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ORIGINAL PAPER
 
CC BY-NC 3.0 Polska
 
 

Effects of benzo(a)pyrene exposure on the ATPase activity and calcium concentration in the hippocampus of neonatal rats

Kai Yang 1,  
Chengzhi Chen 1,  
Shuqun Cheng 1,  
Xianqing Cao 2,  
Baijie Tu 1  
 
1
Chongqing Medical University, Chongqing, China (Innovation Center for Social Risk Governance in Health, Research Center for Medicine and Social Development, School of Public Health and Management, Department of Occupational and Environmental Health)
2
Chongqing Medical University, Chongqing, China (Center of Experimental Teaching for Public Health, Experimental Teaching and Management Center)
Int J Occup Med Environ Health 2017;30(2):203–211
KEYWORDS:
TOPICS:
ABSTRACT:
Objectives: To investigate whether postnatal benzo(a)pyrene (B(a)P) exposure caused the impairments on the process of neurodevelopment and the alteration in the calcium medium in the neonatal rats. Material and Methods: Eighty neonatal Sprague Dawley (SD) rats were randomly divided into 5 groups (untreated control group, vehicle group, 0.02 mg/kg, 0.2 mg/kg and 2 mg/kg B(a)P-exposed group). Rats were treated with B(a)P by the intragastric administration from postnatal day (PND) 4 to 25. Morris water maze (MWM) was employed to observe the spatial memory of rats. The activity of calcium adenosine triphosphatase (Ca2+-ATPase), sodium-potassium adenosine triphosphatase (Na+-K+-ATPase) and calcium-magnesium adenosine triphosphatase (Ca2+-Mg2+-ATPase) in the hippocampus were detected by commercial kits. Fura-2 pentakis(acetoxymethyl) (Fura-2/AM) probe and reactive oxygen species (ROS) reagent kit were used for measuring the concentration of Ca2+ and ROS in the hippocampus synapse, respectively. Results: Rats exposed to B(a)P resulted in the deficits in the spatial memory manifested by the increased escape latency and decreased number of crossing platform and time spent in target quadrant in comparison with the control groups. Benzo(a)pyrene exposure caused the significant decrease in the ATPase activity in the hippocampus and caused Ca2+ overload in the synaptic, besides, the ROS concentration increased significantly which may further induce neurobehavioral impairment of the neonatal rats. Conclusions: Our findings suggest that postnatal B(a)P exposure may cause the neurobehavioral impairments in the neonatal rats, which were mediated by the decreased ATPase activity and elevated Ca2+ concentration. Int J Occup Med Environ Health 2017;30(2):203–211
CORRESPONDING AUTHOR:
Baijie Tu   
Chongqing Medical University, Innovation Center for Social Risk Governance in Health, Research Center for Medicine and Social Development, School of Public Health and Management, Department of Occupational and Environmental Health, 1 Yixueyuan Road, Yuzhong District, Chongqing 400016, China
eISSN:1896-494X
ISSN:1232-1087