呼吸链复合物

帕金森病（PD）的发病机制与线粒体呼吸链复合物I（complexI）活性降低以及氧化应激损伤密切相关。

The inhibition of mitochondrial respiratory chain complex I and oxidative damage have been implicated in the pathogenesis of Parkinson 's disease ( PD ) .

与三磷酸腺苷（ATP）形成有关的呼吸链复合物酶活力在镉暴露后也受到明显抑制，且时间和浓度效应关系显著。

The free radical accumulation will lead to changes in mitochondrial structure and function . ( 2 ) The respiratory chain complex activities which are associated with adenosine triphosphate ( ATP ) formation are also inhibited after cadmium exposure , and such influences are markedly time - and concentration-dependent .

于恢复给氧后0h、24h、48h、72h测定心肌线粒体内Ca2+浓度和呼吸链复合物活性。

Then the concentration of Ca 2 + and the activity of respiratory chain complex ⅳ in myocardial cell mitochondria were measured at 0 hour and 24 , 48 , 72 hours after reoxygenation .

大剂量对复合物活性的增高有进一步增强作用，对复合物活性的增高无明显影响。结论：氧应激可致大鼠心肌线粒体呼吸链复合物损伤。

CONCLUSION : Oxygen stress injury the activities of rat myocardial mitochondria respiratory chain complexes .

3线粒体Ca2+浓度与呼吸链复合物活性呈直线负相关。

The concentration of Ca 2 + in myocardial mitochondria was negatively correlated with the activity of respiratory chain complex ⅳ .

氧应激对体外大鼠心肌线粒体呼吸链复合物的损伤及益心康胶囊含药血清的保护作用

The injury effect of oxygen stress and the protective effect of Yi-Xin-Kang capsule-containing serum on respiratory chain complex in rat myocardial mitochondria

缺氧缺血后心肌线粒体钙超载可能是线粒体呼吸链复合物活性下降的原因之一。

Calcium overload in myocardial mitochondria after hypoxia-ischemia might be one of the causes of the descending activity of respiratory chain complex ⅳ .

方法：利用氧应激损伤体系（Fe2+/抗坏血酸，Fe2+/Vc）在体外攻击线粒体模型，观察对呼吸链复合物I-活性的影响。

METHOD : The effect of drug containing serum on the activities of respiratory chain complexes I ~ⅳ were studied in the model of mitochondria injury induced by oxygen stress ( Fe 2 + / ascorbic acid , Fe 2 + / Vc ) .

用酶动力学和聚合酶链式反应（PCR）对大鼠心肌线粒体呼吸链酶复合物Ⅰ、Ⅳ活性的变化及线粒体DNA的缺失进行测定。

Animal experiments with enzyme kinetics and PCR ( polymerase chain reaction ) technique were conducted .

慢性间断低氧暴露对大鼠心肌线粒体ATP酶及呼吸链酶复合物的影响

Effects of chronic intermittent hypoxic exposure on myocardial mitochondria ATPase and enzyme complexes of respiratory chain in rats

线粒体基因13513G>A突变导致呼吸链酶复合物I缺陷Leigh综合征

A case of Leigh syndrome associated with respiratory chain complex I deficiency due to mitochondrial gene 13513G > A mutation

结论：推测衰老时mtDNA的损伤积累可引起呼吸链酶复合物活性下降，导致呼吸链功能减退致生物衰老。

CONCLUSION : These observations suggest that accumulation of mtDNA damage causes the decreased activities of enzyme compound , hypofunction of respiratory chain when senility , and those may be the foundation of onset of aging regressive disease and organism senility .

丁烯酸内酯对心肌线粒体呼吸链酶复合物活力的影响

Effect of butenolide on the activities of complexes ⅰ - ⅳ in the respiratory chain of myocardium mitochondria

目的：研究慢性间断低氧暴露对大鼠心肌线粒体Na+、K+ATPase和Ca2+、Mg2+ATPase以及呼吸链酶复合物Ⅰ、Ⅱ、Ⅲ、Ⅳ活性的影响。

Aim : To study the effects of acute and chronic intermittent hypoxic exposure on the activities of Na ~ + , K ~ + - ATPase , Ca ~ ( 2 + ), Mg ~ ( 2 + ) - ATPase of myocardial mitochondria and enzyme complexes of !

由清华大学-中科院生物物理所结构生物学联合研究小组完成的线粒体呼吸链膜蛋白复合物II的晶体结构研究成果以Article的方式发表在2005年7月1日出版的Cell上。

An article entitled Crystal Structure of Mitochondrial Respiratory Membrane Protein Complex II was published in the July 1st , 2005 issue of the journal Cell . This research work was accomplished by the Tsinghua - Institute of Biophysics Joint Research Group for Structural Biology .