HUMAN STUDIES- Fluoride's Impact on the Adult Brain:


"The results of the NCTB (neurobehavioral core test battery) testing show the exposed groups with significant differences for various indices as compared to the reference standards and the control, with particular deficits in attention, auditory retention, and physical dexterity and acuity as well as abnormal emotional states. This is consistent with the symptoms of endemic fluoride poisoning, suggesting occupational exposure to fluoride has a harmful effect on the higher functions of the central nervous system, negatively influencing both cognitive and autonomic functioning. There is a definite relationship between the damage caused by fluoride and the level of exposure. The correlation analysis shows that, with the exception of visual retention and digit symbol testing, serum fluoride is negatively correlated with all relevant indices, further demonstrating the cause and effect relationship between occupational fluoride exposure and neurobehavioral function; these tests can be used as early indicators to help protect the health of workers exposed to fluoride as part of their jobs."  SOURCE: Guo Z, et al. (2001). Study on neurobehavioral function of workers occupationally exposed to fluoride. Industrial Health and Occupational Disease 27:346-348.


“Sulfuryl fluoride exposure over the year preceding examination was associated with significantly reduced performance on the Pattern Memory Test and on olfactory testing... CONCLUSIONS: Occupational sulfuryl fluoride exposures may be associated with subclinical effects on the central nervous system, including effects on olfactory and some cognitive functions.”   SOURCE: Calvert GM, et al. (1998). Health effects associated with sulfuryl fluoride and methyl bromide exposure among structural fumigation workers. American Journal of Public Health 88:1774-80.


"Although the blood-brain barrier is relatively impermeable to fluoride, it does not pose an absolute barrier and fluoride has the ability to enter the brain. The literature was examined to assess the quality of the evidence for cerebral impairment occurring due to exposure to fluoride from therapeutic or environmental sources. Several surveys of persons chronically exposed to industrial fluoride pollution reported symptoms related to impaired central nervous system functioning with impaired cognition and memory. Examination of individual case reports showed the evidence for aetiological relationships between symptoms and fluoride exposure to be of variable quality. The evidence was seen as being suggestive of a relationship rather than being definitive. The difficulties with concentration and memory described in relation to exposure to fluoride did not occur in isolation but were accompanied by other symptoms of which general malaise and fatigue were central. Possible mechanisms whereby fluoride could affect brain function include influencing calcium currents, altering enzyme configuration by forming strong hydrogen bonds with amide groups, inhibiting cortical adenylyl cyclase activity, and increasing phosphoinositide hydrolysis."  SOURCE: Spittle B. (1994). Psychopharmacology of fluoride: a review. International clinical psychopharmacology 9:79-82.



ANIMAL STUDIES - Fluoride's Impact on Brain (Behavior/ Learning/ Memory):


"Overall, these results suggest that moderate intoxication with sodium fluoride has potentially deleterious effects on learning and memory."  SOURCE: Chioca LR, et al. (2007). Subchronic fluoride intake induces impairment in habituation and active avoidance tasks in rats. European Journal of Pharmacology Oct 25; [Epub ahead of print]


“The results of the present study indicate that perinatal exposure to sodium fluoride (NaF), at dose levels below those associated with gross malformations and/or overt neurotoxic effects, produces both short and long term sex and dose-specific neurobehavioural alterations in rat offspring."  SOURCE: Bera I, et al. (2007). Neurofunctional effects of developmental sodium fluoride exposure in rats. European Review for Medical and Pharmacological Sciences 11(4):211-24.


"Additional animal studies designed to evaluate reasoning are needed. These studies must be carefully designed to measure cognitive skills beyond rote learning or the acquisition of simple associations, and test environmentally relevant doses of fluoride."  SOURCE: National Research Council. (2006). Fluoride in Drinking Water: A Scientific Review of EPA's Standards. National Academies Press, Washington D.C. p. 187.


"In comparison with control rats, the learning and memory ability of the offspring rats was depressed by high fluoride, low iodine, or the combination of high fluoride and low iodine."SOURCE: Wang J, et al. (2004). Effects of high fluoride and low iodine on biochemical indexes of the brain and learning memory of offspring rats. Fluoride 37: 201-208. ​


"Fluoride intoxicated animals also performed poorly in motor co-ordination tests and maze tests. Inability to perform well increased with higher fluoride concentration in drinking water.”   SOURCE: Bhatnagar M, et al. (2002). Neurotoxicity of fluoride: neurodegeneration in the hippocampus of female mice. Indian Journal of Experimental Biology 40: 546-54.​


“Administration of sodium fluoride with drinking water produced both behavioral and dental toxicities and not lethality in the present study. A suppression of spontaneous motor activity, a shortening of rota-rod endurance time, a decreased body weight gain and food intake, a suppression of total cholinesterase and acetylcholinesterase activities and dental lesion were observed in test animals.”  SOURCE: Ekambaram P, Paul V. (2001). Calcium preventing locomotor behavioral and dental toxicities of fluoride by decreasing serum fluoride levels in rats. Environmental Toxicology and Pharmacology 9(4):141-146.​


“The main results showed that the learning capability of mice drinking a higher concentration of fluoride presented remarkable deterioration.”   SOURCE: Zhang Z, et al. (2001). [Effects of selenium on the damage of learning-memory ability of mice induced by fluoride]. Wei Sheng Yan Jiu. 30(3):144-6.​


“Learning and memory abilities of high-fluoride exposed groups were significantly lower than that of the control group, while the brain ChE activities of high-fluoride exposed groups were significantly higher. Conclusions: High fluoride concentration in drinking water can decrease the cerebral functions of mice. Fluoride is a neurotoxicant.”  SOURCE: Sun ZR, et al. (2000). Effects of high fluoride drinking water on the cerebral functions of mice. Chinese Journal of Epidemiology 19: 262-263.​


“The main results are as follows: the learning ability of mice drinking a high concentration of fluoride presented remarkable deterioration... The results suggested that the impairment on the learning capability induced by fluorosis may be closely related to the pathological changes of synaptic structure in the brain of mice.”  SOURCE: Zhang Z, et al. (1999). [Effect of fluoride exposure on synaptic structure of brain areas related to learning-memory in mice] [Article in Chinese]. Wei Sheng Yan Jiu 28(4):210-2.​


“Sodium fluoride treatment suppressed spontaneous motor activity But no change was observed in the motor coordination of these animals. A suppression of spontaneous motor activity suggests that fluoride has, by a central action, inhibited motivation of these animals to exhibit locomotor behavior.”   SOURCE: Paul V, et al. (1998). Effects of sodium fluoride on locomotor behavior and a few biochemical parameters in rats. Environmental Toxicology and Pharmacology 6: 187–191. ​


"In this experiment, the freeze response to auditory stimuli in the pups showed significant delay, indicating that relatively high doses of fluoride can negatively influence the development of auditory nerves. Guan Zhizhong et al[8] report that the offspring of rats exposed to fluoride have retarded cerebral development and exhibit changes in neural cell ultrastructure. The results of the present experiment suggest that the effects of high doses of fluoride on the behavior development of the offspring are visible primarily as slight delays in response times, particularly with regard to motor and coordination function and well as muscle strength. The measurement of the thickness of the cerebral cortex of offspring on day 21 revealed that the 25 mg/L group had a significantly thinner cerebral cortex as compared to the control; this histological analysis indicates that fluoride slows the growth of brain cells."  SOURCE: Wu N, et al. (1995). Research on the abnormal behavior of rats exposed to fluoride. Chinese Journal of Control of Endemic Diseases 14(5):271.


“This study demonstrates a link between certain fluoride exposures and behavioral disruption in the rat. The effect on behavior varied with the timing of exposure during CNS development. Behavioral changes common to weanling and adult exposures were different from those after prenatal exposures... Experience with other developmental neurotoxicants prompts expectations that changes in behavioral function will be comparable across species, especially humans and rats... [A] generic behavioral pattern disruption as found in this rat study can be indicative of a potential for motor dysfunction, IQ deficits and/or learning disabilities in humans.”   SOURCE: Mullenix P, et al. (1995). Neurotoxicity of Sodium Fluoride in Rats. Neurotoxicology and Teratology 17:169-177.​


" When rats were treated 6 hr a day for 5 mo. with HF concentrations of 3, 1, 0.5, and 0.1 mg/m-3, it caused functional changes in the CNS, as shown by the condition reflex method and the measurement of chronaxy. There was inhibition of the blood alkaline phosphatase activity and pathomorphological changes in the CNS, bone and tooth tissues, and internal organs. The extent of the changes depended on the concentration of HF. The maximum allowable concentration of HF for the air at working places presently accepted, 0.5 mg/m-3, is too high."  SOURCE: Vishnevskii VL, El Nichnykh LN. (1969). (A toxicological and morphological characterization of the action of different concentrations of inhaled hydrogen fluoride on the body.). Tr Tsentr Nauchno-Issled Proektn-Konstr In. 2: 143-147.

"General malaise, asthenia, and apathy developed to a marked degree in the monkeys exposed to the BeF2 (beryllium fluoride) aerosol, and in those under the heaviest BeHPO4 exposure. The monkeys retreated to the furthest corner of their cages and paid no attention to light flashed at them. They remained in this withdrawn and listless condition until death. Monkeys which inhaled the BeSO4 aerosol faired best of all."  SOURCE: Schepers GWH. (1964). The biological action of beryllium: Reaction of the monkey to inhaled aerosols. Industrial Medicine and Surgery 33: 1-16.



ANIMAL STUDIES - Fluoride's Impact on Brain:


"Lipids and phospholipids, phosphohydrolases and phospholipase D, and protein content have been shown to be reduced in the brains of laboratory animals subsequent to fluoride exposure. The greatest changes were found in phosphatidylethanolamine, phosphatidylcholine, and phosphatidylserine. Fluorides also inhibit the activity of cholinesterases, including acetylcholinesterase. Recently, the number of receptors for acetylcholine has been found to be reduced in regions of the brain thought to be most important for mental stability and for adequate retrieval of memories.

It appears that many of fluoride’s effects and those of the aluminofluoride complexes are mediated by activation of Gp, a protein of the G family. G proteins mediate the release of many of the best-known transmitters of the central nervous system. Not only do fluorides affect transmitter concentrations and functions but also are involved in the regulation of glucagons, prostaglandins, and a number of central nervous system peptides, including vasopressin, endogenous opioids, and other hypothalamic peptides. The AlFx binds to GDP and ADP altering their ability to form the triphosphate molecule essential for providing energies to cells in the brain. Thus, AlFx not only provides false messages throughout the nervous system but, at the same time, diminishes the energy essential to brain function.

Fluorides also increase the production of free radicals in the brain through several different biological pathways. These changes have a bearing on the possibility that fluorides act to increase the risk of developing Alzheimer’s disease. Today, the disruption of aerobic metabolism in the brain, a reduction of effectiveness of acetylcholine as a transmitter, and an increase in free radicals are thought to be causative factors for this disease. More research is needed to clarify fluoride’s biochemical effects on the brain."  SOURCE: National Research Council. (2006). Fluoride in Drinking Water: A Scientific Review of EPA's Standards. National Academies Press, Washington D.C. p. 186.


"Studies of rats exposed to NaF or AlF3 have reported distortion in cells in the outer and inner layers of the neocortex. Neuronal deformations were also found in the hippocampus and to a smaller extent in the amygdala and the cerebellum. Aluminum was detected in neurons and glia, as well as in the lining and in the lumen of blood vessels in the brain and kidney. The substantial enhancement of reactive microglia, the presence of stained intracellular neurofilaments, and the presence of IgM observed in rodents are related to signs of dementia in humans. The magnitude of the changes was large and consistent among the studies."   SOURCE: National Research Council. (2006). Fluoride in Drinking Water: A Scientific Review of EPA's Standards. National Academies Press, Washington D.C. p. 187.


"In the present study, levels of glutathione and activities of catalase, GSH-PX, and SOD were significantly decreased, whereas lipid peroxide levels were enhanced in the brain of adult rats by treatment with NaF, As2O, or NaF + As2O3, in agreement with earlier reports."   SOURCE: Chinoy NJ, et al. (2004). Biochemical effects of sodium fluoride and arsenic trioxide toxicity and their reversal in the brain of mice. Fluoride 37: 80-87.


"The histology of the cerebral hemisphere was altered by NaF and/or Arsenic trioxide [As2O3] treatment for 30 days, wherein the effect by As2O3 was greater than by NaF treatment. This result is in agreement with others... The reduced brain acetylcholinesterase (AChE) enzyme activity observed in the present study corroborates data of others in rats exposed for three months to arsenic trioxide and in the brain of NaF-treated mice and rats as compared to controls... The DNA and RNA levels in the cerebral hemisphere were significantly lower in NaF and/or As2O3-treated mice in the present study, which could affect brain function. The ingestion of the antidotes vitamins C and E as well as calcium phosphate, either individually or in combination, during the 30-day withdrawal period, resulted in significant recovery, probably due to the antioxidant properties of vitamins C and E and modulation of fluoride-induced toxicity in rats by calcium."  SOURCE: Shah SD, Chinoy NJ. (2004). Adverse effects of fluoride and/or arsenic on the cerebral hemisphere of mice and recovery by some antidotes. Fluoride 37: 162-171.


"Superoxide dismutase (SOD) activity and the malondialdehyde (MDA) content in the brain of the combined high fluoride and low iodine group were significantly higher during and at the end of the 90-day period than in the control group, but the SOD/MDA ratio in this high fluoride and low iodine group was consistently lower than in the control group. These results suggest that [oxidative] stress from high fluoride and low iodine is one of the causes of reduction in learning and memory in offspring rats."  SOURCE: Wang J, Ge Y, Ning H, Wang S. (2004). Effects of high fluoride and low iodine on biochemical indexes of the brain and learning memory of offspring rats. Fluoride 37: 201-208.


"Brain protein was decreased by low iodine and even more by the combined interaction of high fluoride and low iodine. The activity of cholinesterase (ChE) in the brain was affected to some extent by high fluoride and low iodine but was especially affected by high fluoride and low iodine together."   SOURCE: Wang J, et al. (2004). Effects of high fluoride and low iodine on biochemical indexes of the brain and learning memory of offspring rats. Fluoride 37: 201-208.


“Recently, we have detected the alterations of nicotinic acetylcholine receptors (nAChRs) in rat brains and PC12 cells affected by fluoride toxicity... [O]xidative stress, including protein oxidation of the receptors and lipid peroxidation in the cellular membrane, might be a mechanism of the deficit of the receptors.”
SOURCE: Shan KR, Qi XL, Long YG, Wang YN, Nordberg A, Guan ZZ. (2004). Decreased nicotinic receptors in PC12 cells and rat brains influenced by fluoride toxicity—a mechanism relating to damage at the level in post-transcription of the receptor genes. Toxicology 200: 169–177.

“Fluorosis had an obvious influence on phospholipid and fatty acid composition in brain cells of rats, and its mechanism might be associated with the 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 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.


“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 activity in rat hippocampus]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi 21:102-4.


“Light microscopic study of hippocampal sub-regions demonstrated a significant number of degenerated nerve cell bodies in the CA3, CA4 and dentate gyrus(Dg) areas of sodium fluoride administered adult female mice. Ultrastructural studies revealed neurodegenerative characteristics like involution of cell membranes, swelling of mitochondria, clumping of chromatin material, etc, can be observed in cell bodies of CA3, CA4 and dentate gyrus (Dg).”   SOURCE: Bhatnagar M, et al. (2002). Neurotoxicity of fluoride: neurodegeneration in the hippocampus of female mice. Indian Journal of Experimental Biology 40: 546-54.


“The DNA damage in pallium neurons in rats of the fluoride group was much more serious compared with those of the control group...Sodium fluoride could induce DNA damage and apoptosis in rats' brains.”
SOURCE: Chen J, Chen X, Yang K, Xia T, Xie H. (2002). [Studies on DNA damage and apoptosis in rat brain induced by fluoride]. Zhonghua Yu Fang Yi Xue Za Zhi 36: 222-224.


“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.


“These results suggest that fluoride enhances oxidative stress in the brain, thereby disturbing the antioxidant defense of rats. Increased oxidative stress could be one of the mediating factors in the pathogenesis of fluoride toxicity in the brain.”   SOURCE: Shivarajashankara YM, et al. (2002). Brain lipid peroxidation and antioxidant systems of young rats in chronic fluoride intoxication. Fluoride 35: 197-203.


“rats exposed to 100 ppm fluoride showed significant neurodegenerative changes in the hippocampus, amygdala, motor cortex, and cerebellum... These histological changes suggest a toxic effect of high-fluoride intake during the early developing stages of life on the growth, differentiation, and subcellular organization of brain cells in rats.”   SOURCE: Shivarajashankara YM, et al. (2002). Histological changes in the brain of young fluoride-intoxicated rats. Fluoride 35: 12-21.


“The extent of DNA damage in the fluoride + selenium + zinc group was significantly slighter than that in the fluoride group (P < 0.05). It suggested that fluoride and selenium could induce DNA damage in pallium neural cells of rats respectively.”   SOURCE: Chen J, Chen X, Yang K. (2000). [Effects of selenium and zinc on the DNA damage caused by fluoride in pallium neural cells of rats]. Wei Sheng Yan Jiu. 29: 216-7.


“This study, therefore, shows that both brain and muscle are affected by fluoride with inhibition of some enzymes associated with free-radical metabolism, energy production, and transfer, membrane transport, and synaptic transmission, but with enhanced activity of XOD.”   SOURCE: Lakshmi Vani M, Pratap Reddy K. (2000). Effects of fluoride accumulation on some enzymes of the brain and gastrocnemius muscle of mice. Fluoride 33: 17-26.


“There is a tendency for neuron apoptosis in chronic fluorosis in rats. It is most evident with changes in pathology. It is not likely that only one form of neuron damage exists in the process of chronic fluorosis. There are recessive changes and apoptosis in the process at the same time.”   SOURCE: Lu XH, et al. (2000). Study of the mechanism of neuron apoptosis in rats from chronic fluorosis. Chinese Journal of Epidemiology 19: 96-98.


“Over uptake of fluoride for a long term could cause a 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 strs in the brain of rats with fluorosis]. Zhonghua Yu Fang Yi Xue Za Zhi 34:330-2.


“It was concluded that aluminum interferes with the metabolism of the neuronal cytoskeleton and that this interference is potentiated by fluoride.”   SOURCE: van der Voet GB, et al. (1999). Fluoride enhances the effect of aluminum chloride on interconnections between aggregates of hippocampal neurons. Archives of Physiology and Biochemistry 107:15-21.


"The thickness of post-synaptic density (PSD) was decreased, and the width of the synaptic cleft was remarkably increased. The results suggested that the impairment on the learning capability induced by fluorosis may be closely related to the pathological changes of synaptic structure in the brain of mice.”  SOURCE: Zhang Z, et al. (1999). [Effect of fluoride exposure on synaptic structure of brain areas related to learning-memory in mice] [Article in Chinese]. Wei Sheng Yan Jiu 28:210-2.


“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.


“While the small amount of AlF in the drinking water of rats required for neurotoxic effects is surprising, perhaps even more surprising are the neurotoxic results of NaF at the dose given in the present study [1.0 ppm F]... The results of the present study indicate that more intensive neuropathological evaluations of F effects on the brain may prove to be of value... In summary, chronic administration of AlF and NaF in the drinking water of rats resulted in distinct morphological alterations in the brain, including effects on neurons and cerebrovasculature.”   SOURCE: Varner JA, et al. (1998). Chronic administration of aluminum-fluoride and sodium-fluoride to rats in drinking water: Alterations in neuronal and cerebrovascular integrity. Brain Research 784: 284-298.


“These results indicate that fluoride may penetrate the blood-brain barrier, interact with AChE located on cell membranes, and interfere with their physiological functions and thus induce the neurotoxicities.”   SOURCE: Zhao XL, Wu JH. (1998). Actions of sodium fluoride on acetylcholinesterase activities in rats. Biomedical and Environmental Sciences 11(1):1-6.


“The metabolism of brain phospholipid might be interfered by fluoride accumulated in brain tissue, which is related to the degeneration of neurons. The changes in 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.


“Neuronal abnormalities were observed in the NaF treated animals- especially in the deeper cell layers... The NaF treatment also produced distortions of cells and, in some rats, cell losses could be demonstrated in particular brain regions. Both AlF3 and NaF induced vascular inclusions, although of a different character...”   SOURCE: Issacson R, et al. (1997). Toxin-induced blood vessel inclusions caused by the chronic administration of aluminum and sodium fluoride and their implications for dementia. Annals of the New York Academy of Science 825: 152-166.


“Coenzyme Q content of brain tissue in rats fed with fluorine-containing water decreased at an early stage of fluorosis but increased significantly at the late stage. It is speculated that changes in the 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.


“Excessive fluoride intake decreased 5-hydroxy indole acetic acid and increased norepinephrine in rat brain.”   SOURCE: Li Y, et al. (1994). [Effect of excessive fluoride intake on the mental work capacity of children and a preliminary study of its mechanism] Hua Hsi I Ko Ta Hsueh Hsueh Pao. 25(2):188-91.


“The results reported here indicate that fluoride has a specific effect on the synthesis of proteins in the brain which may lead to degenerative changes in the form of ballooning degeneration of neurons, various degrees of loss of nasal substance, and changes in the Purkinje cells of the cerebellar cortex. Such changes would provide a plausible explanation for some of the diverse neurological complaints in arms and legs such as numbness, muscle spasms and pains, tenaniform convulsions, and spastic paraplegia, encountered in patients with skeletal fluorosis."  SOURCE: Shashi A, et al. (1994). Effect of long-term administration of fluoride on levels of protein, free amino acids, and RNA in rabbit brain. Fluoride 27: 155-159.


“The neurotoxic effect of fluoride on the lipid content of the brain was assessed in rabbits during experimental fluorosis... Fluoride exerts an inhibitory effect on the free fatty acids in the brain of both sexes. The relevance of these results in experimental fluorosis is discussed.”   SOURCE: Shashi A. (1992). Studies on alterations in brain lipid metabolism following experimental fluorosis. Fluoride 25:77-84.




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