Meeting Abstract
Estuarine bivalves are among the champions of hypoxia tolerance and are exposed to cyclic oxygen deficiency due to the tidal cycles and/or formation of the benthic “dead zones” in estuaries. Metabolic adaptations such as efficient anaerobic pathways and metabolic rate depression play a key role in hypoxia tolerance of mollusks; however, it remains unknown how mitochondrial functions are preserved during hypoxia and reoxygenation in these organisms. We studied mitochondrial responses to hypoxia in the hard clam Mercenaria mercenaria and the bay scallop Argopecten irradians. Membrane potential (Δψ) and kinetics of substrate oxidation, proton leak and phosphorylation subsystems were measured in clams and scallops exposed to hypoxia (17 h at <1% O2) followed by a 1 h recovery. In scallops, hypoxia suppressed the capacity of all three mitochondrial subsystems, and mitochondrial condition further deteriorated during reoxygenation, with strong depolarization of mitochondria and decreased capacity for the substrate oxidation and phosphorylation. In contrast, in clams hypoxia increased the Δpsi-dependent capacity of the substrate oxidation subsystem and had weak inhibitory effects on the phosphorylation and proton leak subsystems. During reoxygenation, the substrate oxidation capacity of clam mitochondria further increased and the capacity of the phosphorylation subsystem returned to normal. Upregulation of the substrate oxidation in hypoxia poises clams for a quick recovery upon reoxygenation, while scallops suffer from mitochondrial deterioration limiting their ability to survive hypoxia. Supported by the Charlotte Research Institute and University of North Carolina at Charlotte.
