Abstract

Chronic exposure (up to 42 d) of juvenile brook trout (Salvelinus fontinalis) to sublethal aluminum at pH 5.2 resulted in a damage/repair acclimation phenomenon. The damage developed rapidly (within 24 h), was centered at the gills, and was characterized by substantial accumulation of Al, a corresponding reduction of gill sialic acid content (a measure of gill mucus), and inhibition of branchial Na+ transport. The corresponding internal effects of this initial damage were losses of electrolytes, hemoconcentration, and impaired tissue O2 delivery (as indicated by elevated lactate). Repair was characterized by progressive reduction of gill Al, restoration of sialic acid content, recovery of Na+ transport, and reduction in hemoconcentration and lactate levels. Accompanying the recovery was progressive development (by day 10 onwards) of increased resistance (i.e. acclimation) to acutely lethal Al. This acclimation was characterized by a reduction in both the rate of mortality and in the magnitude of physiological disturbances relative to control (i.e. Al naive) fish. The increased short-term resistance translated to greatly improved survivorship and correspondingly diminished physiological impact in the face of chronically elevated Al levels (2 wk at < 300 μg Al/L). The acclimation process clearly resulted from specific changes at the gills.

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