Abstract

Toxicity tests were performed to determine the 96 h sub-lethal copper concentration at pH 5 (SLCC) for adult brown trout acclimated to 5 °C (Oct.–Mar.) or 15 °C (May–Aug.) in an artificial softwater (Ca 2+ 50 μmol l −1). These were found to be 0.47 and 0.08 μmol l −1 Cu 2+ at 5 and 15 °C respectively. Routine oxygen consumption (M o 2 ) and critical swimming speed (Ucrit) of groups of trout exposed to the SLCC for each temperature were measured and compared to trout maintained in the absence of copper and at pH 7. At 5 °C, an additional group was exposed to the summer copper level of 0.08 μmol l −1 Cu 2+ at pH 5. At the end of each experiment, samples of arterial blood were taken from the dorsal aorta via chronically indwelling cannulae. Copper exposure in acidic water significantly reduced swimming performance. Trout exposed to 0.08 μmol l −1 Cu 2+ at pH 5 achieved a critical swimming speed some 25–50% slower than control trout with no significant temperature effect. Of the six winter trout exposed to 0.47 μmol l −1 Cu 2+ at pH 5, only one swam steadily at the lowest test speed of 0.3 m s −1, the remainder achieving at most a brief burst of activity. Earlier workers suggested that observed increases in aerobic maintenance costs and decreased maximum metabolism arose from copper-induced inefficiencies in ionoregulation and gas exchange and reduced Ucrit to be a consequence of this lower scope for activity. In the present study, plasma sodium and chloride concentrations were reduced some 25–35%, regardless of acclimation temperature or copper concentration. The routine M o 2 of trout exposed to the SLCC at either temperature was elevated (by 72% and 38% at 5 and 15 °C respectively). However, there was no change in that of winter trout exposed to only 0.08 μmol l −1 Cu 2+ at pH 5 although their swimming performance was also reduced. More significantly, there were no changes in the blood oxygen content or lactate concentration of exercised trout at any copper concentration as might be expected if M o 2max was limited by an impaired oxygen uptake. There were, however, some effects of copper and acid exposure, such as increases in haemoglobin and plasma protein concentrations, which may have elevated blood viscosity and which could have led to a disruption of oxygen transport to the tissues. Although the occurrence and magnitude of these effects were not consistent between treatment groups, there is some evidence for a tissue hypoxia from a parallel study.

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