Effects of freshwater hyperoxia and hypercapnia and their influences on subsequent seawater transfer in Atlantic salmon (<i>Salmo salar</i>) smolts

Abstract

Atlantic salmon (Salmo salar) presmolts, smolts, and postsmolts compensate for a respiratory acidosis associated with 96 h of exposure to hyperoxia (100% O 2 ; hO 2 ), hypercapnia (2% CO 2 and 98% air; hCO 2 ), and combined hO 2 /hCO 2 in freshwater (FW) by increasing strong ion difference, predominantly through a reduction in plasma [Cl - ] (presumably via branchial Cl - /HCO 3 - exchange). In smolts, compensation during hO 2 or hCO 2 occurred within 24 h, whereas that in combined hO 2 /hCO 2 was much slower, resulting in 33% mortality by 96 h. FW hO 2 and combined hO 2 /hCO 2 appeared to impair gill function, likely through oxidative cell damage. This resulted in reduced hypoosmoregulatory ability following subsequent transfer to seawater (SW), as indicated by changes in plasma ion levels, osmolality, and muscle water content, resulting in considerable mortalities. Interestingly, FW hCO 2 appeared to enhance hypoosmoregulatory ability during subsequent SW transfer. Smolts are often transported from FW to a subsequent SW release site, and these data indicate that care should be taken to minimize the degree of hyperoxia experienced by the smolts. Hypercapnia, which results from metabolic CO 2 production and inadequate water aeration, does not impair SW transfer, provided it does not occur in conjunction with hyperoxia.