Combined effects of salinity and intermittent hypoxia on mitochondrial capacity and reactive oxygen species efflux in the Pacific oyster, Crassostrea gigas

Abstract

Coastal environments commonly experience fluctuations in salinity and hypoxia/reoxygenation (H/R) stress that can negatively affect mitochondrial functions of marine organisms. Although intertidal bivalves are adapted to these conditions, the mechanisms that sustain mitochondrial integrity and function are not well understood. We determined the rates of respiration and reactive oxygen species (ROS) efflux in the mitochondria of the oysters acclimated to high (33) or low (15) salinity, and exposed to either normoxic conditions (control; 21% O2) or to short-term hypoxia (24 h at <0.01% O2) and subsequent reoxygenation (1.5 h at 21% O2). Further, we exposed isolated mitochondria to anoxia in vitro to assess their ability to recover from acute (∼10 min) oxygen deficiency (<0.01% O2). Our results showed that mitochondria of oysters acclimated to high or low salinity did not show severe damage and dysfunction during H/R stress, consistent with the hypoxia tolerance of C. gigas. However, acclimation to low salinity led to improved mitochondrial performance and plasticity, indicating that salinity 15 might be closer to the metabolic optimum of C. gigas than salinity 33. Thus, acclimation to low salinity increased mitochondrial oxidative phosphorylation rate and coupling efficiency and stimulated mitochondrial respiration after acute H/R stress. However, elevated ROS efflux in the mitochondria of low salinity-acclimated oysters after acute H/R stress indicate possible trade-off of higher respiration. The high plasticity and stress tolerance of C. gigas mitochondria may contribute to the success of this invasive species and facilitate its further expansion to brackish regions such as the Baltic Sea.

Mitochondrial responses to constant and cyclic hypoxia depend on the oxidized fuel in a hypoxia-tolerant marine bivalve Crassostrea gigas

“…Notably, the ROS efflux in the mitochondria of oysters was minimally affected by the H/R stress with no consistent evidence of the oxidative damage to mitochondria. This suggests that unlike the mitochondria of mammals where reoxygenation is associated with ROS burst 19,53,75,76 , mitochondria of stress-tolerant intertidal bivalves like oysters tightly control ROS efflux during environmental stress like oxygen (this study) and salinity 77 fluctuations. In oysters, the robust forward electron flux with succinate combined with suppression of Complex I activity can minimize RET and stabilize ROS production in mitochondria during H/R stress.…”