Abstract

Rainbow trout, common carp, and gibel carp were exposed to sublethal Cu levels (1.0 or 1.7 μM) for 1 week. In rainbow trout, arterial oxygen tension ( P aO 2 ) remained normal and there was no indication of anaerobic metabolism. P aO 2 was considerably lower in common and gibel carp and Cu exposure decreased this further. The decrease was transient for common carp but persistent in gibel carp and coincided with an elevation in arterial carbon dioxide tension ( P aCO 2 ) indicating that all gas exchange was compromised in both cyprinid species. The disturbed gas exchange resulted in acidosis, which was respiratory and metabolic for common carp but mainly respiratory for gibel carp. Gibel carp produced ethanol as end product of their alternative anaerobic pathway. The hypothesis that hypertrophy and hyperplasia, resulting in increased diffusion distances, are reducing P aO 2 appeared invalid. Hypoventilation seems a more likely cause. Ionoregulatory parameters responded more uniform among species. Fast and pronounced decreases in plasma sodium and chloride developed for all three species, independent of the observed gill damage. Rainbow trout lost 20% of their plasma Na in the first 3 days, while common and gibel carp had only lost 13 and 16% respectively at that time. This difference might be crucial when challenged with Cu exposure and allow a fish to survive the first shock phase and supports it the hypothesis that sodium turnover is a key factor in predicting Cu toxicity.

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