急性运动中骨骼肌线粒体氧化应激机制研究

The Mechanism of Oxidative Stress in Muscle Mitochondria during the Acute Exercise

以SD大鼠3级递增负荷跑台运动为实验模型,分别选取安静态和运动45,90,120,150min为实验观察点,测定其骨骼肌线粒体活性氧(ROS)生成、脂质过氧化水平(MDA)和UCP-3mRNA及蛋白表达.实验结果表明:运动过程中ROS生成呈先上升后下降的趋势,运动120min时达到峰值,运动150min时下降并具有显著性,其中运动45,90,120,150min时均较安静时显著性升高;线粒体MDA含量总体呈上升趋势,但变化无显著性;运动过程中UCP-3mRNA和蛋白表达水平总体呈上升趋势,其中UCP-3mRNA在运动90,120,150min时均较安静时呈显著性升高,而蛋白表达水平相对滞后一个时间段,在运动120,150min时较安静时呈显著性增高.运动中线粒体ROS生成显著增加,但MDA水平无明显变化,这可能是运动中抗氧化能力提高,足以清除线粒体产生的过多ROS所致.运动中UCP-3表达的增加减少了线粒体ROS生成及其引发的氧化损伤.在ROS大量生成的情况下未发现线粒体有明显的脂质过氧化损伤,提示ROS在运动中可能具有重要的生理意义,而不仅仅是造成损伤.

SD rats were divided into 5 groups to stay at rest or run for 45,90,120 and 150 rain respectively on the treadmill according to the incremental protocol and sacrificed at rest or immediately after the exercise time courses. The following parameters of skeletal muscle tissue or its mitochondria were determined： 1） Mitochondrial ROS （reactive oxygen species） generation rate; 2） Malondialdehyde （MDA） in skeletal muscle mitochondria; 3） UCP-3 mRNA expression in skeletal muscle tissue; 4） UCP-3 protein in skeletal muscle mitochondria. The results show that mitochondrial ROS generation climbed to the peak at the point of 120 min and subsequently declined,with significantly higher levels at 45,90,120 and 150 min than at rest and obviously lower level at 150 min than at 120 rain; Mitochondrial MDA content slowly in- creased during exercise without significance; There were remarkably higher levels of UCP-3 mRNA at the point of 90,120 and 150 min,and protein content at the point of 120 and 150 rain than at rest. Mitochondrial ROS generation climbed without significant MDA increase. It could be speculated that the enhancement of antioxidant defense eliminated the redundant ROS and UCP-3 played a part in this role. No evident lipid peroxidation of mitochondrial membrane in spite of the increase of ROS generation suggested that ROS may contribute to important physiology events other than causing damage.