摘要
目的观察大鼠经不同时间低压缺氧并复合线粒体蛋白翻译特异抑制剂氯霉素(CAP)处理后,脑组织线粒体呼吸功能和COX活性的变化以及CAP处理对缺氧过程中线粒体氧化呼吸功能的影响。方法成年雄性Wistar大鼠随机分为对照组、单纯药物处理组和缺氧复合药物处理组,后者为模拟海拔5000m高原连续低压缺氧暴露1、5、15d和30d,分别于动物处死前7d按100mg/kg体质量,腹腔注射0·5%CAP。高速离心密度梯度法分离大鼠脑皮质线粒体,Clark氧电极法测定线粒体呼吸活性,极谱法测量COX活性。结果与对照组相比,单纯CAP处理大鼠脑线粒体ST3、RCR、OPR及COX活性显著降低;复合缺氧后则线粒体呼吸功能及COX活性明显改善,且随缺氧时间的延长而基本恢复到平原对照组水平。结论缺氧可以改善氯霉素处理大鼠脑皮质COX活性及线粒体的氧化呼吸功能,提高氧化磷酸化效率,其改善程度具有时间依赖性,随缺氧时间的延长而逐渐恢复。
Objective To understand the changing aspects of CAP-administration on mitochondrial oxidative phosphorylation function and cytochrome c oxidase (COX) activity during hypoxia exposure and their mechanisms. Methods Except the control group (C group), adult male Wistar rats were exposed to a hypobaric chamber simulated 5 000-meter high altitude for 23 h every day for 0, 1, 5, 15, 30 d (H_ 0, 1, 5, 15, 30 ) respectively and administrated CAP (100 mg/kg, intraperitoneal injection) every 12 h for 7 d before sacrificed by decapitation. Mitochondrial respiratory function and COX activity were measured by Clark oxygen electrode and polarography, respectively. Results As compared with C group, mitochondrial state 3 respiration (ST_3) and respiratory control rate (RCR) and oxidative phosphorylation rate (ORP) and COX activity in H_0+CAP group all decreased significantly, but by prolonging hypoxia exposure increased and restored to the control level. Conclusion Mitochondrial respiratory function, oxidative phosphorylation efficiency and COX activity in rat brain could improve by administrating CAP during hypoxia exposure and almost reach to the control level by prolonging hypoxia exposure.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2005年第14期1424-1427,共4页
Journal of Third Military Medical University
基金
国家自然科学基金资助项目(30070290)~~
关键词
缺氧
氯霉素
线粒体
细胞色素氧化酶
hypoxia
choramphenicol
mitochondria
cytochrome c oxidase
