Abstract
Hemolymph acid-base balance and ion concentrations were measured in shore crabs, Carcinus maenas (L.), kept in fullstrength sea water (≈33‰ S) and exposed to sublethal (0.5 mg l-1) and lethal (1 and 2 mg l-1) levels of copper in water. The study was conducted throughout the year 1987 on crabs collected near Arcachon (France). Whatever the dose, waterborne copper induced metabolic acidosis without marked changes of hemolymph ion concentrations. At the sublethal copper level, the acidosis was non-lactic and partly compensated by transitory hypocapnia. Complete recovery was observed within 20 d. At intermediate and lethal copper levels, this primary acidosis was later reinforced by hypercapnia and accumulation of lactic acid, indicating that restriction of respiratory gas exchange is the probable cause of death. A steep increase in the hemolymph calcium concentration before death suggests buffering of the acidosis by calcium-carbonate stores from the exoskeleton.
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