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

Artikel i vetenskaplig tidskrift
Författare E. B. Thorstad
I. Uglem
B. Finstad
F. Kroglund
Ingibjörg Einarsdottir
T. Kristensen
O. Diserud
P. Arechavala-Lopez
I. Mayer
A. Moore
R. Nilsen
Björn Thrandur Björnsson
F. Okland
Publicerad i Estuarine Coastal and Shelf Science
Volym 124
Sidor 34-43
ISSN 0272-7714
Publiceringsår 2013
Publicerad vid Institutionen för biologi och miljövetenskap
Sidor 34-43
Språk en
Länkar dx.doi.org/10.1016/j.ecss.2013.03.0...
Ämnesord Salmo salar, acidification, acid precipitation, aluminium, smolt and post-smolt migration, telemetry, growth-hormone endocrinology, short-term acid, salar smolts, seawater, tolerance, episodic acidification, environmental-factors, migratory, behavior, fjord migration, osmotic-stress, mixing zones
Ämneskategorier Marin ekologi

Sammanfattning

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 ± 4.6 μg l−1 labile Al, 90 h) or high (48.5 ± 6.4 μg l−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.

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