Memory Impairment Induced by Sodium Fluoride is Associated with Changes in Brain Monoamine Levels

Pereira, Marcela; Dombrowski, Patrícia A.; Losso, Estela Maris; Chioca, Lea Rosa; Cunha, Cláudio Da; Andreatini, Roberto

doi:10.1007/s12640-009-9139-5

Cited by 71 publications

(45 citation statements)

References 32 publications

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“…Both the doses of fluoride exposure significantly impaired the acquisition and retention in the present study. Decreased learning and memory abilities induced by fluoride have been reported by various authors [16,[35][36][37]. Since fluoride is known to be neurotoxic, greater accumulation of fluoride in the discrete brain regions in the thirdgeneration rats as found in the present study may have made the subsequent generations more vulnerable to the toxic effects of fluoride.…”

Section: Discussionsupporting

confidence: 67%

Fluoride Toxicity and Status of Serum Thyroid Hormones, Brain Histopathology, and Learning Memory in Rats: A Multigenerational Assessment

Basha

Rai

Begum³

2011

Biol Trace Elem Res

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High-fluoride (100 and 200 ppm) water was administered to rats orally to study the fluoride-induced changes on the thyroid hormone status, the histopathology of discrete brain regions, the acetylcholine esterase activity, and the learning and memory abilities in multigeneration rats. Significant decrease in the serum-free thyroxine (FT4) and free triiodothyronine (FT3) levels and decrease in acetylcholine esterase activity in fluoride-treated group were observed. Presence of eosinophilic Purkinje cells, degenerating neurons, decreased granular cells, and vacuolations were noted in discrete brain regions of the fluoride-treated group. In the T-maze experiments, the fluoride-treated group showed poor acquisition and retention and higher latency when compared with the control. The alterations were more profound in the third generation when compared with the first- and second-generation fluoride-treated group. Changes in the thyroid hormone levels in the present study might have imbalanced the oxidant/antioxidant system, which further led to a reduction in learning memory ability. Hence, presence of generational or cumulative effects of fluoride on the development of the offspring when it is ingested continuously through multiple generations is evident from the present study.

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Section: Discussionsupporting

confidence: 67%

Fluoride Toxicity and Status of Serum Thyroid Hormones, Brain Histopathology, and Learning Memory in Rats: A Multigenerational Assessment

Basha

Rai

Begum³

2011

Biol Trace Elem Res

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“…Fluoride affects the brain by inhibiting some enzymes associated with energy production and transfer, membrane transport, and synaptic transmission [14]. Chronic or subchronic fluoride exposure may lead to reduction of acetylcholinesterase activity and nicotinic acetylcholine receptor level, as well as alteration in the neurotransmitter level [15,16]. The developmental neurotoxicity of fluoride may be closely associated with low glucose utilization and neurodegenerative changes [17].…”

Section: Introductionmentioning

confidence: 99%

Fluoride-Induced Neuron Apoptosis and Expressions of Inflammatory Factors by Activating Microglia in Rat Brain

Yan

Liu

et al. 2015

Mol Neurobiol

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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 effects on microglia of fluoride. In the present study, healthy adult Wistar rats were exposed to 60 and 120 ppm fluoride in drinking water for 10 weeks, and control rats received deionized water. After 10 weeks, rats were sacrificed under anesthesia then apoptosis in neuron and inflammatory factors secreted by microglia were determined. We found that apoptosis of neurons in fluoride-treated rat brain increased and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive immunofluorescence increased with increasing fluoride concentrations. Bax protein expression increased and Bcl-2 protein expression decreased in fluoride-treated rat brain compared with that of the control rat brain. The microglia in the hippocampus and cortex of fluoride-treated rats were activated by immunostaining with OX-42, a marker of activated microglia, and OX-42-positive microglia cells were more abundant in the hippocampus than in the cortex. The levels of IL-1β and IL-6 protein expression in OX-42-labeled microglial cells were significantly increased in the cortex and hippocampus of rats exposed to fluoride, and TNF-α immunoreactivity in microglial cells of the hippocampus was significantly higher in the 120 ppm fluoride-treated group than that in the control group. Our results indicate that fluoride induced neuron apoptosis and expressions of inflammatory factors by activating microglia in rat brain.

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“…For example, Pereira et al [170] studied rats fed 100 mg/L fluoride in drinking water for 30 days -100 times the level in optimally fluoridated water -and noted memory deficits compared with rats who were not dosed with fluoride. Other studies fed rats sodium fluoride by gavage at a level of 5.0 mg/kg/day -again 100 times the recommended level for children (0.05 mg/kg/day).…”

Section: Animal Studiesmentioning

confidence: 99%

Water fluoridation: It really is this simple

2017

Br Dent J

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(RSNZ), and the Ministry of Health, to review the scientific evidence for and against the efficacy and safety of fluoridation of public water supplies. After discussion between the parties, it was agreed that the Office of the PMCSA and the RSNZ would establish a panel to undertake a review. This review would adhere strictly to the scientific issues of safety and efficacy (or otherwise), but take into account the various concerns that have been raised in the public domain about the science and safety of fluoride. It would not consider the ethical and philosophical issues that have surrounded fluoridation and influenced legal proceedings lately. The Prime Minister gave his consent for the Office of the PMCSA to be involved and funding was provided by Councils through your office and by the Ministry of Health.We are pleased to advise the report is being delivered on the timetable agreed. ProcessGiven this is inevitably an issue that arouses passions and argument, we summarise in some detail the process used.As this was the first formal scientific review conducted jointly between the Office of PMCSA and the Royal Society a memorandum of understanding for the process was developed and has been followed.The essence of the process was that the PMCSA appointed an experienced literature researcher to undertake the primary research and literature reviews. Following an initial scoping that included an extensive reading of the literature (informal, grey and peer reviewed) on the subject, a draft table of contents was agreed between the PMCSA and the President of the RSNZ. The RSNZ then appointed a panel of appropriate experts across the relevant disciplines that was approved by the PMCSA.A member of civil society with expertise in local body issues, Ms Kerry Prendergast, was invited to be an observer to the panel and to be included in the discussions and drafting to be sure that it met local body needs. The scientific writer then produced an early partial draft of the report that was presented to a meeting of the expert panel, and their input was sought both as to framing and interpretation of the literature. The panel paid particular attention to the claims that fluoride had adverse effects on brain development, on the risks of cancer, musculoskeletal and hormonal disorders -being the major areas where claims about potential harms have been made. Over the following weeks, the panel members joined in an iterative process with the scientific writer to develop the report. In its advanced form all the members of the panel, together with the PMCSA and the President of the RSNZ, agreed via email exchange on the final wording of the report and its executive summary. In this form it was sent out for international peer review by appropriate scientific experts in Australia, UK and Ireland. Following their suggestions (which were minor and did not affect the panel's conclusions), the report and executive summary were returned to the panel for comment. Findings and recommendationsThe report and its executive summary are very clear i...

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Memory Impairment Induced by Sodium Fluoride is Associated with Changes in Brain Monoamine Levels

Cited by 71 publications

References 32 publications

Fluoride Toxicity and Status of Serum Thyroid Hormones, Brain Histopathology, and Learning Memory in Rats: A Multigenerational Assessment

Fluoride Toxicity and Status of Serum Thyroid Hormones, Brain Histopathology, and Learning Memory in Rats: A Multigenerational Assessment

Fluoride-Induced Neuron Apoptosis and Expressions of Inflammatory Factors by Activating Microglia in Rat Brain

Water fluoridation: It really is this simple

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