Effects of pH and bicarbonate on mitochondrial functions of marine bivalves

Estuarine organisms including molluslcs are exposed to periodic oxygen deficiency (hypoxia) that leads to a decrease in intracellular pH and accumulation of bicarbonate (HCO3-). These changes can affect cellular bioenergetics; however, their effects on mitochondria of estuarine mollusks are not well understood. We determined the interactive effects of bicarbonate (0-10 mM) and pH (7.2 and 6.5) on mitochondrial oxygen consumption ((M) over dot(O2)), membrane potential (Delta psi) and production of reactive oxygen species (ROS) in two common estuarine bivalves hard clams Mercenaria mercenaria, and bay scallops Argopecten irradians. In both species, elevated HCO3- levels suppressed ADP-stimulated (state 3) (M) over dot(O2) but had little effect on the resting (state 4) respiration. These effects were not mediated by the soluble adenylyl cyclase or cyclic AMP. Effects of the low pH (6.5) on mitochondrial traits were species-specific and depended on the substrate oxidized by the mitochondria. Mild acidosis (pH 6.5) had minimal effects on (M) over dotO(2) and Delta psi of the bivalve mitochondria oxidizing pyruvate but led to increased rates of ROS production in clams (ROS production could not be measured in scallops). In succinate-respiring mitochondria of clams, mild acidosis suppressed (M) over dot(O2) and increased mitochondria! coupling, while in scallop mitochondria the effects of low pH were opposite. Suppression of mitochondrial oxidative phosphorylation by bicarbonate and/or acidosis may contribute to the metabolic rate depression during shell closure or environmental hypoxia/hypercapnia. These findings have implications for understanding the physiological mechanisms involved in regulation of mitochondrial bioenergetics during hypoxia exposure in estuarine bivalves. (C) 2016 Elsevier Inc. All rights reserved.