Neuroprotective effects of gallic acid against neurotoxicity induced by sodium arsenite in rats

Arsenic causes a wide range of neurological complications including cognitive impairment, short-term memory and concentration problems. The present study investigated effects of gallic acid (GA) against sodium arsenite (SA)-induced neurotoxicity in rats. Thirty-five adult male rats were randomly divided into five groups. Group 1 received normal saline (2 ml/kg, P.O.) for 21 days. Group 2 received SA (10 mg/kg, P.O., for 14 days). Groups 3 and 4 received GA (10 and 30 mg/kg, P.O., respectively) for 7 consecutive days prior to SA treatment and continued up to 21 days, parallel to SA administration. Group 5 received GA (30 mg/kg, P.O.) for 21 days. The long-term memory, motor performance, locomotor activity, and behavioral parameters were evaluated. The activity of glutathione peroxidase (GPx) and the level of MDA and glutathione (GSH) were measured in hippocampus, corpus striatum, and cortex of brains of rats. Histopathological parameters were also assessed. GA significantly reversed SA-induced reduction of step-through latency, latency to fall, and crossing, rearing, and grooming activity. GA significantly decreased SA-induced increased MDA level, and decreased GSH level and GPx activity in different parts of brain. Our results suggest that GA enhances endogenous antioxidant activity contributing to the improvement of SA-induced neural and behavioral dysfunction.