Psychopharmacology of fluoride

Spittle, Bruce

doi:10.1097/00004850-199400920-00002

Cited by 73 publications

(33 citation statements)

References 7 publications

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“…Locomotor (Spittle 1994) and biochemical (Trivedi et al 1993) deficits have also been found in persons exposed chronically to fluoride. Experimental studies have demonstrated that chronic fluoride exposure is injurious to skeletal (Harrison et al 1984;Choubisa 1999) dental (Boulton et al 1995;Choubisa 1999) and soft tissues (Purohit et al 1999).…”

mentioning

confidence: 99%

Modulation of Fluoride Toxicity in Rats by Calcium Carbonate and by Withdrawal of Fluoride Exposure

Perumal

Paul

2002

Pharmacology & Toxicology

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In order to assess the effect of calcium on the toxic effects of fluoride, adult female Wistar rats were treated with sodium fluoride (NaF, 500 ppm in drinking water) alone or in combination with calcium carbonate (CaCO 3 , 50 mg/ kg by oral intubation) daily for 60 days. Food, water and fluoride intake were measured daily for 60 days. Body weight gain, exploratory motor activity, rota-rod motor coordination, dental structure, activities of acetylcholinesterase (AchE, brain and skeletal muscle) and Na π K π ATPase (erythrocyte membrane and skeletal muscle) and the concentrations of protein (serum and skeletal muscle), calcium (serum) and fluoride (serum) were determined in these animals 24 hr after the last treatment. The same parameters were tested in another group, 60 days after withdrawal of NaF exposure (500 ppm in drinking water daily for 60 days). NaF treatment decreased food and water intake, reduced body-weight gain and impaired exploratory motor activity and rota-rod performance. Dental lesions, inhibition of the activities of AchE and N π K π ATPase and a decrease in the concentration of protein, and serum calcium were also observed in these animals. These effects were accompanied by a marked elevation of fluoride concentration in the serum. CaCO 3 decreased the concentration of fluoride in the serum of NaF-treated animals. A decrease in serum fluoride concentration was found also after NaF withdrawal. A prevention of locomotor behavioural, biochemical and dental toxicities of fluoride was observed both in these groups. It is concluded that the dose of CaCO 3 used in the present study has a potential to prevent the toxicity of fluoride by maintaining serum fluoride at a less toxic level. Further, the toxic effects of fluoride are reversible if its exposure is withdrawn for 2 months.

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confidence: 99%

Modulation of Fluoride Toxicity in Rats by Calcium Carbonate and by Withdrawal of Fluoride Exposure

Perumal

Paul

2002

Pharmacology & Toxicology

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“…Thus NaF exposed pups showed decreased body weight, brain weight and also BSI. F-induced inhibition of motivated behavior has been accompanying with the locomotor behavioral deficit that occurred in workers who have chronic exposure to high level of industrial F 43 . Moreover, increased time to respond thermoceptive pain on hot plate was noted in NaF intoxicated pups which was reverted in AMAE and AMEE treated rats.…”

Section: Discussionmentioning

confidence: 99%

Untitled

2018

IJPSR

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This study reports protective effect of Abelmoschus moschatus seed extract against sodium fluoride (NaF) induced alterations in behavior correlated with neurochemical changes in developing brain of rats. Excessive intake of fluoride during pregnancy cross the blood brain barrier (BBB) and cause adverse effects on neonatal development. As the BBB in fetuses, neonates and infants is immature, it cannot provide protection against the entries. The pregnant wistar rats were randomly categorized into six groups of five animals each. Group I is of control rats received normal tap water. Group II is NaF exposed group with 20 ppm (or 20 mgkg -1 body wt.) in their drinking water. Group III rats were treated with A. moschatus aqueous extract (AMAE) (300 mgkg -1 body wt./day/rat) along with NaF water (20 ppm). Group IV rats were treated with A. moschatus ethanolic extract (AMEE) (300 mgkg -1 body wt./day/rat) along with NaF water (20 ppm).Group V and VI rats were treated with AMAE (300 mgkg -1 body wt./day/rat), and AMEE (300 mgkg -1 body wt./day/rat) respectively. On 1 st , 7 th , 14 th , 21 st and 30 th day (postpartum days), the pups were sacrificed to assess oxidative stress markers (LPO, CAT), and measured body weight, brain weight, BSI, and estimated protein content of brain tissue of all experimental groups. On post-natal day 21 and day 30 pups behavioral activity (rota rod, hot plate test) was measured. Fluoride exposure significantly increased lipid peroxidation and decreased the activity of catalase, and decreased body and brain weight, BSI and also protein content of the brain of pups indicating oxidative stress and inhibited antioxidant system and protein synthesis which were reverted on administration of AMAE and AMEE against NaF intoxication. The altered behavioral responses on NaF exposure were also reversed to that of control. Hence, this study proves the vulnerability of developing brain to fluoride toxicity during development and growth and protection offered by AMAE and AMEE towards neurotoxicity of NaF.

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“…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 [24]. High fluoride exposure can result in damage to brain cells, however, because the damage is usually mild, obvious functional changes will not necessarily be readily observable [25].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Fluoride-Induced Oxidative Stress in Rat Brain: A Multigeneration Study

Basha

Rai

Begum³

2010

Biol Trace Elem Res

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Multigenerational evaluation was made in rats on exposure to high fluoride (100 and 200 ppm) to assess neurotoxic potential of fluoride in discrete areas of the brain in terms of lipid peroxidation and the activity of antioxidant enzyme system. The rats were given fluoride through drinking water (100 and 200 ppm) and maintained subsequently for three generations. Fluoride treatment significantly increased the lipid peroxidation and decreased the activity of antioxidant enzymes viz, catalase, superoxide dismutase, glutathione peroxidase, glutathione S-transferase, and glutathione level in first-generation rats and these alterations were more pronounced in the subsequent second and thirdgeneration rats in both the doses tested. Decreased feed and water consumption, litter size and organ (brain) somatic index, marginal drop in body growth rate and mortality were observed in all three generations. Decreased antioxidant enzyme activity and increased malondialdehyde levels found in the present study might be related to oxidative damage that occurs variably in discrete regions of the brain. Results of this study can be taken as an index of neurotoxicity in rats exposed to water fluoridation over several generations.

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Psychopharmacology of fluoride

Cited by 73 publications

References 7 publications

Modulation of Fluoride Toxicity in Rats by Calcium Carbonate and by Withdrawal of Fluoride Exposure

Modulation of Fluoride Toxicity in Rats by Calcium Carbonate and by Withdrawal of Fluoride Exposure

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Evaluation of Fluoride-Induced Oxidative Stress in Rat Brain: A Multigeneration Study

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