CONICET | Buscador de Institutos y Recursos Humanos

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 O2˙ and 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 specific metabolic rate within the pO2 range in which other authors have shown whole animals to be oxyregulating (21 - 10 kPa). Exposure of the animals to severe anoxia caused an onset of anaerobiosis (succinate) 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 massively during anoxic exposure of the mussels and increased upon reoxygenation. This ROS burst caused induced lipid peroxidation in the gills, but neither were protein carbonyl levels increased (oxidative damage in the protein fraction), nor did the tissue glutathione redox ratio become more oxidized. 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 oxidative stress under these experimental conditions.