Department of Bioscience, Aarhus University, 8000 Aarhus, Denmark
Department of Biomedical Sciences/CFIM, University of Copenhagen, 2200 Copenhagen, Denmark.
J Exp Biol. 2019 Jun 10;222(Pt 11):jeb200410. doi: 10.1242/jeb.200410.
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.
线粒体对于细胞内稳态很重要，但当细胞从缺氧中恢复时，它们可能会成为一个危险的负担。耐缺氧的淡水龟在长时间缺氧后，其线粒体呼吸能力和活性氧（ROS）的产生会减少，但具体机制尚不清楚。在这里，我们通过比较（1）温暖（25°C）正常氧、（2）低温适应（4°C）正常氧和（3）低温适应缺氧海龟的心脏线粒体，来研究这种线粒体抑制是否源于线粒体含量或内在活性的下调。心脏心室的透射电子显微镜显示，这些处理方法并未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、蛋白质含量或超级复合物分布均未发生显著变化。相反，我们的数据表明，海龟通过对 ETC 复合物的轻微抑制累积效应来抑制线粒体呼吸速率和 ROS 的产生。总的来说，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耐缺氧的重要方面。
