运动性疲劳的线粒体膜分子机制研究.Ⅱ.运动性氧自由基代谢途径再探讨

Study on Molecular Mechanism of Mitochondrial Membrane for Exercise-induced Fatigue .Ⅱ. Explores to Pathway of Oxygen Free Radicals Metabolism Induced by Exercise

以大鼠中等强度力竭性跑台跑为运动性疲劳模型 ,采用化学发光法分别直接测定了运动后即刻骨骼肌、心肌和肝脏线粒体超氧阴离子 (O2 ·—)生成量 ;以TBA荧光法测定线粒体丙二醛 (MDA)含量。结果表明 ,骨骼肌和肝脏线粒体O2 ·— 生成较运动前安静时显著增加 (P <0 0 5 ) ,心肌线粒体O2 ·— 生成呈增加趋势 (P >0 0 5 ) ;三种组织线粒体脂质过氧化水平均显著增加 (P <0 0 5 )。结果提示 ,骨骼肌和肝脏线粒体氧自由基代谢以线粒体电子漏机制为主 ,心肌则可能存在黄嘌呤氧化酶途径的参与。

Usingtheincrementalexercisetoexhaustionasanexperimentalanimalmodel,wedeterminedsuperoxideanion (O2 ·—)produc tiondirectlyandtheMDAcontentsinthepreparedmitochondriaofliver,heartandskeletalmusclefromratsimmediatelyafterexhaus tiveexercise Theresultsshowedthefollowing.ThemitochondrialO2 ·— ofliverandskeletalmusclepost -exerciseincreasedsignifi cantlythantheseatrest(P <0 0 5 ) Inheart,theproductionofO2 ·—increasedwithoutsignificance However,Thesignificantincrease ofMDAcontentswereobservedamongthreetissuemitochondria(P <0 0 5 ) Thepresentdatasuggestedthatmitochondrialrespiratory, eg electronleakwasanimportantmechanismofmetabolicpathwayofexercise -inducedoxygenfreeradicalsinliverandskeletal muscle ,butthesamesituationmaybenotexistedinheart,thusotherpathwayshouldbeinvolvedinlipidperoxidation