Contractile activity-induced oxidative stress: cellular origin and adaptive responses
Contractile activity-induced oxidative stress: cellular origin and adaptive responses
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DOI：
10.1152/ajpcell.2001.280.3.c621
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发表时间：
2001-03-01
影响因子：
5.5
通讯作者：
Jackson, MJ
中科院分区：
文献类型：
--
作者：
McArdle, A;Pattwell, D;Jackson, MJ
先前的研究已经报道，在运动过程中产生的氧化自由基物种，并有相当大的兴趣，这些对运动组织的潜在影响。我们假设，收缩的骨骼肌是氧化自由基的主要来源，未经训练的骨骼肌将通过在没有明显细胞损伤的情况下上调细胞保护蛋白的活性来适应单一短期收缩活动的氧化应激。发现15分钟的有氧收缩活动诱导体内小鼠骨骼肌中超氧阴离子的快速释放，并且对收缩培养的骨骼肌肌管的研究证实，这是由于体内肌组织中存在的肌细胞而不是其他细胞类型的释放。这种增加的氧化剂产生引起肌肉蛋白巯基含量的快速，短暂的减少，然后增加超氧化物歧化酶和过氧化氢酶的活性和热休克蛋白的含量。这些变化发生在没有明显损伤肌肉细胞的情况下。
Previous studies have reported that oxidizing free radical species are generated during exercise, and there has been considerable interest in the potential effects of these on exercising tissues. We hypothesized that contracting skeletal muscle was a major source of oxidizing free radical species and that untrained skeletal muscle would adapt to the oxidative stress of a single short period of contractile activity by upregulation of the activity of cytoprotective proteins in the absence of overt cellular damage. Fifteen minutes of aerobic contractile activity was found to induce a rapid release of superoxide anions from mouse skeletal muscle in vivo, and studies with contracting cultured skeletal muscle myotubes confirmed that this was due to release from myocytes rather than other cell types present within muscle tissue in vivo. This increased oxidant production caused a rapid, transient reduction in muscle protein thiol content, followed by increases in the activities of superoxide dismutase and catalase and in content of heat shock proteins. These changes occurred in the absence of overt damage to the muscle cells.