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老年大鼠骨骼肌中的铁负荷与氧化还原应激

Iron load and redox stress in skeletal muscle of aged rats.

作者信息

Altun Mikael, Edström Erik, Spooner Eric, Flores-Moralez Amilcar, Bergman Esbjörn, Tollet-Egnell Petra, Norstedt Gunnar, Kessler Benedikt M, Ulfhake Brun

机构信息

Department of Neuroscience, Karolinska Institute, Retzius väg 8, 171 77 Stockholm, Sweden.

出版信息

Muscle Nerve. 2007 Aug;36(2):223-33. doi: 10.1002/mus.20808.

DOI:10.1002/mus.20808
PMID:17503500
Abstract

Loss of skeletal muscle mass (sarcopenia) is a major contributor to disability in old age. We used two-dimensional gel electrophoresis and mass spectrometry to screen for changes in proteins, and cDNA profiling to assess transcriptional regulations in the gastrocnemius muscle of adult (4 months) and aged (30 months) male Sprague-Dawley rats. Thirty-five proteins were differentially expressed in aged muscle. Proteins and mRNA transcripts involved in redox homeostasis and iron load were increased, representing novel components that were previously not associated with sarcopenia. Tissue iron levels were elevated in senescence, paralleling an increase in transferrin. Proteins involved in redox homeostasis showed a complex pattern of changes with increased SOD1 and decreased SOD2. These results suggest that an elevated iron load is a significant component of sarcopenia with the potential to be exploited clinically, and that mitochondria of aged striated muscle may be more vulnerable to radicals produced in cell respiration.

摘要

骨骼肌质量的丧失(肌肉减少症)是导致老年残疾的主要因素。我们使用二维凝胶电泳和质谱法筛选蛋白质变化,并通过cDNA分析评估成年(4个月)和老年(30个月)雄性Sprague-Dawley大鼠腓肠肌中的转录调控。35种蛋白质在老年肌肉中差异表达。参与氧化还原稳态和铁负荷的蛋白质和mRNA转录本增加,代表了以前与肌肉减少症无关的新成分。衰老过程中组织铁水平升高,与转铁蛋白增加平行。参与氧化还原稳态的蛋白质呈现出复杂的变化模式,超氧化物歧化酶1(SOD1)增加而超氧化物歧化酶2(SOD2)减少。这些结果表明,铁负荷升高是肌肉减少症的一个重要组成部分,具有临床开发潜力,并且老年横纹肌线粒体可能更容易受到细胞呼吸产生的自由基的影响。

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Iron load and redox stress in skeletal muscle of aged rats.老年大鼠骨骼肌中的铁负荷与氧化还原应激
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