Cu is a widely occurring contaminant in aquatic systems and is acutely toxic to fish. The current paradigm of copper’s toxic mechanism of action in fish is believed to be through direct effects on several important functions of the teleost gill; therefore experiments were conducted to examine Cu effects on the osmoregulatory ability and swimming performance of juvenile rainbow trout (Oncorhynchus mykiss) in water of varying hardness. Fish were exposed to three Cu concentrations (0, 20 and 60 µg/L in hard water [100 mg/L CaCO3], and 0, 6 and 16 µg/L in soft water [6 mg/L CaCO3]), for 4, 8 and 16 d and then tested for their ability to osmoregulate and burst swim. Burst swimming speed (Uburst) was not different between control and Cu-exposed fish in either soft or hard water. Osmoregulatory ability following Cu exposure was examined through several biochemical measurements related to osmoregulation and a seawater challenge. Cu exposure did not elicit a change in any osmoregulatory-related measurement or result in mortalities during the seawater challenge. These results indicate that the current paradigm of Cu toxicity may not reflect the mechanism of sublethal Cu toxicity or that compensatory mechanisms are offsetting major physiological disturbances caused by Cu, at concentrations that are near those which typically cause mortality in salmonids.
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