Protective Effects of Calcium Against Chronic Waterborne Cadmium Exposure to Juvenile Rainbow Trout

Abstract

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.

Acute effects of cadmium on osmoregulation of the freshwater teleost Prochilodus lineatus: Enzymes activity and plasma ions

“…This effect is commonly observed at Cd concentrations above 3 g L −1 (Giles, 1988;Reid and McDonald, 1988). For example, Hollis et al (2000) observed no effects in Oncorhynchus mykiss gills when these animals were exposed to 2 g L −1 of Cd for 30 days. In another study involving trout, the plasma levels of Ca 2+ did not decrease after chronic exposure to 3.6 g L −1 of Cd; this effect was only demonstrated in fish exposed to 6.4 g L −1 (Giles, 1988).…”

Acute cadmium biotic ligand model characteristics of laboratory-reared and wild yellow perch (Perca flavescens) relative to rainbow trout (Oncorhynchus mykiss)

“…It was also lower than the values of 1.61 and 3.12 nmol·g wet gill tissue -1 reported in RBT, acclimated to the same water chemistry as that used in the present study, by Hollis et al (1999) and Szebedinszky et al (2001), respectively. This discrepancy in the number of gill binding sites (B max ) among studies was probably due to the size or batch differences in fish and also differences in feeding regime (Hollis et al 2000b) and is certainly an issue that has to be given greater attention for further development of the present acute Cd BLM.…”

“…Toxicity of Cd is generally attributed to the free divalent cation Cd 2+ (Pagenkopf 1983). Waterborne Cd appears to enter mainly through chloride cells in the gills (Wicklund-Glynn et al 1994) and accumulates primarily in kidney, liver, and gills of fish (Hollis et al 1999(Hollis et al , 2000a(Hollis et al , 2000b. At acute waterborne concentrations, Cd severely disrupts Ca homeostasis, which ultimately leads to death (Verbost et al 1987; Reid and McDonald 1988).…”

“…Among various water quality parameters (hardness, pH, alkalinity, and dissolved organic matter (DOM))that could potentially influence the Cd uptake, hardness is often reported to be the major factor influencing Cd toxicity (Calamari et al 1980;Hollis et al 1997Hollis et al , 2000b. As water hardness (defined as the sum of Ca and Mg concentrations, expressed as CaCO 3 equivalents) increases, acute Cd toxicity decreases (Carrol et al 1979;Pascoe et al 1986).…”

Addressing speciation in the effect factor for characterisation of freshwater ecotoxicity—the case of copper

“…The speciation pattern of metals is influenced by the overall composition of the solution (synthetic or natural), in particular, properties like pH, hardness, ionic strength and the presence of complexing ligands such as inorganic ions, EDTA (in synthetic test media) and naturally occurring dissolved organic matter (DOM) expressed as dissolved organic carbon (DOC). The water chemistry and resulting speciation of the metal in the test media thus strongly influence the bioavailability and hence also the ecotoxicity of the metal (Bossuyt et al 2004;Bury et al 1999;Hollis et al 2000;Kramer et al 2004;Macdonald et al 2002;Richards et al 2001). The distribution of the metal among the various metal species, and the resulting concentrations of each of them can be predicted by chemical speciation models (Bhavsar et al 2004), but in spite of the recognised influence on the metal ecotoxicity, chemical speciation and physico-chemical characteristics of the aquatic system are rarely considered when reporting on ecotoxic effects for metals and deriving water quality criteria (Janssen et al 2000).…”