Atlantic salmon (Salmo salar L.) smolts require more than two weeks to recover from acidic water and aluminium exposure.

The detrimental effects of acid rain and aluminium (Al) on salmonids have been extensively studied, yet knowledge about the extent and rate of potential recovery after exposures to acid and Al episodes is limited. Atlantic salmon smolts in freshwater (FW) were exposed for 2 and 7-day episodes (ACID2 and ACID7, respectively) to low pH (5.7±0.2) and inorganic aluminium (Ali; 40±4 μg) and then transferred to good water quality, control water (CW; pH 6.8±0.1; <14±2 μg Ali). Al accumulation on gills after 2 and 7 days of acid/Al exposure was 35.3±14.1 and 26.6±1.8 μg g(-1) dry weight, respectively. These elevated levels decreased 2 days post transfer to CW and remained higher than in control (CON; 5-10 μg Ali) for two weeks. Plasma Na(+) levels in ACID2 and ACID7 smolts decreased to 141±0.8 and 138.6±1.4mM, respectively, and remained significantly lower than CON levels for two weeks post transfer to CW. Similarly, plasma Cl(-) levels in ACID7 smolts (124.3±2.8mM) were significantly lower than in CON, with Cl(-) levels remaining significantly lower in ACID7 (126.2±4.8 mM) and ACID2 (127.6±3.7 mM) than in CON following 9 and 14 days post-transfer to CW, respectively. ACID2 and ACID7 smolts sustained elevated plasma glucose levels post transfer to CW suggesting elevated stress for more than a week following exposure. While gill Na(+), K(+)-ATPase (NKA) activity was only slightly affected in ACID2 and not in ACID7 smolts in FW, acid/Al exposure resulted in a transient decrease in NKA activity following SW exposure in both groups. Acid/Al episodes had limited impact on isoform specific NKA α-subunit mRNA during exposure. However, the transfer of ACID2 and ACID7 smolts to CW showed an increase in NKAα1a mRNA (the FW isoform) and inhibited the up-regulation of NKAα1b (the SW isoform), probably resulting in higher abundance of the enzyme favouring ion uptake. Gill caspase 3B gene transcription did not change in acid/Al treated smolts, indicating no increased apoptosis in gills. ACID2 and ACID7 treatments resulted in lower smolt-related gill transcription of the gene encoding the tight junction protein claudin 10e compared to CON, while the gene encoding claudin 30 showed lower mRNA expression only after 11 days SW exposure in ACID7 fish. Our data suggest that acid/Al conditions affect ion perturbations through a combination of alteration of the preparatory increase in paracellular permeability and negative impact on the SW type NKA α-subunit mRNA transcripts, and raise major concerns regarding the recovery of physiological disruption in smolts following acid/Al exposure. Smolts may require more than two weeks to fully recover from even short moderate episodes of acid/Al exposure. Acid/Al exposure thus probably has greater impact on salmon populations than previously acknowledged.