Meeting Abstract
Rising atmospheric CO2 levels leads to shifts in the carbonate chemistry and pH of marine waters, potentially changing the bioavailability of trace metals such as cadmium (Cd) and copper (Cu) to marine organisms with implications for metal toxicity. We determined the interactive effects of elevated PCO2 levels and Cd or Cu exposure on intracellular metal distribution and metabolic efficiency of the hard clams (Mercenaria mercenaria). Animals were exposed to clean artificial seawater (ASW) or ASW supplemented with 50 µg L-1 Cd or Cu at PCO2 concentrations corresponding to IPCC present day levels, and projections for years 2100, and 2250 (~400, 800 and 2000 ppmv) for 28 days. Cu exposure did not cause significant Cu accumulation in clams indicating tight regulation of this essential metal. In contrast, Cd strongly bioaccumulated in biologically active fractions including mitochondria, lysosomes and high molecular weight cytosolic proteins, but only small fraction of the intracellular Cd burden partitioned to metallothioneins. Cd bioaccumulation in mitochondria and cytosolic proteins was enhanced by hypercapnia. Hypercapnia caused significant (P<0.02) decreases in specific activities of pyruvate kinase, PK, and phosphoenolpyruvate carboxykinase, PEPCK (enzymes that channel glycolytic substrates to aerobic and anaerobic pathways, respectively), indicating metabolic depression. Cd exposure in present-day conditions significantly (P<0.1) decreased PK activity. No significant differences in PK/PEPCK ratio were seen in any treatments, but a trend of lowered anaerobic capacity was detected in response to moderate hypercapnia and Cd exposure, which merits further inquiry. These findings aid our understanding of the long-term effects of increased CO2 levels and pollution on the health of a keystone species and indicate that hypercapnia has a more negative impact on the metabolism of the hard clam than exposure to Cu and Cd at low, environmentally realistic concentrations.
