NEUROBEHAVIORAL PROTECTIVE EFFECTS OF POTASSIUM IODIDE AGAINST POTASSIUM BROMIDE-INDUCED NEUROTOXICITY IN MICE
Abstract
Background: Potassium bromide (KBr) has long been used as an anticonvulsant agent; however, prolonged exposure may induce neurobehavioral disturbances associated with central nervous system depression. Potassium iodide (KI) is an essential iodine source required for normal neurological function, yet its potential protective effect against bromide-induced neurotoxicity remains poorly understood. Objective: This study aimed to evaluate the neurobehavioral effects of repeated potassium bromide administration in mice and to investigate the potential protective role of potassium iodide against bromide-induced behavioral alterations. Materials and Methods: Forty-eight adult male Swiss albino mice were randomly allocated into six experimental groups (n = 8/group). Animals received potassium bromide (90 mg/kg), potassium iodide (0.5 mg/kg), or their combinations three times weekly for 28 consecutive days using either distilled water or physiological saline as administration vehicles. Neurobehavioral performance was assessed using the Open Field test, Negative Geotaxis test, and Poking Head exploratory test. Data were analyzed using one-way analysis of variance (ANOVA) followed by Tukey's post hoc test, with statistical significance accepted at p ≤ 0.05. Results: Repeated potassium bromide administration significantly reduced locomotor activity and exploratory behavior, as evidenced by decreased crossed squares and rearing frequency in the Open Field test, prolonged Negative Geotaxis latency, and reduced head-dipping activity compared with the control group (p ≤ 0.05). These behavioral impairments were most pronounced in mice receiving bromide dissolved in distilled water. Potassium iodide co-administration partially improved several behavioral parameters, although complete restoration to control values was not achieved. Conclusion: Repeated exposure to potassium bromide induced significant neurobehavioral impairment characterized by locomotor suppression, reduced exploratory activity, and impaired neuromotor coordination. Potassium iodide provided partial neurobehavioral protection, suggesting a modulatory effect against bromide-induced toxicity. Further investigations are warranted to elucidate the underlying mechanisms responsible for this protective interaction.