[1]卢国守,刘福玉,高钰琪,等.急性低氧加重氰化钠对大鼠离体肝线粒体能量代谢的抑制作用[J].陆军军医大学学报(原第三军医大学学报),2009,31(10):898-901.
 LU Guo-shou,LIU Fu-yu,GAO Yu-qi,et al.Acute hypoxia exacerbates inhibitory effects of sodium cyanide on energy metabolism in rat in vitro liver mitochondria[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(10):898-901.
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急性低氧加重氰化钠对大鼠离体肝线粒体能量代谢的抑制作用(/HTML )
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陆军军医大学学报(原第三军医大学学报)[ISSN:1000-5404/CN:51-1095/R]

卷:
31卷
期数:
2009年第10期
页码:
898-901
栏目:
论著
出版日期:
2009-05-30

文章信息/Info

Title:
Acute hypoxia exacerbates inhibitory effects of sodium cyanide on energy metabolism in rat in vitro liver mitochondria
作者:
卢国守刘福玉高钰琪杨晓红罗勇军高文祥
第三军医大学高原军事医学系:病理生理学与高原生理学教研室,高原医学教育部重点实验室,全军高原生理与高原病研究重点实验室,军事医学地理学教研室,高原疾病学教研室
Author(s):
LU Guo-shou LIU Fu-yu GAO Yu-qi YANG Xiao-hong LUO Yong-jun GAO Wen-xiang
Department of Pathophysiology and High Altitude Physiology, Key Laboratory of High Altitude Medicine of Ministry of Education, Key Laboratory of High Altitude Physiology and High Altitude Disease of PLA, Department of Military Medical Geography, Department of High Altitude Disease, College of High Altitude Military Medicine, Third Military Medical University, Chongqing 400038, China
关键词:
NaCN低氧线粒体呼吸氧耗膜电位复合酶Ⅳ
Keywords:
NaCN hypoxia mitochondrial oxidative consumption mitochondrial membrane potential the complex Ⅳ of mitochondria
分类号:
R322.47;R992;R995
文献标志码:
A
摘要:
目的   通过观察不同浓度的 NaCN 对模拟高原急性低氧大鼠离体肝脏线粒体呼吸氧耗、膜电位和复合酶Ⅳ活性的影响,探讨急性低氧条件下氰化物中毒大鼠线粒体能量代谢变化特点。   方法   16只SD大鼠按简单完全随机分组法分为对平原照组和急性低氧组,急性低氧组大鼠暴露于低压舱内,模拟海拔5 000 m 高原,23 h/d,连续3 d;对照组大鼠于常压和常氧环境中同时喂养。用差速离心法提取肝线粒体,分别在0、0.01、0.1、0.25 mmol/L NaCN 条件下采用Clark氧电极法测定线粒体呼吸氧耗和复合酶Ⅳ活性并计算Ⅲ态呼吸(state 3 respiration, ST3)、Ⅳ态呼吸(state 4 respiration, ST4)、呼吸控制率(respiratory control rate, RCR)、氧化磷酸化效率(oxidative phosphorylation, OPR)和复合酶Ⅳ耗氧率,用Rhodamine123法测定线粒体膜电位(the mitochondrial membrane potential,MMP)。   结果   0.01、 0.1、0.25 mmol/L NaCN均可显著抑制线粒体呼吸功能,降低线粒体膜电位,且呈剂量依赖关系。与相应NaCN浓度的对照组比较,急性低氧组线粒体功能受抑制程度显著增加。   结论   急性低氧加重NaCN对大鼠肝脏线粒体能量代谢的抑制作用,其机制可能与急性缺氧大鼠线粒体氧化磷酸化脱偶联、呼吸链复合体Ⅳ功能降低及线粒体膜电位改变有关。
Abstract:
Objective   To investigate effect of sodium cyanide (NaCN) at different concentrations on the mitochondrial respiratory oxygen consumption, the mitochondrial membrane potential (MMP) and activity of the complex Ⅳ of mitochondrial breath train in in vitro liver mitochondria from the rats exposed to simulated high altitude hypoxia, and to explore the characteristics of energy metabolism in the mitochondria from the rats subjected to cyanide poisoning during acute hypoxia exposure.    Methods   Adult Sprague-Dawley (SD) rats were set randomly into control and acute hypoxia groups (n=8 in each group). The acute hypoxic rats were exposed to simulate 5 000 m high altitude in a hypobaric chamber 23 h/d for 3 d. Rats in the control group were bred in the normoxia condition at the same time. The liver mitochondria were isolated by centrifugation. Mitochondrial oxidative respiratory consumption and activity of the complex Ⅳ was measured by Clark electrode after the treatment of NaCN at 0, 0.01, 0.1 and 0.25 mmol/L respectively, so as to calculate mitochondrial state 3 respiration (ST3), state 4 respiration (ST4), respiratory control rate (RCR), the rate of oxidative phosphorylation (OPR), and oxygen consumption rate of the complex Ⅳ. MMP was detected by Rhodamine 123 method at the above-mentioned concentrations of NaCN.    Results   NaCN at 0.01, 0.1 and 0.25 mmol/L inhibited the mitochondrial oxidative respiratory function, and decreased MMP significantly. The inhibitory effects of NaCN on energy metabolism in mitochondria was in a dose-dependent manner. Compared with the treatment of NaCN at the corresponding concentration in the control group, mitochondrial function in the acute hypoxia group was inhibited more seriously.    Conclusion   Acute hypoxia exacerbates the inhibitory effects of sodium cyanide on energy metabolism in rat liver mitochondria. Its mechanism might be relevant to the decoupling of oxidative phosphorylation, functional down-regulation of complex  Ⅳ in respiratory chain and changes of the mitochondrial membrane potential in liver mitochondria from rats exposed to acute hypoxia.

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更新日期/Last Update: 2009-05-08