Turtles maintain mitochondrial integrity but reduce mitochondrial respiratory capacity in the heart after cold acclimation and anoxia
Keywords：Electron microscopy; Mitochondria; Oxygen; Reactive oxygen species; Respirometry; Supercomplex
关键词：电子显微镜; 线粒体; 氧; 活性氧； 呼吸测量； 超级复杂
作者：Bundgaard A, Qvortrup K, Rasmussen LJ, Fago A
出版期刊：《Journal of Experimental Biology》 2019/6/10
Abstract：
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°C) normoxic, (2) cold-acclimated (4°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.
文章摘要：
线粒体对细胞稳态很重要，但当细胞从缺氧中恢复时可能会成为危险的负担。耐缺氧淡水龟在长时间缺氧后表现出线粒体呼吸能力和活性氧（ROS）的产生降低，但机制尚不清楚。在这里，我们通过比较（1）温暖（25°C）含氧量正常，（2）冷驯化（4°C）含氧量正常和（3）冷- 适应缺氧海龟。心室透射电子显微镜显示这些治疗不影响线粒体体积密度和形态。此外，电子传递链（ETC）酶的酶活性、蛋白质含量和超复合物分布都没有显着变化。相反，我们的数据表明海龟通过轻微抑制 ETC 复合物的累积效应来抑制线粒体呼吸速率和 ROS 的产生。总之，这些结果表明，在抑制整体酶活性的同时保持线粒体完整性是缺氧耐受性的重要方面。
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