanism of brain damage and learning and memory effects of fluorosis

Wang,

Li,

Tang

et al. 2023

Front. Public Health

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IntroductionFluoride is considered an environmental pollutant that seriously affects organisms and ecosystems, and its harmfulness is a perpetual public health concern. The toxic effects of fluoride include organelle damage, oxidative stress, cell cycle destruction, inflammatory factor secretion, apoptosis induction, and synaptic nerve transmission destruction. To reveal the mechanism of fluorosis-induced brain damage, we analyzed the molecular mechanism and learning and memory function of the SIRT1-mediated BDNF–TrkB signaling pathway cascade reaction in fluorosis-induced brain damage through in vivo experiments.MethodsThis study constructed rat models of drinking water fluorosis using 50 mg/L, 100 mg/L, and 150 mg/L fluoride, and observed the occurrence of dental fluorosis in the rats. Subsequently, we measured the fluoride content in rat blood, urine, and bones, and measured the rat learning and memory abilities. Furthermore, oxidative stress products, inflammatory factor levels, and acetylcholinesterase (AchE) and choline acetyltransferase (ChAT) activity were detected. The pathological structural changes to the rat bones and brain tissue were observed. The SIRT1, BDNF, TrkB, and apoptotic protein levels were determined using western blotting.ResultsAll rats in the fluoride exposure groups exhibited dental fluorosis; decreased learning and memory abilities; and higher urinary fluoride, bone fluoride, blood fluoride, oxidative stress product, and inflammatory factor levels compared to the control group. The fluoride-exposed rat brain tissue had abnormal AchE and ChAT activity, sparsely arranged hippocampal neurons, blurred cell boundaries, significantly fewer astrocytes, and swollen cells. Furthermore, the nucleoli were absent from the fluoride-exposed rat brain tissue, which also contained folded neuron membranes, deformed mitochondria, absent cristae, vacuole formation, and pyknotic and hyperchromatic chromatin. The fluoride exposure groups had lower SIRT1, BDNF, and TrkB protein levels and higher apoptotic protein levels than the control group, which were closely related to the fluoride dose. The findings demonstrated that excessive fluoride caused brain damage and affected learning and memory abilities.DiscussionCurrently, there is no effective treatment method for the tissue damage caused by fluorosis. Therefore, the effective method for preventing and treating fluorosis damage is to control fluoride intake.

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Section: Introductionmentioning

confidence: 99%

Exploration of the SIRT1-mediated BDNF–TrkB signaling pathway in the mechanism of brain damage and learning and memory effects of fluorosis

Wang,

Li,

Tang

et al. 2023

Front. Public Health

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“…Alterations in glutamatergic transmission have been associated with neurological impairment after As or F exposure (Tyler and Allan 2014 ; Agalakova and Nadei 2020 ). Here, we observed crucial differences between glutamate receptor subunit expressions in exposed animals at P90, the time when the behavioral tasks were performed.…”

Section: Resultsmentioning

confidence: 99%

“…This condition has caused detrimental effects on their quality of life due to the higher prevalence of cardiovascular, renal, hepatic, reproductive, and neurological diseases (Mondal and Chattopadhyay 2020 ). Learning and memory impairments have been documented in children exposed to As or F worldwide (Tyler and Allan 2014 ; Agalakova and Nadei 2020 ). Using a mouse model, we have previously reported that exposure to inorganic As in drinking water starting at gestation alters the homeostasis of GSH and disrupts the availability of glutamate in the hippocampus, which was associated with altered ionotropic glutamate receptor expression, and to impaired memory (Ramos-Chavez et al 2015 ; Nelson-Mora et al 2018 ).…”

Section: Discussionmentioning

confidence: 99%

“…Fluoride (F) and arsenic (As) are the most serious contaminants in drinking water worldwide and are of health concern, since approximately over one-third of the world´s population depends on the ground water supply (Schmoll et al 2006 ). Chronic exposure to As and F by drinking water has been linked to toxic effects in several organs and to neurodevelopmental alterations in children (Tyler and Allan 2014 , Agalokova and Nadei 2020 ). As and F can cross the placenta and blood–brain barrier and can incorporate into the central nervous system (CNS).…”

Section: Introductionmentioning

confidence: 99%

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Chronic exposure to inorganic arsenic and fluoride induces redox imbalance, inhibits the transsulfuration pathway, and alters glutamate receptor expression in the brain, resulting in memory impairment in adult male mouse offspring

González-Alfonso,

Pavel,

Karina

et al. 2023

Arch Toxicol

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Exposure to toxic elements in drinking water, such as arsenic (As) and fluoride (F), starts at gestation and has been associated with memory and learning deficits in children. Studies in which rodents underwent mechanistic single exposure to As or F showed that the neurotoxic effects are associated with their capacity to disrupt redox balance, mainly by diminishing glutathione (GSH) levels, altering glutamate disposal, and altering glutamate receptor expression, which disrupts synaptic transmission. Elevated levels of As and F are common in groundwater worldwide. To explore the neurotoxicity of chronic exposure to As and F in drinking water, pregnant CD-1 mice were exposed to 2 mg/L As (sodium arsenite) and 25 mg/L F (sodium fluoride) alone or in combination. The male litter continued to receive exposure up to 30 or 90 days after birth. The effects of chronic exposure on GSH levels, transsulfuration pathway enzymatic activity, expression of cysteine/cystine transporters, glutamate transporters, and ionotropic glutamate receptor subunits as well as behavioral performance in the object recognition memory task were assessed. Combined exposure resulted in a significant reduction in GSH levels in the cortex and hippocampus at different times, decreased transsulfuration pathway enzyme activity, as well as diminished xCT protein expression. Altered glutamate receptor expression in the cortex and hippocampus and decreased transaminase enzyme activity were observed. These molecular alterations were associated with memory impairment in the object recognition task, which relies on these brain regions.

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“…It should be noted that many authors disagree with these conclusions, arguing that population-based studies are incomplete. They also note that many of the behavioural studies were conducted in animal models utilizing acute doses [ 21 , 82 , 83 , 84 ]. Nevertheless, as Till and Green [ 85 ] point out, the evidence is relatively new and should rather be regarded as a potential early warning.…”

Section: Fluoride As An Environmental Toxinmentioning

confidence: 99%

Fluoride in the Central Nervous System and Its Potential Influence on the Development and Invasiveness of Brain Tumours—A Research Hypothesis

Żwierełło

Maruszewska

Skórka-Majewicz

et al. 2023

IJMS

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The purpose of this review is to attempt to outline the potential role of fluoride in the pathogenesis of brain tumours, including glioblastoma (GBM). In this paper, we show for the first time that fluoride can potentially affect the generally accepted signalling pathways implicated in the formation and clinical course of GBM. Fluorine compounds easily cross the blood–brain barrier. Enhanced oxidative stress, disruption of multiple cellular pathways, and microglial activation are just a few examples of recent reports on the role of fluoride in the central nervous system (CNS). We sought to present the key mechanisms underlying the development and invasiveness of GBM, as well as evidence on the current state of knowledge about the pleiotropic, direct, or indirect involvement of fluoride in the regulation of these mechanisms in various tissues, including neural and tumour tissue. The effects of fluoride on the human body are still a matter of controversy. However, given the growing incidence of brain tumours, especially in children, and numerous reports on the effects of fluoride on the CNS, it is worth taking a closer look at these mechanisms in the context of brain tumours, including gliomas.

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Inorganic fluoride and functions of brain

Cited by 37 publications

References 134 publications

Exploration of the SIRT1-mediated BDNF–TrkB signaling pathway in the mechanism of brain damage and learning and memory effects of fluorosis

Exploration of the SIRT1-mediated BDNF–TrkB signaling pathway in the mechanism of brain damage and learning and memory effects of fluorosis

Chronic exposure to inorganic arsenic and fluoride induces redox imbalance, inhibits the transsulfuration pathway, and alters glutamate receptor expression in the brain, resulting in memory impairment in adult male mouse offspring

Fluoride in the Central Nervous System and Its Potential Influence on the Development and Invasiveness of Brain Tumours—A Research Hypothesis

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