Abstract
Fluoride is frequently added to drinking water supplies, various food products, toothpaste, and mouth rinses to prevent tooth damage. However, at high concentrations, fluoride can cause fluorosis and damage to the brain tissue due to its excitotoxicity and oxidative stress effects. The damage of the Purkinje cells of the cerebellum can lead to motor coordination disorders. The present study aimed at investigating the effects of sodium fluoride on the motor coordination and the number of Purkinje cells of the cerebellum of rats. Adult male Wistar rats were divided into four groups, namely a control group which received reverse osmosis distilled water and three treated groups which received sodium fluoride at doses of 5, 10, or 20 mg/kg bw. The treatment lasted for 30 days. The motor coordination of the rats was examined using a rotarod prior and subsequent to the treatments. The number of Purkinje cells was estimated using physical fractionator design. The numbers of Purkinje cells of the F10 and F20 groups were significantly lower than that of the control group. No significant differences in the results of the motor coordination test were found. The administration of sodium fluoride at doses of 10 and 20 mg/kg bw caused a decrease in the number of Purkinje cells of the cerebellum in rats.
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Co-exposure to fluoride and sulfur dioxide on histological alteration and DNA damage in rat brain.
Fluoride (F) and sulfur dioxide (SO2 ) are the two common environmental contaminants that are associated with neurotoxicity. The present study was conducted to explore individual and combined exposure effects of F and SO2 on histological alteration and DNA damage in rat brain. For this, male Wistar albino rats were
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Pre and post natal exposure of fluoride induced oxidative macromolecular alterations in developing central nervous system of rat and amelioration by antioxidants.
The effect of fluoride exposure during gestation and post gestation periods were studied to check the status of oxidant, antioxidant and macromolecular changes in CNS and ameliorative role of antioxidants. The pregnant Wistar albino rats were exposed to 50 and 150 ppm fluoride in drinking water and the pups born
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Neurobehavioral toxicity produced by sodium fluoride in drinking water of laboratory rats
The effect of exposure to different concentrations of sodium fluoride (Na-F) for different durations on learning and memory tasks in rats (non-associative and associative learning) was assessed in our study. Three groups of fifteen pregnant Wistar female rats each, were administered Na-F in drinking water at one of three concentrations;
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Emodin protected against synaptic impairment and oxidative stress induced by fluoride in SH-SY5Y cells by modulating ERK1/2/Nrf2/HO-1 pathway.
Excessive fluoride exposure contributes to neurotoxic effects. Emodin exhibits antioxidative functions in the central nervous system (CNS); however, its neuroprotective mechanism against fluoride remains to be elucidated. Our aim was to explore the neuroprotective efficacy and the possible mechanisms of emodin. In our study, synaptic proteins and oxidative stress damage
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Alterations of apoptosis and expressions of Bax and Bcl-2 in the cerebral cortices of rats with chronic fluorosis
The aim of the study was to investigate the influence of chronic fluorosis on apoptosis and the expression of Bax and Bcl-2 in the cerebral cortices of rats in an attempt to elucidate molecular mechanisms. Sixty Sprague Dawley (SD) rats were divided randomly into three groups of 20 each: an
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