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.
|Title of host publication||CAN. J. ZOOL.|
|Number of pages||11|
|State||Published - May 19 1989|
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