摘要
目的探讨硫酸铍(BeSO4.4H2O)致小鼠肾脏氧化损伤的作用。方法将36只6周龄雄性昆明种小鼠随机分成对照组、低剂量组及高剂量组,每组12只,对照组用灭菌生理盐水(0.9%氯化钠溶液)按0.1 mL/10 g(体质量)隔天腹腔注射,低、高剂量组分别以1mg/kg BeSO4.4H2O和2 mg/kg BeSO4.4H2O生理盐水溶液隔天腹腔注射染毒,连续染毒4周。采集血液测定血清肌酐及尿素氮含量;计算肾脏脏器系数,采用差速离心法制备肾脏线粒体悬液,检测肾线粒体中活性氧(ROS)、丙二醛(MDA)含量及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性。结果与对照组相比,硫酸铍暴露小鼠肾脏脏器系数显著降低,血清中肌酐及尿素氮含量明显升高(P<0.05);硫酸铍暴露小鼠肾脏线粒体活性氧(ROS)、脂质过氧化终产物丙二醛(MDA)含量显著升高(P<0.01);SOD、GSH-Px活性受到明显抑制(P<0.01)。结论硫酸铍可以抑制肾组织线粒体抗氧化系统导致小鼠肾脏功能损害。
Objective To probe into the effects of oxidative stress induced by beryllium sulfate （BeS04 ~ 4H20 ） for mice kidney. Method The thirty-six mice were randomly divided into three groups and administered with physiological saline of beryllium sulfate （ 1 mg/kg, 2 mg/kg） by peritoneal injection once every other day for a month. Then, kidney mitochondria were isolated by differential centrifugation, the organ coefficient of kidney was calculated. The levels of serum creatinine and serum BUN were detected. The Reactive Oxygen Species （ROS） and malondialdehyde （MDA） content, activities of superoxide dismutase （SOD） and glutathione peroxidase （GSH- Px） were detected. Result The results show that beryllium sulfate exposure significantly decreased the organ coefficient of kidney, the activity of superoxide dismutase （SOD） and GSH-Px, and increased the contents of final product of the lipid peroxidization MDA, and the content of ROS, as well as the serum creatinine, BUN in the kidney of mice. Conclusion Beryllium sulfate can lead to mitochondria disfunction of mice kidney, and the lipid peroxidation .
出处
《实验动物科学》
2012年第6期13-16,共4页
Laboratory Animal Science
基金
湖南省科技厅资助项目(No.2011TT2013)
湖南省研究生科研创新项目(No.CX2011B382)
衡阳市科技局资助课题(No.2011ks11)
关键词
硫酸铍
线粒体
脂质过氧化
beryllium sulfate
mitochondria
lipid peroxidation
