Reduced marine survival of hatchery-reared Atlantic salmon post-smolts exposed to aluminium and moderate acidification in freshwater

摘要

Short-term Al-exposure and moderate acidification increased initial marine mortality in migrating post-smolts, and can thereby reduce viability of Atlantic salmon stocks. The delayed impact of short-term aluminium (Al) exposure on hatchery-reared Atlantic salmon smolt in moderately acidified freshwater (pH 5.88-5.98) was investigated during the first 37 km of the marine migration. Smolts were tagged with acoustic tags and exposed to low (28.3 ± 4.6μg~(-1) labile Al, 90 h) or high (48.5 ± 6.4 μg 1~(-1) labile Al, 90 or 48 h) Al concentrations within the hatchery. Thereafter their movements, together with a control group, were monitored throughout the marine fjord. Al-exposure resulted in increased gill-Al and compromised hypoosmoregulatory capacity, as shown by elevated mortality in laboratory seawater challenge tests and reduced Na+, K+-ATPase activity levels. Further, Al-exposure resulted in decreased plasma concentrations of growth hormone (GH), while the insulin-like growth factor (IGF-I) was unaffected. There was a significant mortality in the 90 h high-Al group during exposure, and those surviving until release died during the first 3.6 km of the marine migration. Physiological stress and mortality were not only a result of the Al-concentrations, but also dependent on exposure duration, as shown by results from the 48 h high-Al group. Elevated mortality was not recorded in freshwater or after entering the sea for this group, which highly contrasts to the 100% mortality in the 90 h high-Al group, despite both groups having similarly high gill-Al levels. The low-Al group showed a 20% higher mortality compared to the control group during the first 10 km of the marine migration, but during the next 28 km, mortality rates did not differ. Hence, post-smolts surviving the first 10 km subsequently showed no differences in mortality compared to controls. At least one third of the mortality in both the low-Al and control groups were due to predation by marine fishes, indicating that the proximate cause for elevated mortality due to Al-exposure may have been predation. Migration speeds over 3.6,9.6 or 37.1 km from the release site was not affected by Al-exposure.