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本文引用的文献

1
NADPH oxidase-derived reactive oxygen species in skeletal muscle modulates the exercise pressor reflex.骨骼肌中烟酰胺腺嘌呤二核苷酸磷酸氧化酶衍生的活性氧调节运动升压反射。
J Appl Physiol (1985). 2009 Aug;107(2):450-9. doi: 10.1152/japplphysiol.00262.2009. Epub 2009 Jun 4.
2
Stretch-stimulated glucose uptake in skeletal muscle is mediated by reactive oxygen species and p38 MAP-kinase.骨骼肌中拉伸刺激的葡萄糖摄取由活性氧和p38丝裂原活化蛋白激酶介导。
J Physiol. 2009 Jul 1;587(Pt 13):3363-73. doi: 10.1113/jphysiol.2008.165639. Epub 2009 Apr 29.
3
Tissue-, substrate-, and site-specific characteristics of mitochondrial reactive oxygen species generation.线粒体活性氧生成的组织、底物和位点特异性特征。
Free Radic Biol Med. 2009 May 1;46(9):1283-97. doi: 10.1016/j.freeradbiomed.2009.02.008. Epub 2009 Feb 23.
4
Increased mitochondrial Ca2+ and decreased sarcoplasmic reticulum Ca2+ in mitochondrial myopathy.线粒体肌病中线粒体钙2+增加及肌浆网钙2+减少。
Hum Mol Genet. 2009 Jan 15;18(2):278-88. doi: 10.1093/hmg/ddn355. Epub 2008 Oct 22.
5
Exercise-induced oxidative stress: cellular mechanisms and impact on muscle force production.运动诱导的氧化应激:细胞机制及其对肌肉力量产生的影响。
Physiol Rev. 2008 Oct;88(4):1243-76. doi: 10.1152/physrev.00031.2007.
6
Development of a family of redox-sensitive green fluorescent protein indicators for use in relatively oxidizing subcellular environments.用于相对氧化的亚细胞环境的氧化还原敏感绿色荧光蛋白指示剂家族的开发。
Biochemistry. 2008 Aug 19;47(33):8678-88. doi: 10.1021/bi800498g. Epub 2008 Jul 25.
7
In situ detection and measurement of intracellular reactive oxygen species in single isolated mature skeletal muscle fibers by real time fluorescence microscopy.通过实时荧光显微镜对单个分离的成熟骨骼肌纤维中的细胞内活性氧进行原位检测和测量。
Antioxid Redox Signal. 2008 Aug;10(8):1463-74. doi: 10.1089/ars.2007.2009.
8
Calmodulin in adult mammalian skeletal muscle: localization and effect on sarcoplasmic reticulum Ca2+ release.成年哺乳动物骨骼肌中的钙调蛋白:定位及其对肌浆网Ca2+释放的影响。
Am J Physiol Cell Physiol. 2008 May;294(5):C1288-97. doi: 10.1152/ajpcell.00033.2008. Epub 2008 Mar 5.
9
Skeletal muscle fatigue: cellular mechanisms.骨骼肌疲劳:细胞机制
Physiol Rev. 2008 Jan;88(1):287-332. doi: 10.1152/physrev.00015.2007.
10
Reactive oxygen species and fatigue-induced prolonged low-frequency force depression in skeletal muscle fibres of rats, mice and SOD2 overexpressing mice.活性氧与大鼠、小鼠及超表达SOD2小鼠骨骼肌纤维中疲劳诱导的低频力量长期降低
J Physiol. 2008 Jan 1;586(1):175-84. doi: 10.1113/jphysiol.2007.147470. Epub 2007 Nov 15.

单个完整肌纤维收缩过程中线粒体氧化还原电势。

Mitochondrial redox potential during contraction in single intact muscle fibers.

机构信息

Organizational Systems and Adult Health, University of Maryland School of Nursing, 655 West Lombard Street, Baltimore, Maryland 21201, USA.

出版信息

Muscle Nerve. 2010 Oct;42(4):522-9. doi: 10.1002/mus.21724.

DOI:10.1002/mus.21724
PMID:20730875
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3015179/
Abstract

Although the production of reactive oxygen species (ROS) during muscle contractile activity has been linked to both positive and negative adaptive responses, the sites for ROS generation within working muscle are not clearly defined. We assessed cytosolic ROS production and mitochondrial redox potential with a targeted redox-sensitive green fluorescent protein during repetitive field stimulation of single mature myofibers. Cytosolic ROS production increased by 94%, an effect that was abolished by pretreatment with the reducing agent dithiothreitol. Mitochondrial redox potential was not altered during muscle contraction. In contrast, activity-dependent ROS production was ablated by an inhibitor of NADPH oxidase. We provide the first report on dynamic ROS production from mitochondria in single living myofibers and suggest that the mitochondria are not the major source of ROS during skeletal muscle contraction. Alternatively, our data support a role for NADPH oxidase-derived ROS during contractile activity.

摘要

虽然在肌肉收缩活动过程中产生的活性氧(ROS)与积极和消极的适应性反应都有关联,但工作肌肉中 ROS 产生的部位尚不清楚。我们在对单个成熟肌纤维进行重复场刺激时,使用靶向的氧化还原敏感绿色荧光蛋白来评估细胞浆 ROS 的产生和线粒体氧化还原电势。细胞浆 ROS 的产生增加了 94%,这个效应在用还原剂二硫苏糖醇预处理后被消除。在肌肉收缩过程中线粒体氧化还原电势没有改变。相比之下,NADPH 氧化酶抑制剂可以消除依赖于活动的 ROS 产生。我们首次报道了在单个活肌纤维中线粒体中动态产生 ROS,并且提示在线粒体不是在骨骼肌收缩过程中 ROS 的主要来源。或者,我们的数据支持 NADPH 氧化酶衍生的 ROS 在收缩活动中的作用。