Organisms able to inhabit reef lagoons survive extreme oxygenation fluctuations. Adaptations to withstand anoxia/hypoxia implicate mitochondrial plasticity, yet little is known about hyperoxia-driven plasticity, or the generation and quenching of reactive-oxygen-species (ROS). We used the intertidal crab Eriphia sebana, which occupies an intertidal habitat on Heron Island’s reef platform (Australia), where oxygenation fluctuation reaches 220% of air saturation.
Following collection and 12h of acclimation, crabs were exposed for 4 hours to either: normoxic water; hyperoxic water (≈175% saturation); or air. Compared to normoxic values, whole animal respiration rates were diminished by 37%, while air-exposed animals suppressed respiration by 99.8%. Re-immersed air-exposed crabs only regained 18% of their respiration rate. Hemolymphatic antioxidant levels correlated inversely to respiration rate, with air-exposed crabs displaying the highest antioxidant level. Mitochondrial oxygen consumption and ROS generation was measured in heart fibers from each of the three treatments, using high-resolution respirometry. While mitochondrial respiratory-scope was greater in normoxic-exposed animals, ROS production was similar across treatments. However, mitochondrial ROS-generation at cellular oxygen levels was greater in air-exposed animals. Overall, crabs exposed to hyperoxia appear to suppress respiration at both whole-organism and mitochondrial levels, and quench ROS by increasing antioxidant capacities.