Iron load and redox stress in skeletal muscle of aged rats
Iron load and redox stress in skeletal muscle of aged rats
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DOI：
10.1002/mus.20808
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发表时间：
2007-08-01
期刊：
影响因子：
3.4
通讯作者：
Ulfhake, Brun
中科院分区：
文献类型：
--
作者：
Altun, Mikael;Edstrom, Erik;Ulfhake, Brun
骨骼肌质量的损失（肌肉减少症）是老年残疾的主要原因。我们使用二维凝胶电泳和质谱法筛选蛋白质的变化，并使用cDNA分析法评估成年（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个蛋白质在衰老肌肉中差异表达。参与氧化还原稳态和铁负荷的蛋白质和mRNA转录物增加，代表了以前与肌肉减少症无关的新组分。组织铁水平升高衰老，平行增加转铁蛋白。参与氧化还原稳态的蛋白质表现出复杂的变化模式，增加SOD 1和减少SOD 2。这些结果表明，升高的铁负荷是一个重要的组成部分，肌少症的潜力，可用于临床，和老年横纹肌线粒体可能更容易受到细胞呼吸中产生的自由基。
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.