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• W2030656914 abstract "The elevated rearing densities necessary for profitable aquaculture operations are generally related to declining water quality, which may affect fish welfare and juvenile quality (Conte, 2004; Bjornsson and Olafsdottir, 2006;North et al., 2006; Roncarati et al., 2006). The motivation for this research was to provide information on the potential effects of chronic exposure to ammonia on juvenile Atlantic cod (Gadus morhua) raised in recirculating aquaculture systems (RAS) since ammonia build up is frequently reported in such systems (Webb and Gatlin, 2003). Ammonia can significantly reduce growth, and can adversely affect different organs and functions (Linton et al., 1997; Foss et al., 2003a,b, 2004; Lemarié et al., 2004). There is a general lack of data on ammonia toxicity affecting marine fish. Chronic exposure limits for ammonia in saltwater was considered to be 0.035 mg l−1 as un-ionized ammonia (U.S., 1989). Based on more recent toxicity tests, Boardman et al. (2004) suggested that this value be increased to 0.081 mg l−1. In commercial systems, concentrations ranging from 0.2 to 2 mg l−1 will stress the fish whereas concentration above 2 mg l−1 will result in death (Caldwell, 1998). The one cell-layer design of the branchial tissue makes it particularly susceptible to environmental stressors or damage, and gills are, therefore, the primary target organs for the action of environmental pollutants or conditions (Larsen et al., 1997; Gagnon and Holdway, 1999; Lionetto et al., 2000; Le François and Blier, 2003). The predominant route of entry of unionized ammonia is the gills (Boardman et al., 2004). In response to elevated external or internal ammonia concentrations, effective ammonia detoxification or an excretion system are essential to maintain cellular functions, and to keep cellular and body fluid ammonia levels within an acceptable range (Weihrauch et al., 2004). The branchial cells of teleosts contain a number of enzymes and associated mechanisms that are involved in ammonia homeostasis (Alam and Frankel, 2006). The process involving Na+K+ATPase activity involves the exchange of sodium from the water for ammonia in the fish (Salama et al., 1999; Shrimpton and McCormick, 1999). In fish, branchial gas exchange and oxidative metabolism are disturbed by excess ammonia causing gill damage, excessive mucus production (Smart, 1976; Wilkie, 1997) or osmoregulation imbalance (Rebelo et al., 2000; Lease et al., 2003). This experiment was designed to determine whether ammonia in the external environment could alter the rate of activity of Na+K+ATPase and associated metabolic enzymes at the gill level. Aspartate aminotransferase (AAT) activity reflects the capacity of the tissue to oxidise amino acids for energy production or to mobilise amino acids for protein synthesis. Citrate synthase (CS) is a mitochondrial enzyme indicative of the aerobic capacity of the tissue and chloride cell number. Finally, lactate dehydrogenase (LDH) activity is an indicator of the tissue glycolytic capacity and of lactate oxidation capacity (Le François and Blier, 2003). We propose that chronic exposure to sublethal levels of toxic ammonia will modify the functionality of the branchial tissue, leading to detectable adjustments in enzyme activity level involving Na+K+ATPase, LDH, CS and AAT. This study was conducted using biological material originating from an earlier experiment previously published by Foss et al. (2004) on the effect of chronic exposure to ammonia on growth of juvenile Atlantic cod. Cod eggs originated from wild caught broodstock from Northern Norway and incubated at 4–5°C. After hatching, fish were transferred to start-feeding units and given formulated feed Dan-ex 1362 (Dana Feed, Denmark). Afterwards, the fish were randomly assigned to four tanks (250-L). Initial mean weight of the fish was 16.7 ± 3.4 g and did not differ among tank units. Temperature and pH for the growth trials were measured daily in all experimental groups, and averaged 13°C ±0.7°C and 8.04 ± 0.01 respectively (n = 96). Replicated treatment groups were gradually acclimatised to the experimental UIA-N concentrations 0.0005 (control) and 0.17 mg l−1. The required UIA-N concentrations were obtained by adding a concentrated solution of NH4Cl by two electromagnetic metering pumps to the aerated header tanks. Total ammonia nitrogen (TA-N, mg l−1) was measured daily with an ammonia gas sensing combination electrode (Thermo Orion, Model 95-12; Waltham, MA, USA) connected to an expandable ion analyser (Thermo Orion, EA™ 920). Corrections for pH with low-ionic strength buffers were performed according to Whitfield (1974), and percentage UIA-N was calculated using the equation of Johannsson and Wedborg (1980), which gives the UIA-N/TA-N ratio as a function of pH, temperature and salinity. For further details refer to Foss et al. (2004). The experimental design of the experiment involved the exposure of juvenile cod to three concentrations of ammonia. In the study of Foss et al. (2004) from which our samples originated, a gradual acclimatory response to UIA-N concentrations was reported so it was decided to measure the enzymatic activity in the extreme groups only (control and 0.17 mg l−1 UIA-N, for a total of 40 fish). At day 96, following a 24 h fasting period, 20 fish per group were anaesthetised with metacaine (0.2 g l−1) and bled, and the second gill arches on the left side were dissected and quickly frozen at −80°C in SEI buffer. Gill samples were thawed on ice, carefully blotted dry and the gill filaments separated from the gill arch. The filaments were rapidly weighed and homogenized in 19 volumes of ice-cold SEID (0.1% deoxycholic acid in SEI buffer) with a glass potter for three 10-s periods. Between each period, samples were kept on ice for 1 min. Homogenates were centrifuged at 5000 g for 30 s at 4°C and the supernatant was used for analysis. The assays conditions and homogenate dilutions were optimized. Dilutions were made using Imidazole buffer (50 mm, pH 7.5) for CS (1 : 70) and LDH (1 : 200) analysis. Enzymatic activity was measured at 15°C using a Lambda 11 UV/VIS spectrophotometer equipped with a thermostated cell holder (Perkin Elmer Inc.). Details on the enzymatic assays for Na+K+ATPase (EC 3.6.1.37) can be found in McCormick and Bern (1989), for AAT (EC 2.6.1.1) see Lemieux et al. (2003), and for CS (EC 2.3.3.1) and LDH (EC 1.1.1.27) see Le François et al. (2004). Enzymatic activities were expressed as U mg−1 protein and U g−1 fish. Total protein content was determined using the bicinchoninic acid method (Smith et al., 1985). Assays were conducted at 15°C and protein analyses were carried out at room temperature. All assays were run in duplicate. Enzymatic activities were compared between the two groups by the Student t-test procedure using the Systat 10.2 computer software (SPSS Inc., San Jose, CA, USA). A significance level (α) of 0.05 was used. The mean activities of Na+K+ATPase, AAT, CS and LDH, as well as protein content of the control and 0.17 UIA-N are presented in Table 1 Following the 96-day exposures, we neither detected any significant effect of ammonia exposition on the activity level of all enzymes measured nor on the protein content. The main excretory mechanisms for ammonia detoxification in fish rely on the high activity of the gills and the kidney. It is when detoxification capacities of the fish are surpassed that ammonia will become toxic (Smutna et al., 2002). Recent evidence that ammonia exposure is responsible for enzymatic adjustments at the gill level are numerous. ArasHisar et al. (2004), working on rainbow trout (Oncorhynchus mykiss), reported diminution of gill carbonic anhydrase activity following exposure to ammonia. Alam and Frankel (2006), working on silver perch (Bidyanus bidyanus), reported increases in Na+K+ATPase with increasing ammonia concentrations (0–5 mg l−1). Das et al. (2004) reported increased LDH and aspartate aminotransferase (AAT) activities with increased concentration of ammonia (from 5–25 mg l−1) in the gill of Cirrhinus mrigala. Our results indicate that over a period of 96 days, gill LDH, CS, AAT and Na+K+ATPase activity in juvenile cod were unaffected by the range of sub-lethal external ammonia concentrations used in this experiment (0–0.17 mg l−1). These concentrations are likely to be found in commercial juvenile cod recirculating production systems. In the same experimental fish, Foss et al. (2004) observed significantly lower weight, length and condition factor in the fish exposed to the highest UIA-N concentration after 96 days of experimentation (Table 2). However, they observed an acclimatory growth response to the elevated ammonia concentrations in the rearing environment from day 56. Growth rates were significantly altered by ammonia levels from day 1 until day 56 (reduction of growth rate in the order of 23% in the group exposed to the highest concentration). Conversely, at the end of the experiment (period-day 57–96), growth rates were no longer significantly different among the different exposure levels (mean SGR: 1.1–1.3% per day). Similarly, Lemarié et al. (2004) observed that after 55 days, the growth performances of seabass juveniles (Dicentrarchus labrax) were no longer affected by UIA-N concentrations of 0.24–0.26 mg l−1. But ammonia concentration had a marked effect on plasma K+ and urea-N content. At the same sampling period, Foss et al. (2004) reported plasma K+ values significantly higher at the highest concentration compared to the other experimental groups (mean value of 4.10 ± 0.4 and 3.43 ± 0.4 mm, respectively), whereas plasma urea-N content was significantly reduced in all exposed groups compared to the control (mean value of 1.49 ± 0.3 and 1.03 ± 0.6 mm, respectively) indicating that urea excretion rates increased in juvenile cod when exposed to increased ambient UIA-N. Our results clearly demonstrate that juvenile cod are resistant to some degree of degradation of the ambient rearing water condition such as low levels of ammonia build-up in the RAS. However, the threshold limit for reduced growth in Atlantic cod juveniles of 0.06 mg l−1 UIA-N proposed by Foss et al. (2004) is comparatively low compared to the values of 0.11–0.18 mg l−1 reported for turbot (Rasmussen and Korsgaard, 1996; Person-Le Ruyet et al., 1997), or UIA-N higher than 0.13 mg l−1 for spotted wolffish (Foss et al., 2003a). The authors gratefully acknowledge the participation of Dr. Unn Sørum (NIFA, Norway) for the sampling operations and Dr. Laura C. Halfyard (Marine Institute, MUN, NL Canada) for reviewing the manuscript. This work was funded by the FQRNT to NLF." @default.
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• W2030656914 date "2007-10-17" @default.
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• W2030656914 title "Gill metabolic and osmoregulatory responses of juvenile Atlantic cod (Gadus morhua) to chronic ammonia exposure" @default.
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