scholarly journals Physiological and molecular ontogeny of branchial and extra-branchial urea excretion in posthatch rainbow trout (Oncorhynchus mykiss)

2016 ◽  
Vol 310 (3) ◽  
pp. R305-R312 ◽  
Author(s):  
Alex M. Zimmer ◽  
Chris M. Wood

All teleost fish produce ammonia as a metabolic waste product. In embryos, ammonia excretion is limited by the chorion, and fish must detoxify ammonia by synthesizing urea via the ornithine urea cycle (OUC). Although urea is produced by embryos and larvae, urea excretion (Jurea) is typically low until yolk sac absorption, increasing thereafter. The aim of this study was to determine the physiological and molecular characteristics of Jurea by posthatch rainbow trout ( Oncorhynchus mykiss). Following hatch, whole body urea concentration decreased over time, while Jurea increased following yolk sac absorption. From 12 to 40 days posthatch (dph), extra-branchial routes of excretion accounted for the majority of Jurea, while the gills became the dominant site for Jurea only after 55 dph. This represents the most delayed branchial ontogeny of any process studied to date. Urea transporter (UT) gene expression in the gills and skin increased over development, consistent with increases in branchial and extra-branchial Jurea. Following exposure to 25 mmol/l urea, the accumulation and subsequent elimination of exogenous urea was much greater at 55 dph than 12 dph, consistent with increased UT expression. Notably, UT gene expression in the gills of 55 dph larvae increased in response to high urea. In summary, there is a clear increase in urea transport capacity over posthatch development, despite a decrease in OUC activity.

1998 ◽  
Vol 201 (22) ◽  
pp. 3123-3133 ◽  
Author(s):  
JD Kieffer ◽  
D Alsop ◽  
CM Wood

Instantaneous fuel usage at 5 degreesC or 15 degreesC was assessed by measurement of rates of O2 consumption (O2), CO2 excretion (CO2) and nitrogenous waste excretion (nitrogen =ammonia-N + urea-N) in juvenile rainbow trout (Oncorhynchus mykiss) at rest and during swimming at 45 % and 75 % of aerobic capacity (Ucrit). After 2 weeks of training at approximately 1 body length s-1 (BL s-1), critical swimming speeds (approximately 3.0 BL s-1) and whole-body energy stores (total protein, lipids and carbohydrates) were identical in fish acclimated to 5 degreesC or 15 degreesC. O2 and CO2 increased with swimming speed at both temperatures and were higher at 15 degreesC than at 5 degreesC at all speeds, but the overall Q10 values (1.23-1.48) were low in these long-term (6 weeks) acclimated fish. The respiratory quotient (CO2/O2, approximately 0.85) was independent of both temperature and swimming speed. In contrast to O2 and CO2, the rate of ammonia excretion was independent of swimming speed, but more strongly influenced by temperature (Q10 1. 4-2.8). Urea excretion accounted for 15-20 % of nitrogen, was unaffected by swimming speed and showed a tendency (P<0.07) to be positively influenced by temperature at one speed only (45 % Ucrit). Nitrogen quotients (NQ nitrogen/O2) were generally higher in warm-acclimated fish, remaining independent of swimming speed at 15 degreesC (0.08), but decreased from about 0.08 at rest to 0.04 during swimming at 5 degreesC. Instantaneous aerobic fuel use calculations based on standard respirometric theory showed that both acclimation temperature and swimming speed markedly influenced the relative and absolute use of carbohydrates, lipids and proteins by trout. At rest, cold-acclimated trout used similar proportions of carbohydrates and lipids and only 27 % protein. During swimming, protein use decreased to 15 % at both speeds while the relative contributions of both lipid and carbohydrate increased (to more than 40 %). On an absolute basis, carbohydrate was the most important fuel for fish swimming at 5 degreesC. In contrast, resting fish acclimated to 15 degreesC utilized 55 % lipid, 30 % protein and only 15 % carbohydrate. However, as swimming speed increased, the relative contribution of carbohydrate increased to 25 %, while the protein contribution remained unchanged at approximately 30 %, and lipid use decreased slightly (to 45 %). On an absolute basis, lipid remained the most important fuel in fish swimming at 15 degreesC. These results support the concept that lipids are a major fuel of aerobic exercise in fish, but demonstrate that the contribution of protein oxidation is much smaller than commonly believed, while that of carbohydrate oxidation is much larger, especially at higher swimming speeds and colder temperature.


2000 ◽  
Vol 203 (20) ◽  
pp. 3199-3207 ◽  
Author(s):  
C.M. Pilley ◽  
P.A. Wright

We tested the hypothesis that urea transport in rainbow trout (Oncorhynchus mykiss) embryos is dependent, in part, on a bidirectional urea-transport protein. Acute exposure to phloretin and urea analogs [acetamide, thiourea, 1,(4-nitrophenyl)-2-thiourea] reversibly inhibited urea excretion from the embryos to the external water. Unidirectional urea influx was inhibited by acetamide and thiourea, with IC(50) values of 0.04 and 0.05 mmol l(−1), respectively. Influx of urea from the external water to the embryo tended to saturate at elevated external urea concentrations (V(max)=10.50 nmol g(−1) h(−1); K(m)=2 mmol l(−1)). At very high urea concentrations (20 mmol l(−1)), however, a second, non-saturable component was apparent. These results indicate that urea excretion in trout embryos is dependent, in part, on a phloretin-sensitive facilitated urea transporter similar to that reported in mammalian inner medullary collecting ducts and elasmobranch kidney.


1991 ◽  
Vol 48 (4) ◽  
pp. 583-590 ◽  
Author(s):  
Paul W. Webb

Routine swimming encompasses all volitional motions of fish. It is usually assumed to be quasi-steady, i.e. routine swimming is mechanically equivalent to steady swimming. Routine swimming of rainbow trout, Oncorhynchus mykiss, was dominated by unsteady motions of linear and centripetal (angular) acceleration. Constant-speed swimming was rare. Mean speeds and acceleration rates were small. Tail-beat frequencies were nevertheless strongly correlated with mean swimming speed, but increased more rapidly with increasing speed in routine swimming than in steady swimming. Tail-beat amplitudes and propulsive wavelengths were similar to values seen in steady swimming. The composition of routine swimming and analysis of the force balance showed that routine swimming was not quasi-steady. Therefore, forces and rates of working should be estimated from a complete description of whole-body deformation. This is impractical. Drag dominated resistance in routine swimming, such that average thrust (= resistance) may be computed from mean speed and/or averaged kinematic variables for the trailing edge with a correction factor of approximately 3. Analysis of routine swimming may permit comparisons among a wider range of vertebrates than possible with commonly used methods.


2019 ◽  
Vol 86 ◽  
pp. 764-771 ◽  
Author(s):  
Patrick C. Blaufuss ◽  
T. Gibson Gaylord ◽  
Wendy M. Sealey ◽  
Madison S. Powell

1994 ◽  
Vol 51 (2) ◽  
pp. 372-380 ◽  
Author(s):  
M. G. Rankin ◽  
D. G. Dixon

The 144-h LC50 (95% fiducial limits) of arsenite for 4.5-g rainbow trout (Oncorhynchus mykiss) was 18.5 (17.9–19.1) mg∙L−1. In a pair-fed growth study which exposed trout to 0.0, 0.76, 2.48, or 9.64 mg arsenite∙L−1 over 17 wk, growth was significantly reduced (by 55%) only at 9.64 mg∙L−1. The reduction was attributable to both reduced appetite (primarily) and direct metabolic impact (marginally). Fish at 9.64 mg∙L−1 suffered 10% mortality, usually associated with necrotic erosion of the mandibular and olfactory regions of the head. All fish exposed to 9.64 mg∙L−1 showed inflammation of the gallbladder wall, a lesion absent at lower exposure concentrations. There were no arsenite impacts on hepato- and splenosomatic index, hematocrit, hemoglobin, total plasma lipid, cholesterol, and protein or brain concentrations of norepinephrine, dopamine, and serotonin. Exposure to 0.0, 0.76, 2.48, and 9.64 mg arsenite∙L−1 for 26 wk resulted in mean (SE) equilibrium whole-body As concentrations of 0.3 (0.02), 0.2 (0.02), 0.4 (0.10), and 1.7 (0.40) μg As∙g wet weight−1, respectively, No depuration below these concentrations occurred during a 12-d period in arsenite-free water. The threshold of chronic toxicity was estimated to be 4.9 mg∙L−1.


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