Blog
Long-term high fluoride exposure during adolescence causes hippocampal impairments
Jul
In a recent study published in Scientific Reports, researchers evaluated the impacts of prolonged fluoride exposure during adolescence and maturity on cognition and associated hippocampal alterations.
Study: Prolonged exposure to high fluoride levels during adolescence to maturity elicits molecular, morphological, and functional impairments within the hippocampus. Image Credit: SedovaY / Shutterstock.com
Background
Fluoride, a naturally occurring chemical element with high electronegativity, is utilized in various industries. Water can be treated with fluoride to strengthen teeth and reduce tooth decay rates. Nevertheless, considering its presence in reservoirs and soils at high concentrations, fluoride could also be considered an environmental toxicant.
Previous studies indicate that fluoride exposure might impact cognitive functions in developing organisms. Nevertheless, recent evidence suggests that the World Health Organization (WHO)’ really useful levels of fluoride in drinking water aren’t linked with neurological illnesses, whereas higher levels potentially lower intelligence quotient.
In regards to the study
In the current study, researchers assessed whether long-term fluoride exposure at concentrations typically observed in fluorosis endemic areas and artificially fluoridated water during adolescence and maturity is expounded to learning and memory problems in mice. The morphological elements and hippocampal proteomic profile related to hippocampal fluoride neurotoxicity were also evaluated through a dose-response comparison of the study subjects.
To this end, 21-day-old male mice with a body mass of about 10 g were utilized in the investigation. The mice were randomly divided into three groups, each of which comprised 14 animals.
Mice consumed drinking water with 50 or 10 mg/L of fluoride for 60 days. A fluoride ion-specific electrode was used to measure the plasma fluoride bioavailability.
While the Morris water maze test was used to judge spatial memory, the step-down inhibitory avoidance test was used to evaluate short- and long-term memory. The hippocampal proteomic profile was determined through mass spectrometry.
Low fluoride exposure is secure
Long-term exposure to high fluoride levels was found to cause morphological and molecular alterations within the hippocampus, in addition to learning and memory deficits in mice. While low fluoride concentration exposure didn’t lead to cognitive impairments, exposure to high fluoride concentrations may provoke cognitive impairments.
The onset of short- and long-term memory deficits following high fluoride concentrations was related to the raised plasma fluoride bioavailability. These alterations were linked to a neurodegenerative trend within the hippocampal CA3 and dentate gyrus (DG) regions, in addition to a hippocampal proteomic profile, particularly of proteins involved in synaptic communication.
The step-down inhibitory avoidance test revealed that each short-and long-term memory were impaired following 50 mg/L fluoride exposure, whereas no impairment was observed among the many 10 mg/L group. Mice within the 50 mg/L group also exhibited poor spatial memory relative to the ten mg/L and control groups.
Bioinformatic evaluation of biological processes involving proteins revealed each high and low fluoride concentration exposure significantly affected the proteomic profile. Processes connected to energy metabolism and morphological elements were essentially the most affected.
Chronic exposure to high fluoride levels was linked to a big modification of proteins involved in synaptic transmission. Furthermore, these alterations could also be answerable for the functional deficits observed within the behavioral evaluation, in addition to the morphological and molecular assays. Hippocampal neurodegeneration also reflects how long-term high fluoride concentration exposure may harm cognitive function.
Overall, the study results support the security of exposure to low fluoride concentrations and offer evidence of possible fluoride neurotoxicity molecular targets within the hippocampus at levels considerably higher than those in artificially fluoridated water.
Conclusions
While long-term exposure to artificially fluoridated water on the really useful fluoride level was not linked to cognitive impairments, a better concentration linked to fluorosis caused learning and memory problems and decreased hippocampal neuronal density.
The study findings are essential for future public health regulations regarding the fluoridation of drinking water. To this end, the researchers of the present study emphasize the importance of monitoring fluoride levels in drinking water to verify that they continue to be inside secure ranges.
Although these findings indicate that chronic exposure to high fluoride levels may negatively impact cognitive function, a greater understanding of possible risks involved with long-term fluoride exposure requires additional investigation. Further research at various ages and with longer exposure times can be needed to find out whether the molecular changes observed ad 10 mg/L are innocuous to cognitive function.
