Cytochrome c oxidase deficiency in human posterior cricoarytenoid muscle.
Cytochrome c oxidase deficiency in human posterior cricoarytenoid muscle.
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DOI：
10.1016/j.jvoice.2010.03.002
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发表时间：
2011-07
期刊：
影响因子：
2.2
通讯作者：
Sciote, James J.
中科院分区：
文献类型：
--
作者：
Tellis, Cari M.;Rosen, Clark;Close, John M.;Horton, Michael;Yaruss, J. Scott;Verdolini-Abbott, Katherine;Sciote, James J.
在整个正常衰老过程中，骨骼肌纤维发生线粒体改变，这是由活性氧（ROS）积累增加引起的。这些导致呼吸链异常，从而降低肌纤维的氧化能力，导致收缩力下降，肌肉减少或纤维坏死。喉内肌是一种具有独特基因型、表型和生理特性的颅肌群。它们对氧化应激水平增加的生物过程导致的线粒体改变的易感性可能是这些独特特征之一。测定了人环杓后肌（PCA）和人甲状腺舌骨肌（TH）中COX缺乏症（COX−）的发生率，TH肌是一种作为“对照”肌的喉外肌。10例年龄在55-86岁之间的患者在喉切除术后获得10块PCA和10块TH肌。使用组织切片染色和标准形态计量学分析比较肌肉类型内和肌肉类型之间COX -的差异。在PCA和TH肌中都发现了COX -纤维。PCA肌受影响的纤维是TH肌的10倍，不同肌肉类型和纤维类型的COX -有显著差异（p = 0.003）。几乎所有这些影响都是由于PCA肌肉I型纤维中COX缺乏水平升高（p = 0.002），这与年龄的增长呈正相关。这些结果表明，在正常衰老过程中，PCA肌肉中的线粒体改变可能会增加。
Mitochondrial alterations occur in skeletal muscle fibers throughout the normal aging process, resulting from increased accumulation of reactive oxide species (ROS). These result in respiratory chain abnormalities which decrease the oxidative capacity of muscle fibers, leading to decreased contractile force, sarcopenia, or fiber necrosis. Intrinsic laryngeal muscles are a cranial muscle group which possess some distinctive genotypic, phenotypic and physiologic properties. Their susceptibility to mitochondrial alterations resulting from biological processes that increase levels of oxidative stress may be one of these distinctive characteristics. The incidence of COX deficiency (COX−) was determined in human posterior cricoarytenoid (PCA) muscle, in comparison to the human thyrohyoid (TH) muscle, an extrinsic laryngeal muscle that served as “control” muscle. Ten PCA and 10 TH muscles were harvested post laryngectomy from 10 subjects ranging in age from 55–86 years. Differences in COX− were compared within and between muscle types using tissue section staining and standard morphometric analysis. COX− fibers were identified in both the PCA and TH muscle. The PCA muscle had ten times as may affected fibers as the TH muscle, with significant differences in COX− found between muscle type and fiber type (p = .003). Almost all of this effect was the result of elevated levels of COX deficiency in type I fibers from the PCA muscle (p = .002) that showed a strong positive correlation with increased age. These results suggest that increased mitochondrial alterations may occur in the PCA muscle during normal aging.
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