EXTRA-CELLULAR AND INTRACELLULAR ACID-BASE-BALANCE AND IONIC REGULATION IN COD (GADUS-MORHUA) DURING COMBINED AND ISOLATED EXPOSURES TO HYPERCAPNIA AND COPPER

Cod (Gadus morhua) were exposed to hypercapnia (water Pco(2) = 7.5 mmH g), elevated copper level (0.4 ppm) or a combination of both in order to study extra- and intracellular acid-base regulation and the influen ce hereupon of copper. During pure hypercapnia, the extracellular resp iratory acidosis was completely compensated within 12 to 24 h via a ch loride-mediated increase in extracellular [HCO3-]. Exposure to copper in normocapnic seawater caused a large and progressive increase in pla sma [Na+] and [Cl-] and a metabolic acidosis. Exposure to copper in hy percapnic seawater was associated with smaller elevations of plasma [N af] and [Cl-] than in normocapnic seawater, showing that hypercapnia h ad a protective effect on the copper-induced osmoregulatory disturbanc es. The compensation of the hypercapnic acidosis was, however, slow an d incomplete in fish exposed to both copper and hypercapnia. Extracell ular pH remained depressed by 0.3 pH units after 72 h. The data reveal that acid-base regulation was immediately and persistently inhibited by copper. The limited acid-base regulation during combined copper and hypercapnia exposure was chloride-mediated as during hypercapnia alon e. Intracellular pH recovery was complete and very rapid in ventricula r and skeletal muscle tissues during environmental hypercapnia, wherea s acid-base compensation in liver tissue was slower, the kinetics bein g similar to that in the extracellular compartment. Intracellular pH c ompensation was significantly slowed down by copper. Copper concentrat ion increased drastically in gill tissue already at 3 h, while copper concentrations in liver, muscle and plasma were significantly elevated only after 48 h, with liver showing the largest elevation.