Department of Functional Ecology, Alfred Wegener Institute, Helmholtz Centre for Polar and Marine Research, Am Handelshafen 12, 27570 Bremerhaven, Germany.
Mar Environ Res. 2013 Dec;92:110-9. doi: 10.1016/j.marenvres.2013.09.007. Epub 2013 Sep 24.
Intertidal blue mussels, Mytilus edulis, experience hypoxia reoxygenation during tidal emersion and resubmersion cycles, and this is often suggested to represent a major stress for the animals, especially for their respiratory tissues, the gills. We exposed mussels to experimental short and prolonged anoxia and subsequent reoxygenation and analyzed the respiratory response in excised gill tissue and the effects of treatment on reactive oxygen species (mainly ROS: superoxide anion, O2·- and hydrogen peroxide, H2O2), formation using live imaging techniques and confocal microscopy. Our aim was to understand if this "natural stress" would indeed produce oxidative damage and whether antioxidant defenses are induced under anoxia, to prevent oxidative damage during reoxygenation. Exposure to declining pO2 in the respiration chamber caused an increase of gill metabolic rate between 21 and 10 kPa, a pO2 range in which whole animal respiration is reported to be oxyregulating. Exposure of the animals to severe anoxia caused an onset of anaerobiosis (succinate accumulation) and shifted high and low critical pc values (pc1: onset of oxyregulation in gills, pc2: switch from oxyregulation to oxyconformity) to higher pO2. Concentrations of both ROS decreased strongly during anoxic exposure of the mussels and increased upon reoxygenation. This ROS burst induced lipid peroxidation in the mantle, but neither were protein carbonyl levels increased (oxidative damage in the protein fraction), nor did the tissue glutathione concentration change in the gills. Further, analysis of apoptosis markers indicated no induction of cell death in the gills. To our knowledge, this is the first paper that directly measures ROS formation during anoxia reoxygenation in mussels. We conclude that hypoxia tolerant intertidal mussels do not suffer major oxidative stress in gill and mantle tissues under these experimental conditions.
潮间带贻贝（Mytilus edulis）在潮汐淹没和重新淹没的循环过程中经历缺氧再氧化，这通常被认为是对动物的主要压力，特别是对它们的呼吸组织，鳃。我们将贻贝暴露于实验性短暂和长期缺氧以及随后的再氧化中，并分析了在离体鳃组织中的呼吸反应以及处理对活性氧（主要是 ROS：超氧阴离子，O2·-和过氧化氢，H2O2）的影响，使用活细胞成像技术和共聚焦显微镜进行分析。我们的目的是了解这种“自然压力”是否确实会产生氧化损伤，以及在缺氧条件下是否会诱导抗氧化防御，以防止再氧化过程中的氧化损伤。在呼吸室中 pO2 下降导致鳃代谢率在 21 和 10 kPa 之间增加，这是整个动物呼吸被报道为氧调节的 pO2 范围。动物暴露于严重缺氧会导致无氧呼吸（琥珀酸积累）的发生，并将高和低临界 pc 值（pc1：鳃中氧调节的开始，pc2：从氧调节到氧顺应的转变）转移到更高的 pO2。贻贝在缺氧暴露期间，两种 ROS 的浓度都强烈下降，再氧化时增加。这种 ROS 爆发诱导了外套膜中的脂质过氧化，但蛋白质羰基水平没有增加（蛋白质部分的氧化损伤），鳃组织中的谷胱甘肽浓度也没有变化。此外，对细胞凋亡标志物的分析表明，鳃组织中没有诱导细胞死亡。据我们所知，这是第一篇直接测量贻贝在缺氧再氧化过程中 ROS 形成的论文。我们得出结论，在这些实验条件下，耐缺氧的潮间带贻贝在鳃和外套膜组织中不会遭受重大氧化应激。
