Effects of Cadmium, Copper, and Low pH on Ion Fluxes in the Rainbow Trout, Salmo gairdneri

1988 ◽  
Vol 45 (2) ◽  
pp. 244-253 ◽  
Author(s):  
S. D. Reid ◽  
D. G. McDonald

Adult and juvenile rainbow trout, Salmo gairdneri, acclimated to high and low water Ca levels were statically exposed to equimolor concentrations (~ 6.5 μmolùL−1) of Cd or Cu at circumneutral pH or pH 4.8 either alone or in metal/H+ combinations for 24 h. Unidirectional fluxes of Ca2+ and Na+ were measured by means of radiotracers and terminal blood samples were drawn for analysis of Ca2+ and Na+. Plasma Ca2+ was found not to be a reliable indicator of disturbances in branchial Ca2+ fluxes. Cadmium specifically inhibited Ca2+ influx, while having no effect on Ca2+ efflux and only minor effects on Na+ fluxes. The inhibition of Ca2+ influx by Cd was modulated by water Ca2+ content. Copper altered net Na+ flux and plasma Na+ in trout, while having only a transient effect on Ca2+ homeostasis, the effects of Cu on the net Na+ fluxes of trout were not modulated by either water Ca2+ or pH. Hydrogen ion perturbed Ca2+ dynamics predominantly by stimulating Ca2+ efflux, while reducing influx only slightly. Exposure to elevated H+ (pH 4.8) had no significant effect on net Na+ balance over the 24-h period. These data indicate significant differences in the toxic mechanisms of three metals with similar ligand binding chemistry.

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

1979 ◽  
Vol 36 (6) ◽  
pp. 621-629 ◽  
Author(s):  
Betty A. Hillaby ◽  
David J. Randall

Acute ammonia toxicity in rainbow trout (Salmo gairdneri) was studied by intraarterial injection of NH4Cl and NH4HCO3. Hydrogen ion and total ammonia concentrations were measured in blood sampled from the dorsal aorta both before and after injection. Although injection of NH4HCO3 increased arterial blood pH, and injection of NH4Cl decreased arterial blood pH, the same dose of each was required to kill fish. While the un-ionized form of ammonia in water has been shown to be toxic, in the blood either the ionized form or the total ammonia load is toxic to fish. Ammonia levels were measured in pre- and postbranchial blood. Mean values were not significantly different, but paired values indicated a fall in blood ammonia due to excretion across the gills. There appears to be a more rapid excretion of ammonia following NH4HCO3 infusions, which result in higher un-ionized ammonia levels in blood compared with those following NH4Cl infusions. These results are consistent with the hypothesis that ammonia is excreted in the un-ionized form. Key words: un-ionized ammonia, ionized ammonia, gills, pH, blood


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.


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.


1981 ◽  
Vol 93 (1) ◽  
pp. 101-118 ◽  
Author(s):  
D. G. McDONALD ◽  
C.M. WOOD

Rainbow trout were exposed for 4 days to an environmental pH averaging 4.2, an exposure which resulted in a continuous net branchial influx of acid. The influx provoked a progressive depression in blood pH and [HCO3−], virtually complete by 48 h, and a marked increase in renal acid excretion, also complete by 48 h. The increase in the latter was sufficient to remove, at maximum, about half of the protons entering at the gills; those remaining were buffered in body fluids. The low pH exposure also impaired gill ion regulation as indicated by continuous net branchial losses of Na+, Cl− and K+ and by a progressive decline in plasma Na+ and Cl− levels. Evidence is presented which indicates that there was a significant contribution by the intracellular compartment both to the total body ion losses and to the buffering of the body acid load.


1982 ◽  
Vol 99 (1) ◽  
pp. 397-415 ◽  
Author(s):  
C. LOUISE MILLIGAN ◽  
CHRIS M. WOOD

Exposure of adult rainbow trout to low pH (4.0–4.5) for 3 days resulted in progressive increases in heart rate, mean arterial blood pressure and haematocrit. The haematocrit increase resulted from erythrocyte swelling, a reduction in plasma volume and a mobilization of erythrocytes from the spleen. Erythrocyte swelling probably resulted from plasma acidosis and a reduction in plasma ions (McDonald & Wood, 1981). There was an associated redistribution of body water from extracellular to intracellular compartments, but maintenance of total body water content. Erythrocyte mobilization was reflected in an increase in reticulocyte and erythrocyte counts, and a depletion of splenic blood reserves. Haemoconcentration caused large increases in blood viscosity, which contributed to the rise in blood pressure. Pharmacological analysis revealed an adrenergic component to the cardiovascular disturbance. These events are thought to play a key role in the toxic syndrome.


1983 ◽  
Vol 102 (1) ◽  
pp. 123-140 ◽  
Author(s):  
D. G. McDONALD

Exposure of adult rainbow trout to low pH (pH 4.3) in soft water (Ca2+ = 223 μequiv/1) caused a substantial ionic disturbance which arose primarily because of large net losses at the gills. In contrast, renal ion losses were low initially and declined even further because of a pronounced reduction in urine flow. A net influx of H+ occurred across the gills but this was not sufficient to cause a blood acid-base disturbance or a renal response. Although branchial ion and H+ fluxes declined with time, blood ion levels did not return to normal and many of the fish died. Further reduction in water calcium (Ca2+ = 69 μequiv/l) provoked a higher mortality and a more substantial ionic imbalance. These results contrast sharply with the effects on trout of acid exposure in hard water (Ca2+≥ 1600μequiv/l), where net ion losses and mortality are reduced and H+ uptake increased. A preliminary model for the interaction of low pH and calcium is proposed and evidence for adaptation to acid stress and for the origin of acid lethality is discussed.


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