Fluorides occur naturally in the environment, the daily exposure of human organism to fluorine mainly depends on the intake of this element with drinking water and it is connected with the geographical region In some countries, we can observe the endemic fluorosis—the damage of hard and soft tissues caused by the excessive intake of fluorine Recent studies showed that fluorine is toxic to the central nervous system (CNS) There are several known mechanisms which lead to structural brain damage caused by the excessive intake of fluorine This element is able to cross the blood-brain barrier, and it accumulates in neurons affecting cytological changes, cell activity and ion transport (eg chlorine transport) Additionally, fluorine changes the concentration of non-enzymatic advanced glycation end products (AGEs), the metabolism of neurotransmitters (influencing mainly glutamatergic neurotransmission) and the energy metabolism of neurons by the impaired glucose transporter—GLUT1 It can also change activity and lead to dysfunction of important proteins which are part of the respiratory chain Fluorine also affects oxidative stress, glial activation and inflammation in the CNS which leads to neurodegeneration All of those changes lead to abnormal cell differentiation and the activation of apoptosis through the changes in the expression of neural cell adhesion molecules (NCAM), glial fibrillary acidic protein (GFAP), brain-derived neurotrophic factor (BDNF) and MAP kinases Excessive exposure to this element can cause harmful effects such as permanent damage of all brain structures, impaired learning ability, memory dysfunction and behavioural problems This paper provides an overview of the fluoride neurotoxicity in juveniles and adults

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The Influence of Fluorine on the Disturbances of Homeostasis in the Central Nervous System

Background: People of all ages are exposed to fluoride from a variety of sources including dental products, drinking water, food, beverages and pharmaceuticals. In some developed countries, fluorid...

Systematic Review of Fluoride Exposure and Neurodevelopmental and Cognitive Health Effects

Fluoride decreased the sperm ATP of mice through inhabiting mitochondrial respiration.

Arsenic and fluoride induce apoptosis, inflammation and oxidative stress in cultured human umbilical vein endothelial cells.

Lead-induced oxidative damage in rats/mice: A meta-analysis.

Both fluoride and lead can cross the blood-brain barrier and produce toxic effects on the central neural system, resulting in low learning and memory abilities, especially in children. In order to identify the proteomic pattern in the cortex of young animals, from the beginning of fertilization to the age of postnatal day 56, pregnant female mice and pups were administrated with 150 mg sodium fluoride/L and/or 300 mg lead acetate/L in their drinking water. Two-dimensional electrophoresis (2-DE) combined with mass spectrometry (MS) was applied to identify differently expressed protein spots. Results showed that there were eight proteins in the cortex that significantly changed, whose biological functions were involved in (1) energy metabolism (Ndufs1, Atp5h, Atp6v1b2), (2) cytoskeleton (Spna2, Tuba1a, Tubb2a), (3) glycation repair (Hdhd2), and (4) cell stress response (Hspa8). Based on the previous and current studies, ATPase, Spna2, and Hspa8 were shared by fluoride and lead both as common target molecules.

Proteome alterations in cortex of mice exposed to fluoride and lead.

Fluoride and lead are two common pollutants in the environment. Previous investigations have found that high fluoride exposure can increase the lead burden. In this experiment, in order to study on the molecular mechanisms of central neural system injury induced by the above two elements, differently expressed protein spots in hippocampus of male mice treated with 150 mg sodium fluoride/L and/or 300 mg lead acetate/L in their drinking water were detected by two-dimensional electrophoresis (2-DE) and mass spectrometry (MS). The behavior tests showed that 56 days of fluoride and lead administration significantly reduced the vertical activity and lowered the memory ability of mice. In addition, results of 2-DE and MS revealed that nine spots demonstrated above a twofold change in the same trend in all treatment groups, which were mainly related with (1) energy metabolism, (2) cell stress response/chaperones, (3) cytoskeleton development, (4) protein metabolism, and (5) cell surface signal transduction. The findings could provide potential biomarkers for lesion in nervous system induced by fluoride and lead exposure.

Shuangling Liu

Papers

Proteome alterations in cortex of mice exposed to fluoride and lead.

Proteomic Analysis of Hippocampus in Offspring Male Mice Exposed to Fluoride and Lead