The effects of zinc on rainbow trout (Salmo gairdneri) in hard and soft water

1974 ◽  
Vol 12 (2) ◽  
pp. 193-201 ◽  
Author(s):  
James R. Sinley ◽  
John P. Goettl ◽  
Patrick H. Davies
Keyword(s):  
Rainbow Trout ◽  
Soft Water ◽  
Salmo Gairdneri

Zinc Influx Across the Isolated, Perfused Head Preparation of the Rainbow Trout (Salmo gairdneri) in Hard and Soft Water

1988 ◽  
Vol 45 (12) ◽  
pp. 2206-2215 ◽  
Author(s):  
Douglas J. Spry ◽  
Chris M. Wood
Keyword(s):  
Steady State ◽  
Rainbow Trout ◽  
Hard Water ◽  
Soft Water ◽  
Chloride Cells ◽  
Salmo Gairdneri ◽  
First Order ◽  
Scanning Electron Micrography ◽  
Primary Substrate ◽  
Stimulation Of

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.

The Influence of Calcium on the Physiological Responses of the Rainbow Trout, Salmo Gairdneri, to Low Environmental pH

1980 ◽  
Vol 88 (1) ◽  
pp. 109-132
Author(s):  
D. G. McDONALD ◽  
H. HŌBE ◽  
C. M. WOOD
Keyword(s):  
Rainbow Trout ◽  
Calcium Concentration ◽  
Physiological Responses ◽  
Hard Water ◽  
Low Ph ◽  
Soft Water ◽  
Salmo Gairdneri ◽  
Minor Depression ◽  
Regulatory Failure ◽  
A Minor

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.

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
Keyword(s):  
Rainbow Trout ◽  
Water System ◽  
Respiratory Acidosis ◽  
Carbon Dioxide Tension ◽  
Soft Water ◽  
Cell Swelling ◽  
Salmo Gairdneri ◽  
Flow Through ◽  
Respiratory Gases ◽  
Respiratory Toxicity

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.

Water Quality Modifies Uptake of Waterborne Methylmercury by Rainbow Trout, Salmo gairdneri

1983 ◽  
Vol 40 (6) ◽  
pp. 824-828 ◽  
Author(s):  
D. W. Rodgers ◽  
F. W. H. Beamish
Keyword(s):  
Water Quality ◽  
Rainbow Trout ◽  
Mercuric Chloride ◽  
Relative Efficiency ◽  
Zinc Sulphate ◽  
Hard Water ◽  
Soft Water ◽  
Salmo Gairdneri ◽  
Calcium Dependent ◽  
Sublethal Concentrations

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.

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
Keyword(s):  
Rainbow Trout ◽  
Ammonia Excretion ◽  
Blood Chemistry ◽  
Soft Water ◽  
Acid Exposure ◽  
Salmo Gairdneri ◽  
Plasma Parameters ◽  
Water Effects ◽  
Net Flux

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.

Acute and chronic toxicity of lead to rainbow trout salmo gairdneri, in hard and soft water

1976 ◽  
Vol 10 (3) ◽  
pp. 199-206 ◽  
Author(s):  
P.H. Davies ◽  
J.P. Goettl ◽  
J.R. Sinley ◽  
N.F. Smith
Keyword(s):  
Rainbow Trout ◽  
Chronic Toxicity ◽  
Soft Water ◽  
Salmo Gairdneri ◽  
Acute And Chronic Toxicity

Toxicity of environmental acid to the rainbow trout: interactions of water hardness, acid type, and exercise

1981 ◽  
Vol 59 (8) ◽  
pp. 1518-1526 ◽  
Author(s):  
Mark S. Graham ◽  
Chris M. Wood
Keyword(s):  
Rainbow Trout ◽  
Water Hardness ◽  
Low Ph ◽  
Soft Water ◽  
Activity Level ◽  
Salmo Gairdneri ◽  
Physiological Mechanisms ◽  
Acid Type ◽  
Influence Of Water ◽  
Acid Toxicity

Classical 7-day lethality tests were used to establish the influence of water hardness [Formula: see text], acid type (HCl versus H2SO4) and activity level (rest versus exhaustive exercise) on acid toxicity to fingerling rainbow trout (Salmo gairdneri) at 15 °C. Seven-day mean lethal concentration (LC50) pH's ranged from 4.1 to 4.5. Hardness reduced H2SO4 toxicity at all pH levels during both rest and exericise, but reduced HCl toxicity only at very low pH levels. Hardness increased HCl toxicity at pH's > 3.8. H2SO4 was generally less toxic than HCl, except at pH's > 3.8 in soft water. Exchaustive exercise markedly potentiated H2SO4 toxicity in both hard and soft water except at very low pH levels. Below pH = 4.4–4.6, critical swimming speed declined linearly by about 4% per 0.1 pH unit. Possible physiological mechanisms responsible for these modifying influences and their ecological significance are discussed.

Ion Flux Rates, Acid–Base Status, and Blood Gases in Rainbow Trout, Salmo gairdneri, Exposed to Toxic Zinc in Natural Soft Water

1985 ◽  
Vol 42 (8) ◽  
pp. 1332-1341 ◽  
Author(s):  
Douglas J. Spry ◽  
Chris M. Wood
Keyword(s):  
Rainbow Trout ◽  
Metabolic Acidosis ◽  
Ammonia Excretion ◽  
Blood Gases ◽  
Soft Water ◽  
Salmo Gairdneri ◽  
Acid Base ◽  
Flux Measurements ◽  
Water Base ◽  
Toxic Concentrations

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].

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