30- and 60-days exposure of sodium fluoride induces neurobehavioral deficits and alters neurochemical parameters in adult Wistar rats

Exposure to fluoride above the recommended dose has been shown to have toxicological consequences on several body systems. There is a paucity of information on neurotoxic effect of exposure of varying doses of sodium fluoride (NaF) on specific brain regions. Hence, we investigated the toxicological consequences of 30- and 60-day exposure to varying doses of NaF on neurobehavioral outcomes and region-specific brain alterations in adult Wistar rats, with biochemical analyses conducted in the hippocampus and striatum, and immunohistochemical assessment of astrocytic activation in the striatum and myelin integrity in the corpus callosum. Eighty-four Wistar rats of 100–120 g were randomly divided into six groups. Rats in experimental groups (groups B–F) were administered NaF in deionized water at concentrations of 25, 50, 100, 150, and 300 ppm, respectively, via oral administration for 30 and 60 days. The control group (group A) received only deionized water for the same duration. Neurobehavioral assessments were carried out, and brain samples (striatum and hippocampus) were collected for biochemical assays and immunohistochemistry. Sodium fluoride caused a significant influence on locomotor activities and anxiety. Moreover, NaF caused a significant increase in malondialdehyde and decreased GSH level, superoxide dismutase and glutathione peroxidase activities. The activity of acetylcholinesrase (AchE) was also significantly reduced by all the administered doses of NaF. There was increased GFAP immunoreactivity in the NaF treated rats, and reduced myelin basic protein immunoreactivity in the corpus callosum. NaF exposure compromises brain health by disrupting antioxidant defenses, altering neurochemical balance, promoting astrocytic activation, and inducing demyelination, ultimately resulting in neurobehavioral impairments.