Department of Poultry Science, Center of Excellence for Poultry Science, University of Arkansas, Fayetteville, AR.
J Anim Sci. 2019 Jul 30;97(8):3169-3179. doi: 10.1093/jas/skz219.
Oxidative stress is an unavoidable consequence of aerobic metabolism. Whereas high amounts of mitochondrial reactive oxygen species (ROS) can cause oxidation, low levels play important roles in signal transduction. In a Pedigree male (PedM) broiler model of feed efficiency (FE), the low FE phenotype was characterized by increased ROS in isolated mitochondria (muscle, liver, and duodenum) with a pervasive protein oxidation in mitochondria and tissues. Subsequent proteogenomic studies in muscle revealed evidence of enhanced mitoproteome abundance, enhanced mitochondrial phosphocreatine shuttling expression, and enhanced ribosome assembly in the high FE phenotype. Surprisingly, an enhanced infrastructure would foster greater repair of damaged proteins or organelles through the autophagy and proteosome pathways in the high FE phenotype. Although protein and organelle degradation, recycling, and reconstruction would be energetically expensive, it is possible that energy invested into maintaining optimal function of proteins and organelles contributes to cellular efficiency in the high FE phenotype. New findings in mitochondrial physiology have been reported in the last several years. Reverse electron transport (RET), once considered an artifact of in vitro conditions, now is recognized to play significant roles in inflammation, ischemia-reperfusion, muscle differentiation, and energy utilization. A topology of ROS production indicates that ROS derived from Complex I of the respiratory chain primarily causes oxidation, whereas ROS generated from Complex III are primarily involved in cell signaling. It is also apparent that there is a constant fission and fusion process that mitochondria undergo that help maintain optimal mitochondrial function and enables mitochondria to adjust to periods of nutrient limitation and nutrient excess. Understanding the balancing act that mitochondria play in health and disease will continue to be a vital biological component in health-production efficiency and disease in commercial animal agriculture.
氧化应激是有氧代谢不可避免的后果。虽然大量的线粒体活性氧（ROS）会引起氧化，但低水平的 ROS 在信号转导中起着重要作用。在一个饲料效率（FE）的 Pedigree 雄性（PedM）肉鸡模型中，低 FE 表型的特征是分离的线粒体（肌肉、肝脏和十二指肠）中 ROS 增加，同时线粒体和组织中存在广泛的蛋白质氧化。随后在肌肉中的蛋白质组学研究表明，高 FE 表型中存在增强的线粒体蛋白质组丰度、增强的线粒体磷酸肌酸穿梭表达和核糖体组装的证据。令人惊讶的是，高 FE 表型中增强的基础设施会通过自噬和蛋白酶体途径促进受损蛋白质或细胞器的更大修复。虽然蛋白质和细胞器的降解、回收和重建在能量上是昂贵的，但通过自噬和蛋白酶体途径来维护蛋白质和细胞器的最佳功能的能量投入，可能有助于高 FE 表型中的细胞效率。近年来，在线粒体生理学方面有了新的发现。逆向电子传递（RET），曾经被认为是体外条件下的一种假象，现在被认为在炎症、缺血再灌注、肌肉分化和能量利用中发挥重要作用。ROS 产生的拓扑结构表明，来自呼吸链复合物 I 的 ROS 主要引起氧化，而来自复合物 III 的 ROS 主要参与细胞信号转导。很明显，线粒体经历了一个不断的分裂和融合过程，这有助于维持最佳的线粒体功能，并使线粒体能够适应营养限制和营养过剩的时期。理解线粒体在健康和疾病中的平衡作用将继续成为商业动物农业中健康生产效率和疾病的重要生物学组成部分。
