Sokolova 2014 Abstract MiP2014
|Bioenergetic responses to cyclic hypoxia reveal mitochondrial mechanisms of hypoxia tolerance in marine bivalves.|
Marine organisms are exposed to periodical oxygen deficiency (hypoxia) in estuarine and coastal zones, due to the tidal cycles and/or seasonal formation of the benthic “dead zones”. In sessile organisms, such as bivalves, which cannot escape hypoxic exposures, the ability to survive hypoxia is critically dependent on the physiological and cellular tolerance mechanisms that allow coping with oxygen deficiency and quickly recovering upon reoxygenation. Energy limitation and damage due to reactive oxygen species are major stressors during hypoxia and post-hypoxic recovery, and it is not well known how mitochondria of hypoxia-tolerant marine organisms cope with these challenges.
We studied mitochondrial and cellular responses to hypoxia and post-hypoxic recovery in two common bivalves: a hypoxia-tolerant intertidal hard clam Mercenaria mercenaria and a hypoxia-sensitive subtidal bay scallop Argopecten irradians. Respiration, mt-membrane potential (△ψmt), △ψmt-dependent kinetics of three major mitochondrial subsystems (substrate oxidation, proton leak and phosphorylation), as well as energy reserves and expression of phosphorylated AMPK (pAMPK) and elongation factor (eEF) were measured in clams and scallops exposed to normoxia or short-term hypoxia (17 h at <1% O2), followed by a 1 h period of normoxic recovery. Mitochondrial and cellular responses to hypoxia and reoxygenation dramatically differed in the two studied species.
Labels: MiParea: Respiration, Comparative MiP;environmental MiP
Stress:Ischemia-reperfusion, Oxidative stress;RONS Organism: Other invertebrates
Event: B3, Oral MiP2014
Dep Biol Sc, Univ North Carolina, Charlotte, NC, USA. - ISokolov@uncc.edu
In scallops, hypoxia suppressed the capacity of all three mitochondrial subsystems, especially the phosphorylation subsystem. Mitochondrial condition further deteriorated during reoxygenation, with strong depolarization of mitochondria and a decrease in the flux capacity of the substrate oxidation and phosphorylation subsystems. In contrast, in clams, hypoxia increased the △ψmt-dependent capacity of the substrate oxidation subsystem and had weak inhibitory effects on the flux through 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. Lipid levels increased during hypoxia in clams and scallops, possibly due to the inhibition of mitochondrial catabolism of fats; during reoxygenation, the lipid levels rapidly declined in clams but continued to increase in scallops. Glycogen reserves decreased during hypoxia and reoxygenation in scallops indicating high dependence on glycolysis. Protein levels of phosphorylated eEF increased in clams but not in scallops during hypoxia, indicating suppression of the protein synthesis in the more hypoxia-tolerant species. Levels of pAMPK increased during reoxygenation in scallops indicating energy stress but remained stable throughout hypoxia and reoxygenation in clams. No oxidative damage of the mitochondrial membrane lipids was detected in either species.
Decreased protein synthesis provides an energy-saving mechanism during hypoxia in clams while upregulation of the substrate oxidation capacity poise them for a quick recovery upon reoxygenation. Scallops do not possess these mechanisms and suffer from mitochondrial deterioration and energy deficiency, limiting their ability to survive and recover from hypoxia.
Supported by UNC Charlotte.