Protective effect of N-acetylcysteine on bisphenol A-induced cognitive dysfunction and oxidative stress in rats.

Bisphenol A (BPA) is commonly used as a monomer in polycarbonate plastics. The present study was designed to investigate the effect of BPA on cognitive functions and oxidative stress in the brain tissue of rats and if co-administration of N-acetylcysteine (NAC), an antioxidant, can modulate the effect of BPA on cognitive functions and prevent any possible oxidative stress. The BPA was administered per orally (p.o) in two doses 2 and 20 μg/kg for 28 days. Cognitive functions were assessed using step-down latency (SDL) on a passive avoidance apparatus and spatial navigation task on Morris water maze. Oxidative stress was assessed by examining brain malondialdehyde (MDA) and reduced glutathione (GSH) levels. A significant reduction in SDL, and prolongation of latency in spatial navigation task were observed in BPA (2 and 20 μg/kg) treated group as compared to control group. The co-administration of NAC (100 mg/kg, p.o) antagonized the effect of BPA on SDL and spatial navigation test. NAC treatment also attenuated the BPA-induced increased MDA levels and decreased GSH levels in brain. Results of the present study show that NAC has potential to reverse cognitive dysfunction and oxidative stress induced by BPA exposure in rats.