The toxicity of zinc sulphate to rainbow trout in very hard water

1974 ◽  
Vol 8 (6) ◽  
pp. 389-391 ◽  
Author(s):  
J.F. de L.G. Solbé
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.


1982 ◽  
Vol 60 (9) ◽  
pp. 2079-2084 ◽  
Author(s):  
G. F. Wagner ◽  
B. A. McKeown

An experiment was conducted to determine if the hyperglycemia that is observed in zinc-stressed fish is also accompanied by changes in the levels of plasma insulin and liver glycogen. Juvenile rainbow trout were exposed to three concentrations of zinc sulphate along with a control group over 31 days. Plasma glucose levels were monitored in each group over the course of the experiment. The group demonstrating the most acute and sustained hyperglycemia (0.352 ppm zinc) was then analyzed along with the controls for changes in plasma insulin (using a teleost insulin radioimmunoassay) and liver glycogen levels. Significant depressions in plasma insulin and liver glycogen levels were observed in the zinc-exposed fish when compared with the controls. These changes are discussed with respect to possible influences of epinephrine, which is elevated in stressed fish, and (or) a direct effect of zinc metal on the pancreatic beta cells.


1970 ◽  
Vol 52 (2) ◽  
pp. 481-494
Author(s):  
J. F. SKIDMORE

1. Damage to the gill epithelium occurs when hatched fish are killed rapidly by solutions of zinc sulphate. 2. The rate of routine oxygen uptake by lightly sedated, quiet, rainbow trout did not alter on exposure to a rapidly toxic solution of zinc sulphate. However, oxygen utilization decreased seven-fold, gill ventilation volume increased six-fold, heart rate was halved, coughing rate increased 18-fold and the Po2 of dorsal aortic blood declined. 3. Unsedated trout usually struggled on exposure to zinc. The survival time of struggling fish was reduced and oxygen uptake increased, but other physiological changes were similar to those in quiet fish. 4. The respiratory changes in poisoned trout were generally similar to changes observed earlier in the same fish under hypoxia. 5. The osmotic concentration and the concentrations of sodium, potassium, calcium, magnesium and zinc in blood were largely unaffected by immobilization in zinc sulphate solution. Trout survived a four-fold increase in zinc concentration in the blood by injection. 6. The results suggest that epithelial damage decreased the permeability of the gills to oxygen, and did not increase their permeability to cations. Zinc was not a rapid internal poison. Death was probably caused by tissue hypoxia, when maximum gill ventilation was no longer sufficient to supply the oxygen needs of the fish.


1972 ◽  
Vol 6 (3) ◽  
pp. 217-IN4 ◽  
Author(s):  
J.F. Skidmore ◽  
P.W.A. Tovell

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.


1976 ◽  
Vol 33 (6) ◽  
pp. 1335-1342 ◽  
Author(s):  
Patrick F. Lett ◽  
G. J. Farmer ◽  
F. W. H. Beamish

The influence of sublethal concentrations of total copper on the appetite, growth, and proximate body composition of rainbow trout (Salmo gairdneri) held in hard water (365 mg/liter) was measured over a 40-day interval. The initial response of trout exposed to concentrations of copper ranging from 0.0 to 0.3 mg/liter (the 96-h LC50 was 0.25–0.68) was the cessation of feeding. Thereafter, food intake gradually returned to amounts observed for control fish, the rate of return of appetite being dependent on copper concentration and ration level. Growth rate of trout exposed to copper (0.075–0.225 mg/liter) and fed rations of either 0.25 or 1.5% dry food wt/wet fish wt per day was initially depressed but approached values observed for control fish near the end of the 40-day interval. During this period, lipid, protein, and moisture offish exposed to copper did not change significantly. Initial growth retardation was not attributable to the inability of copper-exposed fish to digest their daily rations. Results are discussed in terms of the ability offish to adapt to stress imposed by sublethal concentrations of heavy metals.


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