Cadmium accumulation, gill Cd binding, acclimation, and physiological effects during long term sublethal Cd exposure in rainbow trout

Abstract

Juvenile rainbow trout, on 3% of body weight daily ration, were exposed to 0 (control), 3, and 10 μg l −1 Cd (as Cd(NO 3) 2 · 4H 2O) in moderately hard (140 mg l −1 as CaCO 3), alkaline (95 mg l −1 as CaCO 3, pH 8.0) water for 30 days. Particular attention focused on acclimation, and on whether a gill surface binding model, originally developed in dilute softwater, could be applied in this water quality to fish chronically exposed to Cd. Only the higher Cd concentration caused mortality (30%, in the first few days). The costs of acclimation, if any, in our study were subtle since no significant effects of chronic Cd exposure were seen in growth rate, swimming performance (stamina and U Crit), routine O 2 consumption, or whole body ion levels. Substantial acclimation occurred in both exposure groups, manifested as 11- to 13-fold increases in 96-h LC 50 values. In water quality regulations, which are based on toxicity tests with non-acclimated fish only, this remarkable protective effect of acclimation is not taken into account. Cd accumulated in a time- and concentration-dependent fashion to 60–120× (gills), 8–20× (liver), 2–7× (carcass), and 5–12× (whole bodies) control levels by 30 days. Chronically accumulated gill Cd could not be removed by ethylenediaminetetraacetic acid (EDTA) challenge. These gill Cd concentrations were 20- to 40-fold greater than levels predicted by the gill-binding model to cause mortality during acute exposure. In short-term gill Cd-binding experiments (up to 70 μg l −1 exposures for 3 h), gill Cd burden increased as predicted in control fish, but was not detectable against the high background concentrations in acclimated fish. In light of these results, Cd uptake/turnover tests were performed using radioactive 109Cd to improve sensitivity. With this approach, a small saturable binding component was seen, but could not be related to toxic response in acclimated fish. Acclimated trout internalized less 109Cd than control fish, but interpretation was complicated by the possibility of radioisotopic exchange and specific activity dilution in the large `cold' Cd pool on the gills. We conclude that gill Cd burden is not predictive of mortality in acclimated fish, that the present gill modelling approach does not work in acclimated fish, and that longer term 109Cd turnover studies are needed for this purpose.