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首页> 外文期刊>American Journal of Physiology >Type II skeletal myofibers possess unique properties that potentiate mitochondrial H(2)O(2) generation.
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Type II skeletal myofibers possess unique properties that potentiate mitochondrial H(2)O(2) generation.

机译：II型骨骼肌纤维具有增强线粒体H（2）O（2）生成的独特特性。

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Mitochondrial dysfunction is implicated in a number of skeletal muscle pathologies, most notably aging-induced atrophy and loss of type II myofibers. Although oxygen-derived free radicals are thought to be a primary cause of mitochondrial dysfunction, the underlying factors governing mitochondrial superoxide production in different skeletal myofiber types is unknown. Using a novel in situ approach to measure H(2)O(2) production (indicator of superoxide formation) in permeabilized rat skeletal muscle fiber bundles, we found that mitochondrial free radical leak (H(2)O(2) produced/O(2) consumed) is two- to threefold higher (P < 0.05) in white (WG, primarily type IIB fibers) than in red (RG, type IIA) gastrocnemius or soleus (type I) myofibers during basal respiration supported by complex I (pyruvate + malate) or complex II (succinate) substrates. In the presence of respiratory inhibitors, maximal rates of superoxide produced at both complex I and complex III are markedly higher in RG and WG than in soleusmuscle despite approximately 50% less mitochondrial content in WG myofibers. Duplicate experiments conducted with +/-exogenous superoxide dismutase revealed striking differences in the topology and/or dismutation of superoxide in WG vs. soleus and RG muscle. When normalized for mitochondrial content, overall H(2)O(2) scavenging capacity is lower in RG and WG fibers, whereas glutathione peroxidase activity, which is largely responsible for H(2)O(2) removal in mitochondria, is similar in all three muscle types. These findings suggest that type II myofibers, particularly type IIB, possess unique properties that potentiate mitochondrial superoxide production and/or release, providing a potential mechanism for the heterogeneous development of mitochondrial dysfunction in skeletal muscle.
机译：线粒体功能障碍与许多骨骼肌病理有关，最明显的是衰老引起的萎缩和II型肌纤维的丢失。尽管氧衍生自由基被认为是线粒体功能障碍的主要原因，但在不同骨骼肌纤维类型中控制线粒体超氧化物生成的潜在因素尚不清楚。使用一种新颖的原位方法来测量透化大鼠骨骼肌纤维束中的H（2）O（2）产生（超氧化物形成指标），我们发现线粒体自由基泄漏（H（2）O（2）产生/ O （2）消耗）（白色，WG，主要为IIB型纤维）的红色（RG，IIA型）腓肠肌或比目鱼（I）型肌纤维在复合呼吸系统I支持的基础呼吸过程中（P <0.05）高2到3倍（丙酮酸+苹果酸）或复合物II（琥珀酸）底物。在存在呼吸抑制剂的情况下，尽管WG肌纤维中的线粒体含量减少了约50％，但在RG和WG中，复合物I和复合物III产生的超氧化物的最大比率均显着高于比目鱼肌。用+/-外源超氧化物歧化酶进行的重复实验显示，WG与比目鱼肌和RG肌肉的拓扑结构和/或超氧化物歧化有显着差异。当线粒体含量归一化时，RG和WG纤维中的总H（2）O（2）清除能力较低，而主要负责线粒体H（2）O（2）去除的谷胱甘肽过氧化物酶活性在所有三种肌肉类型。这些发现表明II型肌纤维，特别是IIB型，具有增强线粒体超氧化物产生和/或释放的独特性质，为骨骼肌线粒体功能障碍的异质发展提供了潜在的机制。

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