Physiological disturbances in rainbow trout (Salmo gairdneri) during acid and aluminum exposures in soft water of two calcium concentrations

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.

1976 ◽  
Vol 11 (1) ◽  
pp. 34-45 ◽  
Author(s):  
S.E. Hrudey ◽  
G.A. Sergy ◽  
T. Thackeray

Abstract Acute toxicity testing using rainbow trout (Salmo gairdneri Richardson) was conducted on two wastewater streams from an oil sands extraction and upgrading plant. The main effluent stream from the upgrading plant was non-acutely toxic in flow-through bioassay while the construction drainage from the tailings pond dyke was acutely lethal in static bioassay with an extrapolated LC50 of 11% (by volume). With no obvious toxicant present, trace organic analysis was undertaken based on the high indeterminate organic carbon content of the sample. Analysis by GC-MS of the sample was able to identify four compounds: 2, 6-di-tert-butyl-p-cresol, (BHT); di-n-butyl phthalate, (DBP); bis (2-ethylhexyl) adipate, (BEHA); and bis (2-ethylhexyl) phthalate, (BEHP). Toxicity testing of the compounds required the evaluation of various schemes for the preparation of the test mixtures. Direct emulsion of the test compounds in water was ultimately adopted. Ninety-six hour static bioassays with rainbow trout indicated LC50 values of 540 mg/l for BEHP, 3 mg/l for BHT, 1.2 mg/l for DBP, and an approximate range of 54–110 mg/l for BEHA. Loss of emulsified components from the test mixture during the bioassays suggested that calculated LC50 values likely underestimate the actual toxicity of the compounds. The contribution by BEHA and BEHP to the whole effluent toxicity was likely minor while BHT and DBP indicated sufficient acute lethal toxicity to warrant further consideration. The feasibility of trace organic analysis and component toxicity testing as a means for conducting longer term research on oil sands wastewaters was demonstrated.


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.


1986 ◽  
Vol 125 (1) ◽  
pp. 347-359 ◽  
Author(s):  
A. P. Farrell ◽  
C. L. Milligan

Myocardial intracellular pH was measured in a perfused rainbow trout, Salmo gairdneri, with DMO (5,5-dimethyl-2,4-oxazlidinedione), to test the hypothesis that catecholamines promote active regulation of myocardial pH in order to protect contractility during a respiratory acidosis comparable to that observed after exercise. Under control conditions (extracellular pH = 8.0; PCO2 = 2 Torr), myocardial pH was 7.53 +/− 0.01 (N = 5). Acidosis (extracellular pH = 7.45; PCO2 = 8.6 Torr) reduced contractility, mechanical efficiency and intracellular pH (7.25 +/− 0.04), but did not affect myocardial O2 consumption. The addition of 0.5 mumol l-1 adrenaline during extracellular acidosis prevented the loss of contractility, restored mechanical efficiency, but did not change intracellular pH significantly. Thus, adrenaline enabled cardiac contractility to recover, without intracellular pH regulation, possibly by modulation of sarcolemmal calcium changes. The absence of a myocardial acidosis after exercise in vivo is discussed with respect to possible intracellular pH regulation via lactate uptake and metabolism.


1974 ◽  
Vol 31 (10) ◽  
pp. 1653-1655 ◽  
Author(s):  
Rosemarie C. Russo ◽  
Charlie E. Smith ◽  
Robert V. Thurston

Flow-through bioassays on the acute toxicity of nitrite to rainbow trout (Salmo gairdneri) of four different sizes (2–235 g) showed median lethal concentration (LC50) values for 4 days ranging from 0.19 to 0.39 mg/liter NO2–N. For 12-g rainbow trout the asymptotic LC50 was 0.14–0.15 mg/liter NO2–N after 8 days.


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.


1983 ◽  
Vol 40 (6) ◽  
pp. 824-828 ◽  
Author(s):  
D. W. Rodgers ◽  
F. W. H. Beamish

We measured the efficiency of uptake of waterborne methylmercury relative to oxygen consumption for rainbow trout, Salmo gairdneri, in hard or soft water and during exposure to sublethal concentrations of mercuric chloride or zinc sulphate. The relative efficiency of methylmercury uptake in soft water was more than double that measured in hard water. When mercuric chloride was added with waterborne methylmercury, uptake efficiency was further increased, with similar values obtained in hard and soft water. In contrast, addition of zinc sulphate decreased the relative efficiency of methylmercury uptake. Water quality thus significantly affects the accumulation of waterborne methylmercury by fish. In particular, calcium-dependent changes in gill permeability may explain elevated methylmercury residues observed in fish from lakes of low alkalinity and pH.


1974 ◽  
Vol 12 (2) ◽  
pp. 193-201 ◽  
Author(s):  
James R. Sinley ◽  
John P. Goettl ◽  
Patrick H. Davies

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.


1981 ◽  
Vol 38 (8) ◽  
pp. 983-988 ◽  
Author(s):  
Robert V. Thurston ◽  
Glenn R. Phillips ◽  
Rosemarie C. Russo ◽  
Susan M. Hinkins

The median lethal concentration (LC50) of aqueous ammonia at reduced dissolved oxygen (D.O.) concentrations was tested in acute toxicity tests with rainbow trout (Salmo gairdneri) fingerlings. Fifteen 96-h flow-through tests were conducted over the D.O. range 2.6–8.6 mg/L, the former concentration being the lowest at which control fish survived. There was a positive linear correlation between LC50 (milligrams per litre un-ionized ammonia) and D.O. over the entire D.O. range tested; ammonia toxicity increased as D.O. decreased. Ammonia LC50 values were also computed for 12, 24, 48, and 72 h; the correlation with D.O. was greater the shorter the time period.Key words: ammonia toxicity, dissolved oxygen, rainbow trout, Salmo gairdneri


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