Differential responses to copper in rainbow trout (Oncorhynchus mykiss) acclimated to sea water and brackish water

Abstract

Rainbow trout, Oncorhynchus mykiss, acclimated to 33% sea water (12 mg·ml-1 salinity) experienced significant (10 meq·1-1) increases in plasma [Na+] and [Cl-] within 5 h of exposure to 6.3 μmol copper·1-1 indicating severe impairment of branchial ionoregulatory capacity. All plasma ion levels subsequently stabilised once the transbranchial [Na+] gradient was reduced to zero. The similar ionic strength of the external medium and their body fluids appeared to protect trout maintained in 33% sea water from further ionoregulatory stress and any secondary physiological disturbances during exposure to copper. Despite three- and fourfold greater transbranchial [Na+] and [Cl-] gradients, trout acclimated to full-strength sea water (35 mg·ml-1 salinity) suffered no major changes in plasma Na+, Cl-, K+, or Ca2+, blood gases or haematology during 24 h exposure to 6.3 μmol copper·1-1. This reduction in toxicity in full strength sea water cannot be explained by differences in copper speciation. We suggest that during acute exposure to waterborne copper, active NaCl extrusion is unaffected due to the basolateral location of the gill Na+/K+-ATPase, but that ionoregulatory disturbances can occur due to gill permeability changes secondary to the displacement of surface-bound Ca2+. However, in full strength sea water the three-fold higher ambient [Ca2+] and [Mg2+] appear to be sufficient to prevent any detrimental permeability changes in the presence of 6.3 μmol copper·1-1. Plasma [NH + 4 ] and [HCO - 3 ] were both significantly elevated during exposure to copper, indicating that some aspects of gill ion transport (specifically the apical Na+/NH + 4 and Cl-/HCO - 3 exchanges involved in acid/base regulation and nitrogenous waste excretion) are vulnerable to inhibition in the presence of waterborne copper.