Long-Term Sublethal Acid Exposure in Rainbow Trout (Salmo gairdneri) in Soft Water: Effects on Ion Exchanges and Blood Chemistry

1988 ◽  
Vol 45 (8) ◽  
pp. 1387-1398 ◽  
Author(s):  
Céline Audet ◽  
R. Stephen Munger ◽  
Chris M. Wood

Long-term sublethal acid exposure (3 mo, pH 4.8) in adult rainbow trout (Salmo gairdneri) acclimated to artificial soft water (Ca2+ = 50, Na+ = 50, Cl− = 100 μeq∙L−1) caused transient net fosses of Na+ and Cl−. Net flux rates of both ions were returned to control levels after 30–52 d of acid exposure through a new equilibrium between unidirectional influx and efflux, where both were lower than control rates. K+ balance remained negative and Ca2+ balance at zero throughout the exposure. No changes in net acidic equivalent flux occurred, indicating the absence of acid–base disturbance, but ammonia excretion increased over time. Muscle K+, Na+, and Cl− fell and Ca2+ increased. Plasma Na+, Cl−, and osmolality decreased, while plasma protein, glucose, and blood hemoglobin increased during the first few weeks of acid exposure. Plasma K+ and Ca2+ did not change. General stabilization of plasma parameters occurred in concert with the stabilization of Na+ and Cl− flux rates, but no recovery to control levels was observed for any of them. We conclude that despite this stabilization at a new steady state, rainbow trout were physiologically affected in a deleterious manner by chronic sublethal acid exposure in soft water.


1988 ◽  
Vol 45 (8) ◽  
pp. 1399-1405 ◽  
Author(s):  
Céline Audet ◽  
Chris M. Wood

Adult rainbow trout (Salmo gairdneri) previously exposed to long-term sublethal acid stress (3 mo, pH 4.8) in artificial soft water (Ca2+ = 50, Na+ = 50, Cl− = 100 μeq∙L−1) were challenged with acute severe acid exposure (4.5–5 h, pH 4.0). Their response in terms of whole-body ionic exchanges and blood chemistry was compared with that of trout that had no previous history of acid exposure (naive fish). Acute pH 4.0 exposure caused significant ionoregulatory disturbances in both acid-preexposed and naive fish. Rates of net Na+ and Cl− body losses were twice as large in acid-preexposed fish as in naive fish. The two groups showed similar slight net uptake of acidic equivalents. However, the dynamics of acid–base exchange differed, especially with regard to ammonia excretion which was elevated in acid-preexposed fish and inhibited in naive fish. A larger decrease in plasma Na+, red blood cell swelling, and the maintenance of high-stress indicators (elevated plasma glucose and ammonia excretion, depressed osmolality) confirmed that osmo-ionoregulatory disturbances were more intense in acid-preexposed fish than in naive fish. Thus, long-term sublethal acid exposure did not improve but rather significantly decreased the ability of rainbow trout to respond to more severe acid stress. We conclude that acclimation to acid stress does not occur in rainbow trout.



1985 ◽  
Vol 42 (8) ◽  
pp. 1332-1341 ◽  
Author(s):  
Douglas J. Spry ◽  
Chris M. Wood

Exposure to 0.8 mg Zn2+/L in natural soft water for up to 72 h was toxic to rainbow trout, Salmo gairdneri, causing an acid–base disturbance and net branchial ion losses. Mean arterial pH fell from 7.78 to 7.58. Both [Formula: see text] and lactate rose, indicating a mixed respiratory and metabolic acidosis, despite maintenance of high [Formula: see text] Net branchial uptake of Na+ and Cl− became a net loss immediately following exposure to Zn2+, and this continued during 60 h of exposure. Net K+ loss was exacerbated, and net Ca2+ uptake was abolished. Unidirectional flux measurements with 22Na+ and 36Cl− indicated an increased efflux immediately following zinc exposure. Both influx and efflux of Na+ and Cl− were stimulated after 48–60 h in Zn2+. Both net branchial ammonia excretion and net branchial uptake of acidic equivalents from the water (=base loss) were greatly stimulated, the latter contributing to metabolic acidosis. Kidney function, as measured by urine flow rate and excretion of ammonia, acidic equivalents, Na+, Cl−, K+, and Zn2+, was relatively insensitive to the effects of zinc. The only renal component to be affected was Ca2+ excretion, which decreased during a single flux period, possibly in response to the reduced entry of Ca2+ at the gill. We conclude that toxic concentrations of zinc are capable of altering gill function so as to cause ionoregulatory and acid–base disturbances without disturbance of [Formula: see text].



1984 ◽  
Vol 32 (1) ◽  
pp. 732-741 ◽  
Author(s):  
A. A. Oladimeji ◽  
S. U. Qadri ◽  
A. S. W. deFreitas


1989 ◽  
Vol 6 (4) ◽  
pp. 221-229 ◽  
Author(s):  
Per-Erik Olsson ◽  
Åke Larsson ◽  
Amund Maage ◽  
Carl Haux ◽  
Keith Bonham ◽  
...  


1979 ◽  
Vol 36 (6) ◽  
pp. 621-629 ◽  
Author(s):  
Betty A. Hillaby ◽  
David J. Randall

Acute ammonia toxicity in rainbow trout (Salmo gairdneri) was studied by intraarterial injection of NH4Cl and NH4HCO3. Hydrogen ion and total ammonia concentrations were measured in blood sampled from the dorsal aorta both before and after injection. Although injection of NH4HCO3 increased arterial blood pH, and injection of NH4Cl decreased arterial blood pH, the same dose of each was required to kill fish. While the un-ionized form of ammonia in water has been shown to be toxic, in the blood either the ionized form or the total ammonia load is toxic to fish. Ammonia levels were measured in pre- and postbranchial blood. Mean values were not significantly different, but paired values indicated a fall in blood ammonia due to excretion across the gills. There appears to be a more rapid excretion of ammonia following NH4HCO3 infusions, which result in higher un-ionized ammonia levels in blood compared with those following NH4Cl infusions. These results are consistent with the hypothesis that ammonia is excreted in the un-ionized form. Key words: un-ionized ammonia, ionized ammonia, gills, pH, blood



1980 ◽  
Vol 37 (9) ◽  
pp. 1421-1425 ◽  
Author(s):  
Larry J. Paulson

Ammonia excretion by brook trout (Salvelinus fontinalis) and rainbow trout (Salmo gairdneri) was measured in relation to nitrogen consumption, body weight (15–154 g for rainbow trout and 50–360 g for brook trout), and temperature (11.2–21.0 °C) under laboratory conditions. Four natural diets, collected from Castle Lake, California, and a commercial pellet diet were fed to the trout in gelatin capsules at feeding rates from 2.5 to 5% body weight∙d−1. Nitrogen consumption was the most important factor influencing ammonia excretion, followed by body weight and temperature. Testing the models with an independent data set revealed good agreement between measured and predicted rates of excretion. The models seem to estimate adequately ammonia excretion by trout in both natural and artificial aquatic systems.Key words: models, ammonia excretion, nitrogen consumption, body weight, temperature, multiple regression, rainbow trout, brook trout



1983 ◽  
Vol 40 (4) ◽  
pp. 420-425 ◽  
Author(s):  
W. Roscoe Miller III ◽  
Albert C. Hendricks ◽  
John Cairns Jr.

Wytheville strain rainbow trout (Salmo gairdneri) were used in an 11-mo study designed to establish normal ranges for several hematological and blood chemistry characteristics. Two nonparametric techniques, percentile estimation and tolerance interval, were used and produced comparable ranges to those based on the Gaussian distribution. Serum glucose levels appeared to coincide with the condition of the gonads; low glucose levels corresponded with approximate spawning times at the hatchery. Total serum protein and gonadal condition were similarly related. High variability of the serum enzymes LDH and SGOT was partially explained by a positive linear relationship between enzyme activity and acclimation temperatures. In addition to physiological significance, determination of normal ranges for rainbow trout has promise in diagnosis of pathological, disease, and toxicant-induced stresses.



1988 ◽  
Vol 45 (12) ◽  
pp. 2206-2215 ◽  
Author(s):  
Douglas J. Spry ◽  
Chris M. Wood

At a waterborne [Zn] of 1.9 mg∙L−1 in hard water (~1 mmol Ca∙L−1), Zn influx across an isolated, saline-perfused head preparation of rainbow trout (Salmo gairdneri) was about 1.5 nmol∙kg−1∙h−1 through the lamellar pathway and about 1 nmol∙kg−1∙h−1 through the filamental route. Flux rates came rapidly to steady state in both pathways. Trout preexposed to artificial soft water (~0.05 mmol Ca∙L−1) for 5 d showed differential stimulation of flux rates to about 42 and 5 nmol Zn∙kg−1∙h−1 through the lamellar and filamental pathways, respectively. Under these conditions, steady-state fluxes across the lamellae did not occur until 15–20 min after the start of perfusion. Preparations from hardwater-acclimated trout tested in soft water gave typical hardwater fluxes showing that these changes in influx were not simply due to acute exposure of the gill surface to low waterborne [Ca]. Influxes in softwater trout, studied over [Zn] from 0.4 to 7.5 mg Zn∙L−1, revealed a saturable, first-order uptake with apparent Jmax and Km of 150 nequiv∙kg−1∙h−1 and 1.5 mg Zn∙L−1 (23 μmol∙L−1), respectively. Because the apparent Km is in the toxic range, Zn is clearly not the primary substrate. Scanning electron micrography revealed hypertrophy and increased apical exposure of chloride cells; this stimulation, coupled with the increase in Zn influx, suggests that chloride cells may be the site of entry of Zn across the gill.



1980 ◽  
Vol 88 (1) ◽  
pp. 109-132
Author(s):  
D. G. McDONALD ◽  
H. HŌBE ◽  
C. M. WOOD

The physiological responses of 1- to 2-year-old rainbow trout to low pH are dependent on the environmental calcium concentration. Trout, maintained for 5 days in moderately hard water ([Ca2+] = 1·6–2·7 m-equiv/1) at a mean pH of 4·3, developed a major blood acidosis but exhibited only a minor depression in plasma ion levels. In acidified soft water ([Ca2+] = 0·3 m-equiv/1), only a minor acidosis occurred, but plasma ion levels fell and there were substantially greater mortalities. Lethal bioassays performed on fingerling trout over a range of pH levels (3·0–4·8) revealed an important influence of external [Ca2+] on resistance to acid exposure. Terminal physiological measurements on adult fish succumbing to low pH in soft water indicate the singular importance of iono-regulatory failure as the toxic mechanism of action under these circumstances.



1989 ◽  
Vol 67 (2) ◽  
pp. 314-324 ◽  
Author(s):  
Richard C. Playle ◽  
Greg G. Goss ◽  
Chris M. Wood

Rainbow trout (Salmo gairdneri) fitted with dorsal aortic cannulae were exposed in a flow-through soft water system to three acidities (pH 5.2, 4.8, or 4.4) and two concentrations of Ca (45 or 410 μequiv.∙L−1), in the presence (105 μg∙L−1) or absence of Al. Blood was sampled for respiratory gases, ions, metabolites, and hematology before and at 4, 18, 28, 42, and 66 h exposure. Two toxic mechanisms of Al and acidity were seen: (i) ionoregulatory toxicity, which was caused by Al at pH 5.2 and 4.8 and by acidity at pH 4.4, and (ii) respiratory toxicity, which was caused solely by Al, and was greatest at higher pH. Ionoregulatory toxicity involved decreases in plasma Na+ and Cl−, red cell swelling, and hemoconcentration. Respiratory toxicity involved reduced blood oxygen tension, elevated blood carbon dioxide tension, and increases in blood lactate. Blood acidosis was a combination of respiratory acidosis (due to CO2 accumulation in the blood; higher pH exposures) and metabolic acidosis (probably due to differential Na+ and Cl− loss into the external, acidic environment; lower pH exposures). Higher water Ca reduced ionoregulatory disturbances due to acidity alone but not those due to Al at higher pH. Higher water Ca also reduced respiratory disturbances at lower pH but not at higher pH. The results are discussed with reference to the chemistry of Al and changes in the gill epithelium associated with acid and Al exposure.



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