四氯化碳诱发大鼠肾损伤的机制研究  

Study on mechanism of rat renal injury induced by carbon tetrachloride

作　　者：阳建莹[1] 李文良[1] 李先华[1] 肖业伟[1] 

机构地区：[1]泸州医学院,四川泸州646000

出　　处：《工业卫生与职业病》2012年第6期336-338,共3页Industrial Health and Occupational Diseases

摘　　要：目的探讨四氯化碳(CCl4)致大鼠慢性肾损伤的毒性机制。方法将健康的Wistar大鼠随机分为对照组和染毒组,对照组腹部皮下注射生理盐水;染毒组腹部皮下注射CCl4大豆油溶液。于第8周末分别检测血清中尿素氮(BUN)和肌酐(CRE)含量;血清和肾组织中丙二醛(MDA)、NO含量及超氧化物歧化酶(SOD)的活力,并作肾组织病理检查。结果与对照组比较,染毒组血清中BUN、CRE明显增高(P<0.01),血清和肾组织中SOD活力明显降低、MDA和NO含量增加(P<0.01)。染毒组肾组织病理学变化明显。结论CCl4能诱发肾脏损伤,其机制可能与体内自由基增加和细胞脂质过氧化有关。Objective To explore the toxic mechanism of chronic kidney injury induced by carbon tetrachloride（CC14）in rat. Methods Healthy Wistar rats were randomly divided into the control group and exposure group. Normal saline was intraperitoneally injected in control group. CC14 soybean oil solution was intraperitoneally injected in exposure group. Blood serum samples of all rats were collected in the 8th week for detecting BUN, CRE, SOD and MDA contents. In addition, kidney tissues were collected in the 8th week for measuring SOD activity, MDA content and observing pathologic findings. Results Levels of BUN and CRE in serum were significantly higher （P〈 0.01）, levels of MDA and NO in serum and kidney tissue increased significantly, while SOD activity was significantly lower than the control group（P〈0. 01）. Severe morphological changes were clearly seen in rat renal of the exposure group. Conclusions CC14 could induce renal injury. The mechanism might be closely related with increased free radicals and lipid peroxidation.

关 键 词：四氯化碳 肾损伤 自由基 脂质过氧化 

分 类 号：R134[医药卫生—劳动卫生]