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264 Fluoride 2004;37(4):264–277 Research Report Fluoride 2004;37(4) Dr Blaylock is a Board-certified neurosurgeon, a member of the Editorial Board of the Journal of the American Nutraceutical Association (JANA), and the author of three books on excitotoxicity: Excitoxicity: the taste that kills, Health and nutrition secrets, and Natural strategies for cancer patients. EXCITOTOXICITY : A POSSIBLE CENTRAL MECHANISM I N FLUORIDE NEUROTOXICITY Russell L Blaylock a Ridgeland, MS, USA SUMMAR Y : Recent evidence indicates that fluoride produces neuronal destruction and synaptic injury by a mechanism that involves free radical production and lipid peroxidation. For a number of pathological disorders of the central nervous system (CNS), excitotoxicity plays a critical role. Var ious studies have shown that many of the neurotoxic metals, such as mercury, lead, aluminum, and iron also injure neural elements in the CNS by an excitotoxic mechanism. Free radical generation and lipid peroxidation, especially in the face of hypomagnesemia and low neuronal energy production, also magnify excitotoxic sensitivity of neurons and their elements. This paper reviews briefly some of the studies that point to a common mechanism for the CNS neurotoxic effects of fluoride and calls for research directed toward further elucidation of this mechanism. Keywords: Aspartate; Excitotoxicity; Fluoride neurotoxicity; Fluoroaluminum complexes; Glutamate; 4-Hydroxynonenal; Melatonin; Neurodegeneration; Peroxynitrite; Reactive nitrogen species; Reactive oxygen species. INTRODUCTION Compelling evidence indicates that fluoride produces injury to the central ner- vous system (CNS) by several mechanisms. Of particular interest is the ability of fluoride to induce free radical generation and lipid peroxidation in the brain, especially in the hippocampus. In addition, fluoride enhances aluminum absorp- tion from the gastrointestinal mucosa and across the blood-brain barrier. Of par- ticular concern is the recent demonstration that fluoride readily forms a chemical complex with aluminum, similar to the phosphate ion, which is toxic to neurons at low concentrations and can act as an activator of G-proteins, a membrane link to second messenger activation. While it appears that the toxicity of fluoride is secondary to many widely diver- gent and unrelated processes, there is compelling evidence that a central mecha- nism may be involved c alled excitotoxicity (Figure and Table). a For correspondence: Russell L Blaylock, MD, 315 Rolling Meadows Road, Ridgeland, MS 39157, USA. E-mail: [email protected]

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