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饮水铅暴露对大鼠脑组织 APE1 表达的影响及与氧化应激的关系研究
引用本文:任清风,李炜娟,徐群英,张中伟,李伟,冯建高,任晓慧,肖元梅 ?.饮水铅暴露对大鼠脑组织 APE1 表达的影响及与氧化应激的关系研究[J].天津医药,2016,44(2):170-173.
作者姓名:任清风  李炜娟  徐群英  张中伟  李伟  冯建高  任晓慧  肖元梅 ?
作者单位:1南昌大学公共卫生学院 (邮编330006); 2九江学院临床医学院·附属医院; 3南昌大学抚州医学院
基金项目:国家自然科学基金资助项目(81160342); 江西省自然科学基金资助项目(20122BAB205047); 江西省教育厅科技项目 (GJJ11312)
摘    要:目的 探讨饮水铅暴露对大鼠大脑皮质、 小脑、 海马组织中脱嘌呤脱嘧啶核酸内切酶 1(APE1)表达的影响及其与氧化应激的关系。方法 40 只刚断乳雄性 SD 大鼠按体质量随机区组法均分为 5 组, 对照组自由饮用去离子水, 4 个铅暴露组分别饮用 100、 200、 400 和 800 mg/L 醋酸铅溶液, 连续染毒 60 d 后, 取大脑皮质、 小脑和海马组织, 测定各组的超氧化物歧化酶 (SOD) 活力、 过氧化氢 (H2O2) 水平和丙二醛 (MDA) 含量, 蛋白印迹法检测 APE1 蛋白在各组织中的表达。结果 铅暴露后, 大脑皮质、 小脑、 海马中 APE1 蛋白表达水平均低于对照组, 且随染铅剂量的升高呈逐渐下降趋势(P<0.05); 随着染铅剂量的升高, 大脑皮质、 小脑和海马中的 SOD 活力基本呈下降趋势; 而 H2O2及 MDA 含量随染铅剂量的升高基本呈逐渐升高趋势, 大脑皮质、 小脑和海马组织的 APE1 蛋白表达水平与其 SOD 活力呈正相关(r 分别为 0.619、 0.380、 0.375, P < 0.05) ,而与 H2O2水平和 MDA 含量呈负相关(r 分别为-0.472、 -0.535、 -0.436, -0.514、 -0.486、 -0.316, P < 0.05)。结论 饮水铅暴露可导致大鼠脑组织 APE1 蛋白表达水平改变,且此种改变与铅所致的氧化应激有关。

关 键 词:  脑组织  氧化应激  脱嘌呤脱嘧啶核酸内切酶  1  超氧化物歧化酶  过氧化氢  丙二醛  
收稿时间:2015-09-07
修稿时间:2015-10-30

Effects of lead exposure through drinking water on expression of APE1 protein and their relationships with oxidative stress in brain tissues of rats
REN Qingfeng,LI Weijuan,XU Qunying,ZHANG Zhongwei,LI Wei,FENG Jiangao,REN Xiaohui,XIAO Yuanmei?.Effects of lead exposure through drinking water on expression of APE1 protein and their relationships with oxidative stress in brain tissues of rats[J].Tianjin Medical Journal,2016,44(2):170-173.
Authors:REN Qingfeng  LI Weijuan  XU Qunying  ZHANG Zhongwei  LI Wei  FENG Jiangao  REN Xiaohui  XIAO Yuanmei?
Affiliation:1 School of Public Health, Nanchang University, Nanchang 330006, China; 2 Clinical Medical College, Jiujiang University; 3 Fuzhou Medical College of Nanchang University
Abstract:Objective To observe the effects of lead exposure through drinking water on the expression of APE1 pro? tein in cerebral cortex, cerebellum and hippocampus of rats and its relationship with oxidative stress. Methods Forty weaned male SD rats were randomly assigned to five groups (control group and four exposure groups) according to body weights of rats. Rats in control group were given deionized water as drinking water. Rats in four exposure groups were given 100 mg/L, 200 mg/L, 400 mg/L and 800 mg/L lead acetate solution for 60 days. The activity of superoxide dismutase (SOD), the contents of hydrogen peroxide (H2O2) and malondialdehyde (MDA) in cortex, cerebellum and hippocampus were measured using kits. The protein level of APE1 in cortex, cerebellum and hippocampus were detected by Western blotting assay. Results After being exposed to lead, the APE1 protein levels were significantly decreased in cortex, cerebellum and hippocampus (P < 0.05). The protein level showed a trend of gradual decline with the increase of exposed lead (P < 0.05). With the increase of dye lead dose, the activity of SOD in cortex, cerebellum and hippocampus showed a downward trend, while the contents of H2O2 and MDA showed a rising trend. The activity of SOD was positively correlated with APE1 protein level in cortex, cerebellum and hippocampus (r=0.619, 0.380 and 0.375, P < 0.05). While the contents of H2O2 and MDA were neg? atively correlated with APE1 protein level in cortex, cerebellum and hippocampus (r=-0.472, -0.535, -0.436, -0.514, -0.486 and - 0.316, P < 0.05). Conclusion Lead exposure through drinking water can affect the expression of APE1 protein through inducing oxidative stress in brain tissues of rats.
Keywords:lead  brain tissue  oxidative stress  APE1  superoxide dismutase  hydrogen peroxide  malonaldehyde  
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