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

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.

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.


1986 ◽  
Vol 43 (8) ◽  
pp. 1488-1496 ◽  
Author(s):  
Darrel Jon Laurén ◽  
D. G. McDonald

Juvenile rainbow trout were exposed to 25–400 μg copper∙L−1 for 24 h. Water hardness, pH, and alkalinity were varied independently at a constant [Na+]. Net and unidirectional sodium fluxes were measured in hard and soft, low-alkalinity water and in hard, high-alkalinity water at neutral pH and pH 5.0. In low alkalinity water, Na+ uptake (Jin) was inhibited at copper concentrations as low as 25 μg∙L−1, and sodium efflux (Jout) was stimulated above 100 μg∙L−1. High-alkalinity water significantly reduced the effects of copper on Jin and Jout, but there was no significant effect of increasing water hardness. The effects of pH 5.0 and copper were additive from 25 to 100 μg∙L−1, but a pure copper effect was found from 200 to 400 μg∙L−1. Fish died when they had lost about 50–55% of their exchangeable Na+ pool. Water hardness and alkalinity had no effect on the apparent uptake of copper, but copper uptake was reduced by about 50% at pH 5.0.


1988 ◽  
Vol 22 (1) ◽  
pp. 69-77 ◽  
Author(s):  
Dorthy A. Klaprat ◽  
S. B. Brown ◽  
Toshiaki J. Hara

1973 ◽  
Vol 30 (8) ◽  
pp. 1047-1052 ◽  
Author(s):  
L. E. Olson ◽  
L. L. Marking

The lampricide TFM (3-trifluoromethyl-4-nitrophenol) was tested against the following life stages of rainbow trout (Salmo gairdneri): green eggs, eyed eggs, sac fry, swim-up fry, fry, and fingerlings in four water hardnesses (12, 44, 170, and 320 mg/liter as CaCO3). The eyed-egg stage was one of the most resistant stages tested, and the sac-fry stage was one of the least resistant. Increased water hardness decreases toxicity to all stages. The LC50’s range from 0.532 mg/liter to 40.0 mg/liter depending upon life stage, water hardness, and duration of exposure. The margin of safety for coexisting species exposed to TFM ranges from 3.2 to 4.1 in natural waters. The margin of safety for early life stages of rainbow trout and larval lamprey under controlled laboratory conditions ranges from 4.2 to 12.2. Therefore, all six early life stages of rainbow trout are safe in minimum lampricidal concentrations of TFM.


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.


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.


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

1985 ◽  
Vol 42 (4) ◽  
pp. 731-736 ◽  
Author(s):  
R. W. Bradley ◽  
J. B. Sprague

The acute lethality of dissolved zinc to rainbow trout (Salmo gairdneri) was significantly increased at higher pH and lower hardness levels. Changes in pH from 5.5 to 7.0 increased zinc toxicity by factors of 2 to 5, depending on total hardness levels. A decrease in hardness from 386 to 31 mg CaCO3/L increased zinc toxicity by more than an order of magnitude at both pH levels. These effects of pH and hardness were not caused by changes in the chemical speciation of zinc. An increase in carbonate alkalinity from 8.4 to 24 mg CaCO3/L at pH 7.0 did not significantly alter zinc toxicity at either hardness level. Thus, carbonate alkalinity is not an important factor at or below pH 7.0. At low hardness, dissolved zinc was more than 10 times as toxic at pH 9.0 as at pH 5.5. Two competing mechanisms appear to operate: as the pH rises, dissolved zinc becomes increasingly toxic, but at higher pH levels it is increasingly replaced by zinc precipitate, which is of very low toxicity to fish.


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