The effect of low pH and aluminum on the olfactory organ of rainbow trout, Salmo gairdneri

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


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.


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.


1963 ◽  
Vol 41 (7) ◽  
pp. 1233-1236 ◽  
Author(s):  
Wolfgang Pfeiffer

The surface area of the olfactory epithelium of Pacific salmon (Oncorhynchus spp.) is about 40% of the retinal area in 10- to 60-cm fish. In salmon up to 12 cm, growth of the olfactory epithelium occurs by increase in the size and number of the olfactory lamellae, in larger fish only by increase in the size of the lamellae. In adult salmon these primary lamellae develop secondary lamellae which can be seen in the unfixed tissue. The secondary lamellae, up to 10 in each primary lamella, consist only of a non-sensory mucous epithelium. Similar secondary lamellae were found in large rainbow trout (Salmo gairdneri) and seem to be characteristic of salmonids.


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.


1991 ◽  
Vol 69 (8) ◽  
pp. 2239-2245 ◽  
Author(s):  
D. Saucier ◽  
L. Astic ◽  
P. Rioux ◽  
F. Godinot

Sequential histopathological changes related to a long-term sublethal copper exposure were investigated in the olfactory organ of rainbow trout, Oncorhynchus mykiss (formerly Salmo gairdneri Richardson, 1836). Fish were continuously exposed to an average copper level of 22 μg/L from the 14th day after fertilization (embryo group) or from hatching (alevin group) for a period of 41 and 37 weeks, respectively. A control group was reared in well water. Specimens of the exposed and the control groups were sacrificed every month for histological examination by light microscopy. Morphological alterations were identical in both embryo and alevin groups and appeared at the same posthatching periods. The first change, noted from the 8th week posthatch, was an increase in goblet cells. Epithelial lesions, which looked like patches of necrotic tissue randomly distributed in the olfactory sheet, were reported from the 28th week posthatch. From the 32nd week, cellular shrinkage related to degeneration and necrosis of individual cells led to a pattern of loose epithelium in many olfactory areas. These sequential histopathological changes suggest an initial increased mucus production which, however, does not appear effective enough to ensure long-term protection of the olfactory rosette. Stopping the copper exposure led to some morphological restoration. Ten weeks after copper removal, a few epithelial lesions and shrinkage were still noted. The delay between morphological and functional recoveries supports the concept of an anatomical redundancy of the epithelium-to-bulb connections.


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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