New regulatory approaches to metal toxicity (e.g., biotic ligand model [BLM]) focus on gill metal binding and tissue-specific accumulation of waterborne metals; the dietary route of exposure and dietary/waterborne interactions are not considered, nor are the consequences of chronic exposure by either route. Therefore, we studied the effect of the same gill Cd load (approximately 2.5 microg/g), achieved by a chronic, 30-d exposure to Cd either via the diet (1,500 mg/kg) or the water (2 microg/L), on tissue-specific Cd distribution and subsequent uptake of waterborne Cd in juvenile rainbow trout (Oncorhynchus mykiss). These two exposure regimes resulted in a branchial Cd load that had been taken up across either apical gill membranes (waterborne Cd) or basolateral gill membranes (through the bloodstream for dietary Cd). The BLM characteristics of the gills (i.e., short-term Cd uptake kinetics) were altered: affinity (log K(Cd Gill) [95% confidence level]) decreased from 7.05 (6.75-8.76) for control to 6.54 (6.32-7.03) for waterborne Cd and 5.92 (5.83-6.51) for dietary Cd, whereas binding capacity (Bmax) increased from 3.12 (2.14-4.09) to 4.80 (3.16-6.43) and 5.50 (2.86-8.17) nmol x g(-1) for control, waterborne, and dietary Cd, respectively. Fish exposed to dietary Cd accumulated a much greater overall chronic Cd body burden relative to fish exposed to waterborne Cd or control fish. The carcass accumulated the greatest percentage of total body Cd in control and waterborne-exposed fish, whereas the intestinal tissue accumulated the greatest percentage in dietary-exposed fish. Tissue-specific Cd burdens were highest in the kidney in both dietary and waterborne treatments. We conclude that chronic Cd exposure alters Cd uptake dynamics, and that the route of Cd exposure, whether waterborne or dietary, results in differences of internal Cd accumulation and branchial Cd uptake characteristics. These factors should be considered in future BLM development.

Juvenile rainbow trout (Oncorhynchus mykiss [Walbaum]) on 1% daily ration were exposed to 0 (control) or 2 g of cadmium as Cd(NO 3 ) 2 ·4H 2 O per liter added to four different calcium (Ca) concentrations: 260 (background), 470 (low), 770 (medium), or 1200 (high) M of Ca added as Ca(NO 3 ) 2 ·4H 2 O in synthetic soft water for 30 d. Mortality was highest (ϳ80%) in the background ϩ Cd treatment. Approximately 40% mortality was observed in the low ϩ Cd exposure; mortality was 10% or less for all other treatments. No growth effects were seen for any of the exposures. Kidneys accumulated the greatest concentration of Cd during the 30 d, followed by gills and livers. Accumulation of Cd in gills, kidney, and liver decreased at higher water Ca concentrations. No differences in whole-body or plasma Ca concentrations were found. Swimming performance was impaired in the low ϩ Cd-exposed fish. Influx of Ca 2ϩ into whole bodies decreased as water Ca concentrations increased; influx of Ca 2ϩ into background ϩ Cd-treated fish was significantly reduced compared to that in control fish. Experiments that measured uptake of new Cd into gills showed that the affinity of gills for Cd (K Cd-gill ) and the number of binding sites for Cd decreased as water Ca concentrations increased. Acute accumulation of new Cd into gills and number of gill Cd-binding sites increased with chronic Cd exposure, whereas the affinity of gills for Cd decreased with chronic Cd exposure. Longer-term gill binding (72 h) showed reduced uptake of new Cd at higher water Ca levels and increased uptake with chronic Cd exposure. Complications were found in applying the biotic ligand model to fish that were chronically exposed to Cd because of discrepancies in the maximum number of gill Cdbinding sites among different studies.

No abstract

Juvenile rainbow trout were fed diets containing control (0.26 mmol/g) or elevated (1.3 mmol/g) dietary Na+ in combination with either background (19 nmol/L) or moderately elevated levels (55 or 118 nmol/L) of waterborne Cu for 21 d. Unidirectional waterborne Na+ uptake rates (measured with 22Na) were up to four orders of magnitude higher than those of Cu (measured with 64Cu). Chronic exposure to elevated dietary Na+ alone or in combination with elevated waterborne Cu decreased whole-body uptake rates of waterborne Na+ and Cu. Accumulation of new Cu and Na+ at the gills was positively and highly significantly correlated and responded to the experimental treatments in a similar fashion, suggesting that Na+ and Cu have common branchial uptake pathways and that dietary Na+ preexposure modifies these pathways. Chronic exposure to elevated waterborne Cu significantly increased Cu concentrations in the liver but caused only modest increases in total Cu concentrations in the whole body and gill. Chronic exposure to elevated dietary Na+ slightly decreased whole-body Cu concentration on day 14 and greatly reduced liver Cu concentration on days 14 and 21; new Cu accumulation in whole-body, gill, and internal organs was reduced on all days. Chronic exposure to elevated waterborne Cu or dietary Na+ alone reduced short-term gill Cu binding at low waterborne Cu concentrations. At high waterborne Cu concentrations, chronic exposure to elevated waterborne Cu had no effect, while elevated dietary Na+ increased Cu binding to the gills. Combined chronic exposure to elevated dietary Na+ and waterborne Cu decreased gill Cu binding over the entire range of Cu concentrations tested. Clearly, chronic exposure to elevated dietary Na+ and waterborne Cu appears to modify gill Cu-binding characteristics and may be important considerations in future development of a chronic biotic ligand model for Cu.