Turtles maintain mitochondrial integrity but reduce mitochondrial respiratory capacity in the heart after cold acclimation and anoxia
Turtles maintain mitochondrial integrity but reduce mitochondrial respiratory capacity in the heart after cold acclimation and anoxia
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DOI：
10.1242/jeb.200410
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发表时间：
2019-06-01
影响因子：
2.8
通讯作者：
Fago, Angela
中科院分区：
文献类型：
--
作者：
Bundgaard, Amanda;Qvortrup, Klaus;Fago, Angela
线粒体对细胞内稳态很重要，但当细胞从缺氧中恢复时，线粒体可能成为一种危险的责任。耐缺氧的淡水龟在长期缺氧后表现出线粒体呼吸能力和活性氧（ROS）产生的降低，但其机制尚不清楚。在这里，我们研究了这种线粒体抑制是否源于线粒体含量或内在活性的下调，通过比较心脏线粒体（1）温暖（25摄氏度）常氧，（2）冷驯化（4摄氏度）常氧和（3）冷驯化缺氧海龟。心室透射电镜观察显示，这些处理并没有影响线粒体的体积密度和形态。此外，无论是酶活性，蛋白质含量，也没有电子传递链（ETC）酶的超复合物分布的显着变化。相反，我们的数据表明，海龟抑制线粒体呼吸速率和ROS生产的ETC复合物的轻微抑制的累积效应。总之，这些结果表明，维持线粒体的完整性，同时抑制整体酶活性是缺氧耐受性的重要方面。
Mitochondria are important to cellular homeostasis, but can become a dangerous liability when cells recover from hypoxia. Anoxia-tolerant freshwater turtles show reduced mitochondrial respiratory capacity and production of reactive oxygen species (ROS) after prolonged anoxia, but the mechanisms are unclear. Here, we investigated whether this mitochondrial suppression originates from downregulation of mitochondrial content or intrinsic activity by comparing heart mitochondria from (1) warm (25 degrees C) normoxic, (2) cold-acclimated (4 degrees C) normoxic and (3) cold-acclimated anoxic turtles. Transmission electron microscopy of heart ventricle revealed that these treatments did not affect mitochondrial volume density and morphology. Furthermore, neither enzyme activity, protein content nor supercomplex distribution of electron transport chain (ETC) enzymes changed significantly. Instead, our data imply that turtles inhibit mitochondrial respiration rate and ROS production by a cumulative effect of slight inhibition of ETC complexes. Together, these results show that maintaining mitochondrial integrity while inhibiting overall enzyme activities are important aspects of anoxia tolerance.