Mitochondrial response to pH and bicarbonate in marine mollusks
Supervisor: Inna Sokolova (University of North Carolina, Charlotte, USA)
Estuarine environments are naturally exposed to broad variations of temperature, salinity, as well as changes in dissolved oxygen (DO) and carbon dioxide (CO2) due to tidal, diurnal and seasonal cycles. In estuaries, periods of reduced DO (hypoxia) and elevated CO2 levels (hypercapnia) commonly coincide. Mollusks are champions of tolerance to hypoxic conditions but the physiological mechanisms of this exceptional tolerance are not well understood. We determined the effects of conditions mimicking hypercapnic hypoxia (elevated bicarbonate concentrations and reduced pH) on mitochondrial respiration (MO2) and membrane potential of hard clams Mercenaria mercenaria (a hypoxia tolerant species) and scallops Argopecten irradians (a hypoxia sensitive species). Mitochondrial MO2 plays a vital role in response to hypoxia by adjusting ATP production rates to match ATP demand during hypoxia and recovery. State 3 and 4 respiration of mitochondria (indicative of ADP-stimulated and resting respiration, respectively), respiratory control ratio (an index of mitochondrial coupling) and rates of production of reactive oxygen species (ROS) were measured to understand metabolic effects of elevated bicarbonate and reduced pH. With pyruvate as a metabolic substrate typical of normoxic conditions, low pH stimulated mitochondrial MO2 in both studied species and but elevated HCO3-only affected mitochondrial respiration of scallops. When succinate (a substrate that accumulates in hypoxia) was used, mitochondrial respiration of clams and scallops was suppressed by elevated HCO3– but only scallop mitochondria were sensitive to pH. Increasing bicarbonate levels led to a progressive decrease in mitochondrial coupling, especially pronounced in scallops. Unlike mammals, effects of bicarbonate on mitochondrial respiration of bivalves were not mediated by activation of soluble Adenylyl Cyclase (sAC) or by cyclic AMP (cAMP) indicating evolutionary divergence of signaling pathways involved in response to bicarbonate.