摘要
目的观察慢性砷中毒小鼠齿状回内生化指标和神经元的改变,探讨慢性砷中毒对小鼠齿状回神经元的毒性。方法 80只健康成年昆明小鼠随机分为对照组(蒸馏水)、1.1、4.5、9.0 mg/kg As2O3染毒组,每组20只,雌雄各半,连续灌胃3个月,每天1次,检测小鼠海马组织中超氧化物歧化酶(SOD)、丙二醛(MDA)水平。利用免疫组织化学和蛋白印迹技术检测齿状回神经元特异性烯醇化酶(neuron specific enolase,NSE)蛋白表达。结果砷中毒组小鼠海马组织中MDA水平高于对照组,而SOD水平则低于对照组(P<0.01);免疫组化染色显示砷中毒组小鼠齿状回NSE阳性细胞减少(P<0.01),阳性反应产物平均光密度降低(P<0.01),同时蛋白印迹结果显示随着砷染毒剂量的增加,小鼠齿状回NSE蛋白含量减少(P<0.01),各组性别差异无统计学意义(P>0.05)。结论慢性砷中毒导致小鼠齿状回神经元氧化损伤,并抑制小鼠齿状回神经元NSE表达。
Objective To investigate the effects of different doses of chronic arsenic exposure on neurons and enzymes in dentate gyrus in adult mice. Methods A total of 80 healthy adult Kunming mice were randomly divided into four groups： control group, high-dose group, moderate-dose group and low-dose group, 20 in each, each group was treated respectively with distilled water, 9.0,4.5 and 1.1 mg/kg AS203 through gavage for three consecutive months, and the dose was adjusted according to their weight changes. The levels of SOD and MDA were measured. The expression of neuron-specific enolase （NSE） in dentate gyrus neurons was detected by Western blotting and immunohistochemistry, and analyzed by morphology methods. Results In arsenic poisoning groups, higher levels of MDA and lower levels of SOD were found, NSE immunohistochemieal staining positive cells reduced significantly （P〈0.01）, and there was lower expression of NSE, compared with those in the control group （P〈0.01）. There was no significant gender difference in indexes mentioned above. Conclusion Chronic arsenic exposure may induce oxidative damage and the changes of NSE expression in the dentate gyrus in mice.
出处
《环境与健康杂志》
CAS
CSCD
北大核心
2013年第12期1062-1065,F0003,共5页
Journal of Environment and Health
基金
贵阳市科技局大学生创新基金[(2007)筑科计合同字第6-13号
(2009)筑科大合同字第4号]
关键词
砷中毒
神经元特异性烯醇化酶
齿状回
氧化损伤
Arsenic poisoning
Neuron-specific enolase
Dentate gyrus
Oxidative damage
