Vasilaki A, Mansouri A, Van Remmen H, van der Meulen J H, Larkin L, Richardson A G, McArdle A, Faulkner J A, Jackson M J
Division of Metabolic and Cellular Medicine, School of Clinical Sciences, University of Liverpool, Liverppol L69 3GA, UK.
Aging Cell. 2006 Apr;5(2):109-17. doi: 10.1111/j.1474-9726.2006.00198.x.
Oxidative modification of cellular components may contribute to tissue dysfunction during aging. In skeletal muscle, contractile activity increases the generation of reactive oxygen and nitrogen species (ROS). The question of whether contraction-induced ROS generation is further increased in skeletal muscle of the elderly is important since this influences recommendations on their exercise participation. Three different approaches were used to examine whether aging influences contraction-induced ROS generation. Hind limb muscles of adult and old mice underwent a 15-min period of isometric contractions and we examined ROS generation by isolated skeletal muscle mitochondria, ROS release into the muscle extracellular fluid using microdialysis techniques, and the muscle glutathione and protein thiol contents. Resting skeletal muscle of old mice compared with adult mice showed increased ROS release from isolated mitochondria, but no changes in the extracellular levels of superoxide, nitric oxide, hydrogen peroxide, hydroxyl radical activity or muscle glutathione and protein thiol contents. Skeletal muscle mitochondria isolated from both adult and old mice after contractile activity showed significant increases in hydrogen peroxide release compared with pre-contraction values. Contractions increased extracellular hydroxyl radical activity in adult and old mice, but had no significant effect on extracellular hydrogen peroxide or nitric oxide in either group. In adult mice only, contractile activity increased the skeletal muscle release of superoxide. A similar decrease in muscle glutathione and protein thiol contents was seen in adult and old mice following contractions. Thus, contractile activity increased skeletal muscle ROS generation in both adult and old mice with no evidence for an age-related exacerbation of ROS generation.
细胞成分的氧化修饰可能在衰老过程中导致组织功能障碍。在骨骼肌中，收缩活动会增加活性氧和氮物种（ROS）的生成。老年人骨骼肌中收缩诱导的ROS生成是否会进一步增加是一个重要问题，因为这会影响对他们运动参与的建议。我们使用了三种不同的方法来研究衰老是否会影响收缩诱导的ROS生成。成年和老年小鼠的后肢肌肉进行了15分钟的等长收缩，我们通过分离的骨骼肌线粒体检测ROS生成，使用微透析技术检测ROS释放到肌肉细胞外液中的情况，以及肌肉谷胱甘肽和蛋白质巯基含量。与成年小鼠相比，老年小鼠的静息骨骼肌显示出分离线粒体释放的ROS增加，但超氧化物、一氧化氮、过氧化氢、羟自由基活性的细胞外水平或肌肉谷胱甘肽和蛋白质巯基含量没有变化。收缩活动后，从成年和老年小鼠分离的骨骼肌线粒体显示过氧化氢释放与收缩前值相比显著增加。收缩增加了成年和老年小鼠的细胞外羟自由基活性，但对两组的细胞外过氧化氢或一氧化氮没有显著影响。仅在成年小鼠中，收缩活动增加了骨骼肌中超氧化物的释放。收缩后，成年和老年小鼠的肌肉谷胱甘肽和蛋白质巯基含量出现了类似的下降。因此，收缩活动增加了成年和老年小鼠骨骼肌中的ROS生成，没有证据表明ROS生成存在与年龄相关的加剧情况。
