Effect of cadmium and environmental anoxia and re-oxygenation on metabolism of eastern oysters (Crassostrea virginica)


Meeting Abstract

P3.16  Tuesday, Jan. 6  Effect of cadmium and environmental anoxia and re-oxygenation on metabolism of eastern oysters (Crassostrea virginica). IVANINA, Anna*; KUROCHKIN, Ilya; EILERS, Silke; SOKOLOVA, Inna; University of North Carolina at Charlotte; University of North Carolina at Charlotte; Hochschule Bremen, Bremen, Germany; University of North Carolina at Charlotte aivanina@uncc.edu

Heavy metal pollution is a worldwide problem, and cadmium (Cd) is an important toxicant in estuarine and coastal environments. Alternating hypoxia/anoxia and re-oxygenation during the tidal cycle is a common stress in the marine intertidal zone, but physiological consequences of these cycles and effect of Cd contamination in intertidal organisms are not fully understood. We have studied the effects of air exposure (1-6 days) and the subsequent recovery in normoxic water on metabolism of control and Cd-exposed intertidal bivalves, the eastern oyster (Crassostrea virginica). Determination of hemolymph oxygen content (PO2) indicates that oysters become anoxic very rapidly (after 10-20 minutes of air exposure). The hearts also stopped beating in air-exposure oysters indicating cessation of the tissue hemolymph supply. During air exposure control and Cd-exposed oysters accumulated anaerobic end products (succinate, acetate and L-alanine) in tissues, but the concentrations of anaerobic metabolites were significantly higher in control oysters compared to the Cd-exposed ones indicating lower anaerobic capacity in Cd-exposed oysters. There was a significant decrease in ATP levels and ATP/ADP ratio during the air exposure. Concentration of tissue metabolites (including anaerobic end products and adenylates) returned to the control levels after 12h of re-oxygenation in control but not in Cd-exposed oysters. These findings show that in presence of Cd the metabolic response of oysters to anoxia and subsequent recovery of upon reoxygenation are inhibited. Supported by NSF CAREER (IBN-0347238).

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