Adult brook trout (Salvelinus fontinalis) were exposed for up to 11 d to one of a matrix of 18 Al, low pH, and Ca2+ combinations, chosen as representive of acidified softwater environments in the wild. Reduction in water pH led to pH-dependent net losses of Na+ and Cl− exacerbated by the presence of Al in the water and reduced by elevating Ca2+. Any animal losing more than 4% of its total body Na+ over the first 24 h of Al exposure had a greater than 90% likelihood of eventual mortality. Na+ losses arose from inhibition of influx and stimulation of efflux. The inhibition was persistent and pH dependent. Addition of Al to acidified water had a slight further inhibitory effect on Na+ influx and a large stimulatory effect on efflux. The latter was dependent on Al concentration, was the main cause of initial ion losses and mortality, and declined with time in surviving animals. All Al-exposed fish accumulated Al on their gills, but this was apparently mainly surface or subsurface bound, since no internal Al (plasma or liver) could be detected. Nonsurviving fish had substantially higher gill Al levels than survivors.

The relative importance of ionoregulatory and respiratory disturbances in brook trout (Salvelinus fontinalis) under acid/Al stress in soft water is dependent upon water pH and Ca2+ levels. Trout acclimated to Ca2+ = 25 or 400 μequiv/L were fitted with arterial catheters and exposed to acid/Al for 10 d under flow-through conditions. Parameters monitored included pHa, [Formula: see text], [Formula: see text], HCO3−, ΔH+m, Na+, Cl−, K+, Ca2+, protein, lactate, glucose, hemoglobin, and hematocrit. Exposure to pH = 4.8 (no Al) at Ca2+ = 25 μequiv/L caused no mortality and negligible physiological disturbance. Addition of Al (333 μg/L or 12.3 μmol/L) resulted in >80% mortality (LT50 = 39.0 h) preceded by a marked decrease of plasma Na+ and Cl−, a moderate disturbance of blood gases, but no acidosis. At higher Ca2+ (400 μequiv/L), this same exposure (pH = 4.8, Al = 333 μg/L) caused similar mortality (LT50 = 38.5 h) but smaller ionic disturbances, much larger decreases in blood O2, increases in blood CO2, and respiratory acidosis. Exposure to pH = 4.4 (no Al) at Ca2+ = 25 μequiv/L caused 60% mortality (LT50 = 170.0) preceded by marked ionic disturbances and metabolic acidosis, but little change in blood gases. Addition of Al (333 μg/L) increased mortality to >80% (LT50 = 78.2 h) with smaller ionic but greater respiratory disturbances.

Epithelial ion regulation by larval Rana clamitans (developmental stages III to XX) and early stage juveniles (stage XXV) was examined in soft water (Ca2+ = 300 μequiv./L) at circumneutral pH and during exposure to low pH (nominally 4.0). In tadpoles and juveniles, the acute acid exposure initially caused substantial increases in transepithelial net ion losses and in net acid uptake, and a slight inhibition of active ion transport. In tadpoles, these disturbances had largely disappeared by 7 h of acid exposure but they persisted in early stage juveniles with no apparent sign of recovery. Prior acclimation of tadpoles to a sublethal pH (12 days at pH 5.0) did not reduce the ionoregulatory disturbance at pH 4.0 and the acclimated animals were less able to restore those losses at circumneutral pH compared with a control group. It is concluded that larval amphibians show many similarities with fish in ionoregulatory responses to acid exposure including an inability to adapt to low pH, but the magnitude and duration of disturbances are generally less. This suggests that larval amphibians may be more able to resist acid exposure than many acid-intolerant fish species such as the salmonids.

1988. Physioisgical evidence of acclimation to acid/aluminum stress in adult brook trout (SaBve%inus dowtiwalis). 1. Blood composition and net sodium fluxes. Can. 1. Fish. Aquat. Sci. 45: 1587-1 596.Brook trout (SaBveBi wus dowtina%is) adapt to chronic sublethal acid/Al stress. The accompanying acclimation confers greater resistance to short-term increases in Al and acidity. A d~~l t trout were exposed in flowing soft water to eight combinations of pH (6.5, 5.2) X Ca2+ (25, 400 ~equiv/L) X Al (8, 75, 150 p@L = 0, 2.8, 5.6 pmoI/L). After '80 wk, blood sampling by caudal puncture revealed no significant variations in osmo8ality, plasma protein, or hemoglobin and only minor differences (~1 5 % ) in plasma Na+ and CI-. Bvera$l, most electrolytes were higher in fish exposed to higher water Ai and/or CaZ+; only plasma Ca2+ was directly depressed by low pH. Hematoerit was raised by both low pH and elevated Al. When trout naive to both acid and Al were challenged with pH = 4.8, Al = 333 p@L under flow-through conditions, there were large negative whole-body Na+ fluxes and marked depressions of plasma Na+ and Cl-, hemsconcentration, and substantial mortality over 48 h. Prior exposure for 10 wk to pH = 5.2 plus either 75 or 150 p g Al/L prevented mortality and ameliorated or abolished these effects through a more rapid recovery of net Na+ balance. Prior exposure to pH = 5.2 alone ameliorated these effects only slightly.Lbomble de fontaine (SaBveiinus fowtiwalis) s%dapte A un stress chronique entrain6 par des teneurs subletales en acide et en Ai; l'aaccoutumance concornitante lui conf&re une plus grande resistance A des augmentations A court terme de la teneur en Al et die Itacidit$. On a expos4 des ornbles aduites A huit difl6rentes combinaisons de pH (6,s et 5,2), de teneurs en Cac2 (25 et 400 pequiv/L) et dde teneurs en Al (0, 75 et 150 p@L = 63, 2,8 et 5,6 garno$/ L) en eau douce 21 debit csntinu. AprGs 10 sem, l%chantillsnnage du sang par ponction caudale n'a pas rev$l6 de variations significatives de Ibsmolalit6, des niveaux de proteine dans le plasma ou du taux de I%~moglobine, mais on a observe de l6g$res diff6rences (GI 5 %) des teneurs en Na+ et Cl-du plasma. En g6n6ralf les niveaux de la plupart des 6lectrolytes etaient plus e5leves chez les poissons exposes des teneurs eBev6es en Al evou en Ca+2 en milieu aqueux; seule la teneur en Cac2 du plasma a 6t6 directement abaisske par un faible pH. Un faible pH et une teneur $levee en Al ont tous deux entrain4 une augmentation du taux de I'h$matocrite. Chez des ombies jamais exposes A un milieu acide ajout6 d%l et provoqu6s dans un milieu de pH 4,8 et de teneur en Al de 333 pg/L en dkbit continu, on a observe d'imprtants flux n6gatifs de la teneur en Nac dans tout [krganisme et des baisses marquees de la teneur en Na+ et Cl-du plasma et de l'h6moconcentratisn ainsi qufune importante mortalit6 6chelonn4e sur 48 k. Une exposition pr6alable pendant 10 sem au pH 5,2 en presence de $5 obi f 58 gsgAI/L a prevenu cette mortalit6 et a am6Iior6 ou 6limin6 ces effets par suite du...

Brook trout (Salvelinus fontinalis) exposed for 10 wk to sublethal acid (pH = 5.2) plus Al (150 μg/L) in flowing soft water (Ca2+ = 25 μequiv/L) did not exhibit chronic respiratory disturbance or elevated stress indices, as revealed by sampling of arterial blood gases, acid–base status, glucose, and cortisol via an indwelling catheter. Acclimation occurred, which prevented mortality and greatly attenuated the disturbances of respiratory, acid–base, and stress parameters normally seen upon challenge with more severe acid (pH = 4.8) plus Al conditions (333 μg/L} for 3 d. Ionoregulatory, fluid volume, and hematological disturbances were similarly reduced. Higher water Ca2+ (400 μequiv/L) slightly delayed but did not prevent this suite of toxic responses in naive fish. These disturbances did not occur in naive fish challenged with acid alone (pH = 4.8). However, long-term adaptation to acid alone (pH = 5.2) resulted in elevated glucose and cortisol levels and offered no protection against the more severe acid plus Al challenge. Thus the acclimation was to Al rather than to acidity itself, and low levels of Al may be beneficial to fish under chronic acid stress.