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

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.

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.


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.


1973 ◽  
Vol 30 (4) ◽  
pp. 485-492 ◽  
Author(s):  
J. C. MacLeod ◽  
E. Pessah

Mercury toxicity in rainbow trout fingerlings was related to temperature and chemical formulation of the mercury. At 10 C, the 24-hr TLm concentration (median tolerance limit) for mercuric chloride (HgCl2) was approximately 30 times that for phenyl mercuric acetate (PMA). The 96-hr TLm values for mercuric chloride at 5, 10, and 20 C were 0.40, 0.28, and 0.22 mg Hg/liter. The velocity of mortality, (V = reciprocal of time to death in hours), was linearly related to temperature. For a mercuric chloride concentration of 0.5 mg Hg/liter, V =.002 +.0023t, where t = temperature in centigrade degrees.Temperature also affected accumulation rate of mercury in the fish muscle. At 5, 10, and 20 C a mercuric chloride concentration of 0.1 mg Hg/liter in the water produced biological magnification factors (conc. in fish ÷ conc. in water) of 4, 10, and 22 ×, respectively, PMA produced higher magnification factors of 80–100 × at 10 C.Active metabolic rate, though increased by higher temperatures, was depressed by mercuric chloride, and higher temperatures augmented the depressant effect.


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.


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

1978 ◽  
Vol 35 (1) ◽  
pp. 35-42 ◽  
Author(s):  
L. S. McCarty ◽  
J. A. C. Henry ◽  
A. H. Houston

Variations in cadmium form and concentration and in selected water quality parameters (pH, dissolved oxygen, total hardness, total alkalinity, conductivity) were monitored during static bioassays conducted with relatively soft (~ 20 mg/L as CaCO3) and hard (~ 140 mg/L as CaCO3) waters. Cadmium concentrations were reasonably stable in soft water, and with the exception of total hardness, water quality was not greatly altered during assay. Cumulative mortality curves were of a simple sigmoidal type and readily analyzed by conventional procedures. LC50 values of 2.76, 2.13, and 1.78 mg Cd/L were estimated on the basis of 48-, 96-, and 240-h periods of observation. During hard-water trials there were transient increases in the amount of particulate cadmium present and sharp decreases in total cadmium levels. Several parameters (pH, total alkalinity, conductivity) exhibited transient and/or sustained variations of a cadmium concentration-dependent type. Mortality curves were typically biphasic. The extent of first-phase mortality was significantly correlated with the magnitude of the initial pH decline and the amount of cadmium present in centrifugable form. Conventional procedures did not result in rectification of 240-h cumulative mortality curves, and the 240-h LC50 value (40.2 mg Cd/L) is considered to be inherently less precise than those obtained on the basis of 48- and 96-h periods of observation (46.9, 46.8 mg Cd/L). Key words: goldfish, Carassius auratus, cadmium toxicity, hard water, soft water, mortality


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.


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