Abstract

Highlights

• long-term exposure to fluoride during the development leads to the decrease in the expression of COX1 and COX2 in the brain.
• a statistically significant increase in PGE2 concentration and COX2 immunexpression was observed in hippocampus.
• exposure to fluoride in the prenatal and neonatal period may result in the development of inflammation in the brain.
• Neurotoxic mechanism of fluoride may be associated with an increase in COX2 activity and in PGE2 concentration in the hippocampus.

BACKGROUND: Sixty percent of the mammalian brain is composed of lipids including arachidonic acid (AA). AA released from cell membranes is metabolised in the cyclooxygenase (COX) pathway to prostanoids – biologically active substances involved in the regulation of many processes including inflammation. It has been shown that long-term exposure to fluoride in pre and neonatal period is dangerous because this element is able to penetrate through the placenta and to cross the blood-brain barrier. Exposure to fluoride during the development affects metabolism and physiology of neurons and glia which results in the impairment of cognitive functions but the exact mechanisms of fluoride neurotoxicity are not clearly defined.

OBJECTIVE: The aim of this study was to determine whether exposure to fluoride during the development affects COXes activity and the synthesis of prostanoids.

MATERIAL AND METHODS: Pre- and postnatal toxicity model in Wistar rats was used. Experimental animals received 50 mg/L of NaF in drinking water ad libitum, while control animals received tap water. In cerebral cortex, hippocampus, cerebellum and striatum were measured fluoride concentration, COX1 and COX2 genes expression, immunolocalization of the enzymatic proteins and concentration of PGE2 and TXB2.

RESULTS: of this study showed statistically significant changes in the concentration of fluoride in brain structures between study group and control animals. Moreover, significant changes in the expression level of COX1 and COX2, and in the concentration of PGE2 and TXB2 were observed.

CONCLUSION: Exposure to fluoride in the prenatal and neonatal period result in the increase in COX2 activity and increase in PGE2 concentration in rats brain, which may lead to disturbances in central nervous system homeostasis.

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