摘要
目的观察慢性砷中毒对成年小鼠齿状回神经元的形态学影响,探讨慢性砷中毒对成年小鼠脑部的神经毒性机制。方法选取健康成年昆明小鼠80只,雌雄各半,分为对照组、高、中、低剂量砷染毒组,每组20只,高、中、低剂量砷染毒组分别以As2O3的1/5、1/10、1/40 LD5(09、4.5、1.1 mg/kg)灌胃染毒,对照组以蒸馏水灌胃,连续3个月。利用免疫组织化学和蛋白印迹技术观察小鼠齿状回部位神经元半胱氨酸蛋白水解酶-3(caspase-3)蛋白的表达。结果免疫组化染色显示,与正常对照组比较,砷染毒组小鼠齿状回caspase-3阳性细胞明显增多(P<0.01),阳性反应产物平均光密度增高(P<0.01),同时蛋白印迹结果显示随砷中毒剂量的增加,小鼠齿状回caspase-3蛋白含量随之增加(P<0.01),各剂量组雌雄间各数据差异无统计学意义(P>0.05)。结论慢性砷中毒导致脑齿状回神经元细胞凋亡可能与齿状回细胞caspase-3增加有关,同时脑细胞caspase-3随砷浓度增加而增高。
Objectlve To investigate the effects of chronic arsenic exposure at different doses on dentate gyrus neurons in adult mice. Methods Eighty healthy adult Kunming mice, 20-22 g, were randomly divided into four groups： normal control group, low-dose group, moderate dose group and high dose group, 20 in each （10 males and 10 females in each group）, each group was fed respectively with distilled water, 1/5 LD50, 1/10 LD50 and 1/40 LD50 As2O3 for 3 consecutive months, and adjusting the dose according to their weight changes. The content of arsenic in brain was determined. The expression of easpase-3 in dentate gyrus neurons was detected by western blotting and immunohistochemistry and analyzed by morphology methods. Results Compared with normal control group, groups of arsenic poisoning had been the main changes： caspase-3 immunohistoehemical staining positive cells increased significantly （P〈0.01）, and there were the higher expression than that of the control group by western bloting （P〈0.01）, and no significant difference was seen between male and female mice （P〉0.05）. Conclusion The obvious up-regulated expression of caspase-3 in dentate gyrus neurons may play a role in the apoptosis of the neurons induced by chronic arsenic poisoning.
出处
《环境与健康杂志》
CAS
CSCD
北大核心
2011年第7期579-582,F0003,共5页
Journal of Environment and Health
基金
[2007]筑科计合同字第6-13号
[2009]筑科大合同字第4号
