The effects of soft-water acclimation on gill structure in the rainbow trout Oncorhynchus mykiss

1996 ◽  
Vol 285 (1) ◽  
pp. 75-82 ◽  
Author(s):  
Anna Maria Greco ◽  
James C. Fenwick ◽  
Steve F. Perry
1996 ◽  
Vol 69 (6) ◽  
pp. 1419-1441 ◽  
Author(s):  
S. F. Perry ◽  
S. G. Reid ◽  
E. Wankiewicz ◽  
V. Iyer ◽  
K. M. Gilmour

1991 ◽  
Vol 48 (10) ◽  
pp. 2028-2033 ◽  
Author(s):  
J. Freda ◽  
D. A. Sanchez ◽  
H. L. Bergman

The objective of this study was to investigate possible sites for Na+ loss in fish exposed to low environmental pH. In rainbow trout (Oncorhynchus mykiss) exposed to pH 4.0 for 1 h, a net loss of Na+ was stimulated, and changes in gill structure occurred. In addition to epithelial lifting and necrosis in the gills of acid-exposed fish, tight junctions between pavement epithelial cells and chloride cells decreased in length by 25% whereas tight junctions between adjacent pavement cells did not significantly change. In a second experiment where fish were moved from pH 4.0 or 3.5 water to pH 6.5 water, we observed that Na+ loss declined immediately and approached control levels. The reversible nature of the stimulation of Na+ loss indicates that the site of Na+ loss in the fish gill can be reversibly opened and closed, which is consistent with the known properties of tight junctions. We hypothesize that the opening of tight junctions contributes to the loss of plasma electrolytes at low environmental pH. However, the relative magnitude of electrolyte loss through the tight junctions remains unknown.


1994 ◽  
Vol 51 (3) ◽  
pp. 527-535 ◽  
Author(s):  
Rod W. Wilson ◽  
Harold L. Bergman ◽  
Chris M. Wood

Juvenile rainbow trout (Oncorhynchus mykiss, 5–13 g) became acclimated (i.e., increased their resistance to lethal Al levels, 162 μg∙L−1, pH 5.2) after only 5 d when exposed to sublethal AS (38 μg∙L−1) in acidified soft water (Na+ = 85, Ca2+ = 28 μEq∙L−1, pH 5.2). Acclimation was associated with reduced ionoregulatory and respiratory disturbances during lethal Al challenge and was maintained for at least 34 d. Acclimation was relatively specific to Al because no consistently improved resistance to lethal Cu (32 μg∙L−1, pH 5.2) was observed. Exposure to sublethal acid alone (pH 5.2) did not result in acclimation to lethal [H+] (pH 4.0) and caused a pronounced reduction in whole-body Na+ and Cl−. Sublethal acid + Al resulted in a more rapid loss of ions than sublethal acid alone over the first 10 d, but both groups subsequently recovered ionoregulatory status after 34 d. Exposure to sublethal acid alone had a negligible effect on feeding or growth. However, growth was impaired by 29% in Al-exposed trout, primarily the result of reduced appetite during the first 10 d. Decreased growth must be considered one of the costs of acclimation during chronic sublethal exposure to Al.


1999 ◽  
Vol 77 (7) ◽  
pp. 1035-1047 ◽  
Author(s):  
Jeff G Richards ◽  
Richard C Playle

We report that an elevated aqueous calcium (Ca) concentration protects against acute respiratory and osmoregulatory action due to exposure to a combination of cadmium (Cd) and copper (Cu) in rainbow trout (Oncorhynchus mykiss), but does not protect against longer term ionoregulatory disruption. Trout exposed to 0.18 µM Cd and 0.80 µM Cu in soft water (40 µM Ca, 440 µM Na, pH 6.6) experienced a 60-torr decrease in arterial oxygen tension, a 5.5 mM increase in blood lactate concentration, and severe haemoconcentration as indicated by a 1.4-fold decrease in mean cell haemoglobin concentration, all of which occurred within 24 h. The addition of Ca to soft water (to reach 910 µM Ca, added as CaCl2; 430 µM Na, pH 6.8) eliminated these severe effects and slowed Cd uptake by the gills, plasma, and liver of trout, probably through competition for binding at gill Ca channels, but Ca did not affect Cu uptake by the gills or its entry into the plasma. Associated with slower Cd accumulation and unchanged Cu accumulation in the plasma were slow decreases in plasma concentrations of Na, Cl, and Ca, which were prevented initially by adding Ca to the water. Modelling using a modified aqueous chemistry computer program, MINEQL+, and previously published gill binding constants accurately simulated the initial (18 h) accumulation of Cd and Cu by trout gills and thus predicted acute toxicity, but our model did not adequately simulate the physiological mechanisms of Cd accumulation by trout gills over longer exposures up to 130 h.


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