Introduction A series of cytotoxic effects exposed to zinc oxide nanoparticles (ZnO NPs) are observed, such as oxidative damage and cell death. Oxidative stress has been recognized as an important mechanism underlying the toxic effects of metal oxide NPs, which has been extensively studied in vitro and in vivo . Oxidative stress is definitely caused by an imbalance between production of various reactive oxygen species (ROS) and antioxidant defense. ROS has been identified as signaling molecules in various pathways regulating both cell survival and cell death. This study focused on the effects of ZnO NPs on spatial learning and memory and number of CA1 pyramidal neurons in the hippocampus of male rats. Methods The experimental groups consist of control group, care groups with ZnO NPs (0.25, 0.5, 1, 1.25 mg/kg) and group treated with ZnO NPs(1.25) +N-acetyl-cysteine (300 mg/kg). Intraperitoneal administration of saline or ZnO NPs was down 30 minutes before training. The animals memory were examined with passive avoidance test and the number of intact neurons in CA1 area in experimental groups were counted. The statistical analysis were performed using SPSS software and one-way analysis of variance and Graph Pad prism software. Results Injections of ZnO NPs(1.25 mg/kg) significantly reduced memory retention (p<0.01) and intact neurons in CA1 area (p<0.0001) compared to the control group.In the group of ZnO NPs(1.25) + NAC (300 mg/kg), NAC improved the effect of ZnO NPs on memory retrival and intact neurons in CA1 area. Conclusion: Injection of ZnO NPs in high dose lead to memory deficiency and reduced hippocampal CA1 neurons.
