luenced by fluoride toxicity—a mechanism relating to a damage at the level in post-transcription of the receptor genes. Toxicology200: 169–177.
“These findings suggest that selective decreases in the number of nAChRs may play an important role in the mechanism(s) by which fluoride causes dysfunction of the central nervous system.”
SOURCE: Chen J, Shan KR, Long YG, Wang YN, Nordberg A, Guan ZZ. (2003). Selective decreases of nicotinic acetylcholine receptors in PC12 cells exposed to fluoride. Toxicology 183: 235-42.
“In order to investigate the molecular mechanism(s) underlying brain dysfunction caused by chronic fluorosis, neuronal nicotinic acetylcholine receptors (nAChRs) in the brain of rats receiving either 30 or 100 ppm fluoride in their drinking water for 7 months were analyzed in the present study employing ligand binding and Western blotting… Since nAChRs play major roles in cognitive processes such as learning and memory, the decrease in the number of nAChRs caused by fluoride toxicity may be an important factor in the mechanism of brain dysfunction in the disorder.”
SOURCE: Long YG, Wang YN, Chen J, Jiang SF, Nordberg A, Guan ZZ. (2002). Chronic fluoride toxicity decreases the number of nicotinic acetylcholine receptors in rat brain. Neurotoxicology and Teratology 24:751-7.
“Over uptake of fluoride for a long term could cause potential increase in the level of oxidative stress in the brain tissue.”
SOURCE: Shao Q, Wang Y, Guan Z. (2000). [Influence of free radical inducer on the level of oxidative stress in brain of rats with fluorosis]. Zhonghua Yu Fang Yi Xue Za Zhi 34:330-2.
“The results demonstrate that the contents of phospholipid and ubiquinone are modified in brains affected by chronic fluorosis and these changes of membrane lipids could be involved in the pathogenesis of this disease.”
SOURCE: Guan ZZ, Wang YN, Xiao KQ, Dai DY, Chen YH, Liu JL, Sindelar P, Dallner G. (1998). Influence of chronic fluorosis on membrane lipids in rat brain. Neurotoxicology and Teratology 20: 537-542.
“Coenzyme Q content of brain tissue in rats fed with fluorine-containing water decreased at early stage of fluorosis, but increased significantly at late stage. It is speculated that changes in content of coenzyme Q could correlate with changes in free radical levels induced by fluorine.”
SOURCE: Wang Y, Guan Z, Xiao K. (1997). [Changes of coenzyme Q content in brain tissues of rats with fluorosis]. Zhonghua Yu Fang Yi Xue Za Zhi. 31: 330-3.
“The metabolism of brain phospholipid might be interfered by fluoride accumulated in brain tissue, which is related with the degeneration of neuron. The changes of brain phospholipid could be involved in the pathogenesis of chronic fluorosis.”
SOURCE: Guan Z, Wang Y, Xiao K. (1997). [Influence of experimental fluorosis on phospholipid content and fatty acid composition in rat brain]. Zhonghua Yi Xue Za Zhi. 77: 592-6.
Other references (no abstract available):
2) Animal Studies from other research teams
“Fluorosis had obvious influence on phospholipid and fatty acid composition in brain cells of rats, and its mechanism might be associated with action of lipid peroxidation, and 0.03 mg/L KI (potassium iodine) is the optimal concentration for the antagonistic action with this influence from fluorosis.”
SOURCE: Shen X, Zhang Z, Xu X. (2004). [Influence of combined iodine and fluoride on phospholipid and fatty acid composition in brain cells of rats] Wei Sheng Yan Jiu. 33:158-61.
“These neurotoxic changes in the brain suggested that there was a direct action of fluoride upon the nerve tissue which was responsible for central nervous system problems such as tremors, seizures, and paralysis indicating brain dysfunction seen at the two highest doses.”
SOURCE: Shashi A. (2003). Histopathological investigation of fluoride-induced neurotoxicity in rabbits. Fluoride 36: 95-105.
“CONCLUSION: Fluoride may go through the blood-brain barrier and accumulate in rat hippocampus, and inhibit the activity of cholinesterase.”
SOURCE: Zhai JX, et al. (2003). [Studies on fluoride concentration and cholinesterase 