Chandwaney R, Leichtweis S, Leeuwenburgh C, Ji L L
Age (Omaha). 1998 Jul;21(3):109-17. doi: 10.1007/s11357-998-0017-5.
The rate of oxidative phosphorylation was investigated in isolated mitochondria from hindlimb muscles of young (4.5 mo) and old (26.5 mo) male Fischer 344 rats with or without endurance training. Further, the susceptibility of the muscle mitochondria to exogenous reactive oxygen species was examined. State 3 and 4 respiration, as well as the respiratory control index (RCI), were significantly lower in muscle mitochondria from aged vs. young rats (P<0.05), using either the site 1 substrates malate-pyruvate (M-P) and 2-oxoglutarate (2-OG), or the site 2 substrate succinate. In both young and old rats, training increased state 4 respiration with M-P, but had no effect on state 3 respiration, resulting in a reduction of RCI. Training also increased state 4 respiration with 2-OG and decreased RCI in young rats. When muscle mitochondria were exposed to superoxide radicals (O2 (·-)) and hydrogen peroxide (H2O2) generated by xanthine oxidase and hypoxanthine, or H2O2 alone in vitro, state 3 respiration and RCI in both age groups were severely hampered, but those from the old rats were inhibited to a less extent than the young rats. In contrast, state 4 respiration was impaired by O2 (·-) and/or H2O2 to a greater extent in the old rats. Muscle mitochondria from trained young rats showed a greater resistance to the O2 (· -) and/or H2O2-induced state 3 and RCI inhibition than those from untrained young rats. Muscle from aged rats had significantly higher total activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPX), and glutathione reductase than that from young rats, however, training increased SOD and GPX activities in young but not old rats. The results of this study suggest that mitochondrial capacity for oxidative phosphorylation is compromised in aging skeletal muscle. Further, the increased mitochondrial resistance to reactive oxygen species demonstrated in aged and young trained muscles may be attributed to enhanced antioxidant enzyme activities.
研究了耐力训练与否的年轻（4.5月龄）和老年（26.5月龄）雄性Fischer 344大鼠后肢肌肉分离线粒体的氧化磷酸化速率。此外，还检测了肌肉线粒体对外源性活性氧的敏感性。使用位点1底物苹果酸 - 丙酮酸（M - P）和2 - 氧代戊二酸（2 - OG）或位点2底物琥珀酸时，老年大鼠肌肉线粒体的状态3和状态4呼吸以及呼吸控制指数（RCI）显著低于年轻大鼠（P<0.05）。在年轻和老年大鼠中，训练均增加了使用M - P时的状态4呼吸，但对状态3呼吸无影响，导致RCI降低。训练还增加了年轻大鼠使用2 - OG时的状态4呼吸并降低了RCI。当肌肉线粒体在体外暴露于黄嘌呤氧化酶和次黄嘌呤产生的超氧阴离子（O2(·-)）和过氧化氢（H2O2）或单独的H2O2时，两个年龄组的状态3呼吸和RCI均受到严重阻碍，但老年大鼠受到的抑制程度低于年轻大鼠。相反，老年大鼠的状态4呼吸受到O2(·-)和/或H2O2的损害程度更大。训练后的年轻大鼠的肌肉线粒体对O2(·-)和/或H2O2诱导的状态3和RCI抑制的抵抗力比未训练的年轻大鼠更强。老年大鼠肌肉中的超氧化物歧化酶（SOD）、过氧化氢酶、谷胱甘肽过氧化物酶（GPX）和谷胱甘肽还原酶的总活性显著高于年轻大鼠，然而，训练增加了年轻大鼠而非老年大鼠的SOD和GPX活性。本研究结果表明，衰老骨骼肌中线粒体的氧化磷酸化能力受损。此外，老年和年轻训练肌肉中线粒体对活性氧的抵抗力增加可能归因于抗氧化酶活性的增强。
