Aging and acute exercise enhance free radical generation in rat skeletal muscle
Aging and acute exercise enhance free radical generation in rat skeletal muscle
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DOI：
10.1152/jappl.1999.87.1.465
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发表时间：
1999-07-01
影响因子：
3.3
通讯作者：
Ji, LL
中科院分区：
文献类型：
--
作者：
Bejma, J;Ji, LL
活性氧（ROS）参与了生物衰老和运动诱导的氧化损伤机制。本研究检测了急性运动对年轻成年（8月龄，n = 24）和老年（24月龄，n = 24）雌性Fischer 344大鼠细胞内ROS生成、脂质和蛋白质过氧化以及骨骼肌GSH状态的影响。年轻大鼠在跑步机上以25米/分钟和5%的速度奔跑，直到精疲力竭（55.4 +/- 2.7分钟），而年老大鼠以15米/分钟和5%的速度奔跑，直到精疲力竭（58.0 +/- 2.7分钟）。二氯荧光素（DCFH）氧化率是股外侧深层匀浆中ROS和其他细胞内氧化剂产生的指标，在休息的老年大鼠中比年轻大鼠高77% （P < 0.01）。运动使年轻大鼠和老年大鼠DCFH氧化分别增加38% （P < 0.09）和50% （P < 0.01）。老年大鼠与年轻大鼠相比，分离的股外侧深层线粒体中含有1位底物的DCFH氧化增加了57% (P < 0.01)，但运动没有改变。在无底物的实验培养基中加入ADP、NADPH和Fe（3+）时，衰老肌肉线粒体中DCFH氧化率显著升高（P < 0.01），而匀浆中DCFH氧化率无显著升高。以丙二醛含量测定的肌肉脂质过氧化无年龄效应，但随运动而增加20% （P < 0.05）。肌肉蛋白质羰基的形成不受年龄或运动的影响。老龄大鼠线粒体GSH/GSSG比值显著高于幼龄大鼠（P < 0.05），运动增加GSSG含量，降低GSH/GSSG （P < 0.05）。这些数据提供了直接证据，证明骨骼肌中氧化剂的产生在老年和长时间运动中增加，线粒体呼吸链和NADPH氧化酶都是潜在的来源。肌脂过氧化和线粒体GSH状态的改变与这些结论一致。
Reactive oxygen species (ROS) are implicated in the mechanism of biological aging and exercise-induced oxidative damage. The present study examined the effect of an acute bout of exercise on intracellular ROS production, lipid and protein peroxidation, and GSH status in the skeletal muscle of young adult (8 mo, n = 24) and old (24 mo, n = 24) female Fischer 344 rats. Young rats ran on a treadmill at 25 m/min and 5% grade until exhaustion (55.4 +/- 2.7 min), whereas old rats ran at 15 m/min and 5% grade until exhaustion (58.0 +/- 2.7 min). Rate of dichlorofluorescin (DCFH) oxidation, an indication of ROS and other intracellular oxidants production in the homogenate of deep vastus lateralis, was 77% (P < 0.01) higher in rested old vs. young rats. Exercise increased DCFH oxidation by 38% (P < 0.09) and 50% (P < 0.01) in the young and old rats, respectively. DCFH oxidation in isolated deep vastus lateralis mitochondria with site 1 substrates was elevated by 57% (P < 0.01) in old vs. young rats but was unaltered with exercise. Significantly higher DCFH oxidation rate was also found in aged-muscle mitochondria (P < 0.01), but not in homogenates, when ADP, NADPH, and Fe(3+) were included in the assay medium without substrates. Lipid peroxidation in muscle measured by malondialdehyde content showed no age effect, but was increased by 20% (P < 0.05) with exercise in both young and old rats. Muscle protein carbonyl formation was unaffected by either age or exercise. Mitochondrial GSH/GSSG ratio was significantly higher in aged vs. young rats (P < 0.05), whereas exercise increased GSSG content and decreased GSH/GSSG in both age groups (P < 0.05). These data provided direct evidence that oxidant production in skeletal muscle is increased in old age and during prolonged exercise, with both :mitochondrial respiratory chain and NADPH oxidase as potential sources. The alterations of muscle lipid peroxidation and mitochondrial GSH status were consistent with these conclusions.