Data from: Mitochondrial responses to prolonged anoxia in brain of Red-eared slider turtles

AbstractMitochondria are central to aerobic energy production and play a key role in neuronal signalling. During anoxia, however, the mitochondria of most vertebrates initiate deleterious cell death cascades. Nonetheless, a handful of vertebrate species, including some freshwater turtles, are remarkably tolerant of low oxygen environments and survive months of anoxia without apparent damage to brain tissue. This tolerance suggests that mitochondria in the brains of such species are adapted to withstand prolonged anoxia, but little is known about potential neuroprotective responses. In this study, we address such mechanisms by comparing mitochondrial function between brain tissues isolated from cold-acclimated red-eared slider turtles (Trachemys scripta elegans) exposed to two weeks of either normoxia or anoxia. We found that brain mitochondria from anoxia-acclimated turtles exhibited a unique phenotype of remodelling relative to normoxic controls, including: (i) decreased citrate synthase and F1FO-ATPase activity but maintained protein content, (ii) markedly reduced aerobic capacity, and (iii) mild uncoupling of the mitochondrial proton gradient. These data suggest that turtle brain mitochondria respond to low oxygen stress with a unique suite of changes tailored towards neuroprotection., Usage notesOroboros data filesOroboros Instruments DatLab Data (DLD) files.

摘要
线粒体（mitochondria）是有氧能量产生的核心枢纽，同时在神经元信号传导中发挥关键作用。然而，在缺氧（anoxia）条件下，大多数脊椎动物的线粒体会启动有害的细胞死亡级联反应。尽管如此，少数脊椎动物类群（包括部分淡水龟）对低氧环境具备极强的耐受性，可在长达数月的缺氧状态下存活，且脑组织未出现明显损伤。这种耐受性提示，此类物种大脑中的线粒体已进化出适应长期缺氧的能力，但目前对其潜在的神经保护应答机制仍知之甚少。

本研究通过对比经两周常氧（normoxia）或缺氧处理的冷驯化红耳滑龟（Trachemys scripta elegans）脑组织分离所得的线粒体功能，探究了上述相关机制。研究发现，相较于常氧对照组，缺氧驯化的龟脑线粒体呈现出独特的重塑表型，具体包括：（i）柠檬酸合酶（citrate synthase）与F1FO-ATP合酶（F1FO-ATPase）活性降低，但蛋白质含量保持稳定；（ii）有氧代谢能力显著下降；（iii）线粒体质子梯度出现轻度解偶联。上述数据表明，龟脑线粒体可通过一系列针对性的独特适应性变化，响应低氧应激以实现神经保护。

使用说明
奥罗博罗斯仪器（Oroboros Instruments）数据文件，即奥罗博罗斯仪器公司的DatLab数据（DLD）文件。