力竭性运动中肝脏线粒体电子漏对电子传递与质子转移偶联的影响

Enhancement in Mitochondrial Electron Leak Induced by Acute Exhaustive Exercise And Its Effects on the Coupling of Electron transfer and Proton Pump in Rat Liver

以SD大鼠递增负荷急性力竭跑台运动为疲劳模型,分别测定了运动后即刻肝脏线粒体:(1)超氧阴离子(O_2)生成及膜脂质过氧化水平;(2)呼吸链复合体Ⅰ+Ⅲ和Ⅱ+Ⅲ0电子传递与质子泵出比值(H^+/2e)。结果表明:线粒体电子漏(O_2)和膜脂质过氧化水平(MDA含量)显著增加(P<0.05);苹果酸及谷氨酸和琥珀酸两种呼吸底物启动的呼吸链复合体Ⅰ+Ⅲ和Ⅱ+Ⅲ的总H^+/2e分别降低18.63和15.89％(均 P<0.001)。研究提示,线粒体电子漏是运动性内源自由基的重要来源,而且线粒体电子传递—质子转移之间的偶联破坏与运动诱导线粒体电子漏生成增多有关。

Rats running with incremental intensity to exhaustion were used as experimental model to investigate the effect of acute exhaustive exercise on the production of mitochondrial electron leak (superoxide free radicals, O2 ) and its effect on the coupling of electron transfer and proton pump of mitochondrial respiratory chain in liver. The experiment was designed to determine the changes of prrepared mitochondria immediately after exhaustive exercise: 1. Mitochondrial O2 production and the level of lipid peroxidation (MDA content); 2. Rate of electron transfer to proton pump of mitochondrial respiratory chain complex I + III and II +III (H+ /2e). It was showed in exhausted rats that there were significant increases of O2 and peroxidation (p<0. 05), and the parameter of complex I + III and II + III total H+ /2e decreased with 18. 63% and 15. 89% (respectively, p<0. 001 ), in the presence of Malate and Glutate (M + G), and Succi-nate (S). The present research suggested that enhanced mitochondrial election leak may be an important source of exercise-induced free radicals and it may be related with the destroyed coupling of electron transfer and proton pump of mitochondrial respiratory chain.