Effects of long term sublethal Cd exposure in rainbow trout during soft water exposure: implications for biotic ligand modelling

Abstract

The objectives of the study were to determine the physiological and toxicological effects of chronic cadmium exposure on juvenile rainbow trout in soft water. Particular attention focused on acclimation, on comparison to an earlier hard water study, and on whether a gill surface binding model, originally developed in dilute soft water, could be applied in this water quality to fish chronically exposed to Cd. Juvenile rainbow trout, on 3% of body weight daily ration, were exposed to 0 (control), 0.07, and 0.11 μg l −1 Cd [as Cd(NO 3) 2·4H 2O] in synthetic soft water (hardness=20 mg l −1 as CaCO 3, alkalinity=15 mg l −1 as CaCO 3, pH 7.2) for 30 days. Mortality was minimal for all treatments (up to 14% for 0.11 μg l −1 Cd). No significant effects of chronic Cd exposure were seen in growth rate, swimming performance (stamina), routine O 2 consumption, or whole body/plasma ion levels. In contrast to the hard water study, no acclimation occurred in either exposure group in soft water, with no significant increases in 96-h LC 50 values. Cadmium accumulated in a time-dependent fashion to twice the control levels in the gills and only marginally in the liver by 30 days. No significant Cd accumulation occurred in the gall bladder or whole body. Cadmium uptake/turnover tests were run using radioactive 109Cd for acute (3 h) exposures. Saturation of the gills occurred for control fish but not for Cd-exposed fish when exposed to up to 36 μg l −1 Cd for 3 h. Cd-exposed trout accumulated less ‘new’ Cd in their gills compared to controls and they internalized less 109Cd than control fish. This effect of lowered Cd uptake by the gills of acclimated trout was earlier seen for the fish acclimated to 10 μg l −1 Cd in hard water. The affinity of the gill for Cd was greater in hard water (log K Cd-gill=7.6) than in soft water (log K Cd-gill=7.3) but the number of binding sites ( B max=0.20 μg g −1 gill) was similar in both media. In addition, there was a shift in affinity of the gill for Cd (i.e. lowered log K Cd-gill) and increased B max with chronic Cd exposure in both soft water and hard water. We conclude that the present gill modelling approach (i.e. acute gill surface binding model or Biotic Ligand Model) does work for soft and hard water exposures but there are complications when applying the model to fish chronically exposed to cadmium.