Recovery of Atlantic salmon smolts following aluminum exposure defined by changes in blood physiology and seawater tolerance (original) (raw)
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Estuarine, Coastal and Shelf Science, 2013
Salmo salar acidification acid precipitation aluminium smolt and post-smolt migration telemetry Regional index terms: Europe Norway Møre and Romsdal County Romsdalsfjord a b s t r a c t Short-term Al-exposure and moderate acidification increased initial marine mortality in migrating postsmolts, 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 5.88e5.98) was investigated during the first 37 km of the marine migration. Smolts were tagged with acoustic tags and exposed to low (28.3 AE 4.6 mg l À1 labile Al, 90 h) or high (48.5 AE 6.4 mg l À1 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 þ , K þ -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.
Exposure to moderate acid water and aluminum reduces Atlantic salmon post-smolt survival
Aquaculture, 2007
Acidification is acknowledged as the cause for extinction or catch reductions in numerous Atlantic salmon (Salmo salar L.) populations in Norway. In freshwater, labile (cationic/inorganic) forms of Al (LAl) accumulate in fish gills, where high concentrations result in mortality due to respiratory and ionoregulatory dysfunction. At lower concentrations, Al may still have population effects by inhibiting gill Na + ,K + -ATPase activity, thereby reducing hypoosmoregulatory capacity and marine survival. Over the years 1999 to 2003 we exposed groups of 1150 to 1200 one-year old hatchery reared, Carlin tagged Atlantic salmon smolts of the Imsa strain (South-Western Norway) to moderately acidified water (pH 5.8; 5-15 μg LAl L − 1 ) from 3 (short term exposure) to 60 (long term exposure) days. Fish exposed to Lake Imsa water (pH N 6.5 and b 5 μg LAl L − 1 ) acted as controls. Control fish had gill-Al concentrations in the range of 5 to 10 μg Al g − 1 gill dry weight (dw), while Al-exposed fish had gill-Al concentrations exceeding 20 μg Al g − 1 gill dw prior to seawater release. The physiological responses measured as plasma Cl − and glucose were related to the LAl concentration in water and to the accumulation of Al onto the gills. Gill Na + ,K + -ATPase activity was depressed in all groups having N 25 μg Al g − 1 gill dw. Following exposure, the smolts were released into River Imsa to monitor downstream migration and ocean return rates. Acid exposed smolts migrated out of the river together with controls. Adult return rates were reduced by 20 to 50% in all Al-exposed groups relative to the control groups, although marine growth was unaffected. The results suggest that even moderately and/or episodically acidified rivers containing 5-15 μg LAl L − 1 can cause substantial reductions in returns of Atlantic salmon.
Aquatic Toxicology, 2010
Na + , K +-ATPase (NKA) is involved, through its role as a major driving force for electrochemical gradients, in a range of transmembrane transport processes. Maintenance of homeostasis in anadromous salmonids requires modulation of several gill ion secretory proteins as part of the preparatory adaptation and acclimation to marine life. Atlantic salmon smolts were exposed to combinations of low pH and inorganic aluminum (acid/Al i) in freshwater (FW) and were then transferred to seawater (SW) for studies of postsmolt performance. Gill mRNA levels of four NKA-␣ isoforms (␣1a, ␣1b, ␣1c and ␣3) of the catalytic NKA subunit and NKA enzyme activity were measured. Moderate acid/Al treatment (MOD, pH 5.9 ± 0.3, 15 ± 9 g l −1 Al i) prevented the FW preparatory increase in NKA activity observed in control (CON, pH 6.9 ± 0.1, 8 ± 3 g l −1 Al i) smolts, while high acid/Al treatment (SEV, pH 5.6 ± 0.2, 30 ± 7 g l −1 Al i) caused a rapid and persistent reduction in NKA activity. Correspondingly, a 3.3-fold increase in plasma glucose levels in the SEV groups concurrent with a decrease in plasma chloride levels suggest that acid/Al exposed fish were stressed and experienced problems maintaining ion homeostasis. Gill NKA activities in acid/Al exposed groups were re-established after 28 days in SW. Both long (9 days) and short-term (2.5 days) treatments had significant impact on isoform-specific Na + , K +-ATPase ␣-subunit mRNA abundance in the FW period. Acid/Al exposed groups lacked the preparatory increases in all NKA-␣ isoform mRNA levels seen in the CON group, except for ␣1a. In contrast to the other isoforms measured, ␣1a mRNA abundance decreased sharply upon SW transfer, supporting the hypothesis of isozyme shifting as a mechanism of altering the gill from an ion absorbing to an ion excreting tissue during smoltification and SW exposure. Adult return rates to the Imsa river were significantly reduced both in short-term (78% of controls) and long-term (55% of controls) acid/Al exposures, emphasising the physiological and ecological consequences of acid/Al exposure during smoltification.
Water, Air, and Soil Pollution, 1986
Physiological stress, measured as changes in plasma chloride, and mortality were measured on different year-classes of landlocked and migratory Atlantic salmon, two strains of brown trout, and brook trout, in a flow-through system with acidic Al-rich soft water. The oldest year-classes of salmon were smolts. Water from Lake Byglandsfjord (pH = 5.9), was enriched with inorganic AI (as AICI3) ~nd H2SO 4 to pH = 5.1, total AI = 225 ug L-I, and labile AI = 135 ug L-~. As a reference, lake water was limed by means of a shellsan~ filter to pH = 6.2, increasing Ca-concentration from 1.0 to 1.5 mg L-~. During the 83 hr experiment, neither mortality nor physiological stress occurred in any species or year-class in the limed water. In the acid water, no mortality occurred on any stage of brown trout or brook trout. Among the migratory and landlocked salmon, however, 5% of the alevins died after 49 and 70 hr, respectively. All smolts of both the landlocked and the migratory salmon died after 83 and 35 hr, respectively, the co~responding loss rate of plasma chloride was-0.76 and-1.26 meq CI hr-~. Brook trout, however, increased plasma ion concentration during the experimental period, and hence showed no stress.
Water, Air, and Soil Pollution, 1988
The respiratory, acid-base, and ionoregulatory responses of juvenile rainbow trout (Salmo gairdneri) were monitored during exposure of the fish in the laboratory to inorganic A1 (2.8 rtM) over the pH range 4.0 to 6.5. Responses to A1 were most severe at pH 6.1 and 4.5, mortality being primarily due to asphyxia at pH 6.1 and to electrolyte loss at pH 4.5. Competition between the H+-ion and A1 for binding at the gill surface is offered as an explanation for the decreased toxicity of A1 at pH 4.0, one which is compatible with the free-ion toxicity model that has been developed for other metals. The physiologically distinct response of S. gairdneri to A1 at pH 6.1 is less amenable to unambiguous interpretation. If a mixed ligand hydroxo-At complex is incorporated in the free-ion model, and if it is assumed that the two A1 species, [A1-L-gill] and [HO-A1-L-giU], provoke distinct toxicological responses, then a bimodal toxicological response to A1 is indeed predicted. An alternative explanation of the apparent toxic action of A1 at pH 6.1, i.e., at pH values close to that of minimum AI solubility, is the precipitation of solid AI(OH)3 at the gill surface, i.e., a 'physical' effect rather than a biochemical one.
Marine Chemistry, 2003
Acute mortality of Atlantic salmon has been described from fjord-based fish farms in Western Norway. Mortality is often related to snowmelt and heavy rainfall in the catchment areas during the winter. Increased freshwater runoff reduces the surface water salinity from >20 to < 10, while water temperature is reduced from 8 to 3 jC. Recent studies have suggested that aluminium transported by acid rivers to the fjords during these episodes can be the cause for mortality. During the present study, we documented an increased deposition of aluminium (Al) on gills of Atlantic salmon (from < 10 to >200 Ag g À 1 dry weight). The increases in gill Al were related to increased discharge episodes where acidic, Al-rich freshwater elevated the surface water concentrations of Al from < 20 to >70 Ag Al l À 1. Increased mobility of reactive Al (Al a) and increased Al accumulation on gills during flood episodes was the probable cause of the massive salmon mortality.
Sensitivity of early-life-stage golden trout to low pH and elevated aluminum
Environmental Toxicology and Chemistry, 1993
Early-life-stage golden trout (Oncorhynchus uguubonitu uguubonitu) were exposed to acid and A1 to examine the response and determine the sensitivity of a western, alpine salmonid to conditions simulating an episodic pH depression. Freshly fertilized eggs, alevins, and swim-up larvae were exposed for 7 d to one of 12 combinations of pH and Al, and surviving fish were held to 40 d post-hatch to determine the effect of exposure on subsequent survival and recovery. Golden trout are sensitive to conditions simulating episodic acidification events typically observed in the field.
Canadian Journal of Fisheries and Aquatic Sciences, 1996
Smolts from several stocks of Atlantic salmon were released in the estuaries of, and 5 km upstream in, an acid river and a neighbouring limed river in southern Norway. There was good agreement between recapture rates of released smolts and physiological effects and mortality of fish retained over the same period in floating cages at the different release sites. Of the smolts released upstream in the acid river, scarcely any were recaptured as adults. The smolts retained in the cages in this river suffered from severe osmoregulatory failure and high mortality within a few hours. Gill Na + ,K +-ATPase activities were significantly reduced. Exposure for a few hours to the acid river impaired the seawater tolerance of the fish. The results suggest that simple physiological challenge tests of smolts after exposure to the water in which they are to be released may be a useful tool for predicting survival after release, and may help decide when and where smolts should be released. Résumé : Dans le sud de la Norvège, des smolts de plusieurs stocks de saumon atlantique ont été relâchés dans l'estuaire et à 5 km en amont d'un cours d'eau acidifié et d'un cours d'eau chaulé avoisinant. On a noté une bonne concordance entre le taux de recapture des smolts libérés et les effets physiologiques et la mortalité des poissons gardés, pendant la même période, dans des cages flottantes aux différents sites de lâchers. Parmi les smolts libérés en amont dans le cours d'eau acidifié, très peu ont été recapturés à l'état adulte. Chez les smolts gardés en cages dans ce cours d'eau, en moins de quelques heures, on a observé une défaillance grave de l'osmorégulation et un taux de mortalité élevé. L'activité de la Na + ,K +-ATPase des branchies a été nettement réduite. Une exposition de quelques heures à l'eau acidifiée de ce cours d'eau a rendu les poissons moins tolérants à l'eau de mer. D'après les résultats, des tests de provocation physiologique simples appliqués aux smolts après une exposition à l'eau dans laquelle ils seront relâchés peuvent être un moyen utile pour prévoir la survie après le lâcher, et choisir le moment et le lieu du lâcher. [Traduit par la Rédaction]