EFFECTS OF CHRONIC Cd EXPOSURE VIA THE DIET OR WATER ON INTERNAL ORGAN-SPECIFIC DISTRIBUTION AND SUBSEQUENT GILL Cd UPTAKE KINETICS IN JUVENILE RAINBOW TROUT (ONCORHYNCHUS MYKISS)

Abstract

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.

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

“…Taylor et al (2003) also reported no significant differences in log K Cu in hard water as well as in soft water between the same two species, although they observed significantly greater binding capacity for Cu in YP relative to RBT in both hard and soft water. The log K Cd value in RBT of the present study (7.34) was in reasonable agreement with those (7.60 and 7.05) reported earlier by Hollis et al (1999) and Szebedinszky et al (2001), respectively, in RBT in moderately hard water. However, the value in this study is much less than the value (8.60) reported by Playle et al (1993aPlayle et al ( , 1993b in fathead minnow, which translates to a more than 20-fold greater affinity of fathead minnow gills for Cd compared with RBT.…”

Toxic effects of two sources of dietborne cadmium on the juvenile cobia, Rachycentron canadum L. and tissue-specific accumulation of related minerals

“…In the equivalent Cd treatments, Cd concentration in gills was lower than in other tissues except for the muscle. Szebedinszky et al (2001) reported that gills are important in taking up dissolved Cd across the apical cell membranes, and resulted in the highest branchial Cd concentration in the waterborne Cd exposed fish, but in dietborne Cd exposed fish, the Cd in gills was probably transferred from the bloodstream across the basolateral cell membranes. The difference of transport mechanism led to lower gill Cd concentration in fish exposed to dietbrone that those exposed to waterborne Cd (Dang and Wang, 2009).…”

Conducting Ecological Risk Assessments of Inorganic Metals and Metalloids: Current Status

“…For example, Weston et al (2000) concluded that the principal route of metals bioaccumulation for deposit-feeding organisms is ingestion of contaminated sediment, desorption of metals in the gut, and absorption across the gut wall. However, although the gill is not a primary target for dietary metal accumulation, dietary metals such as Cu (Handy 1992;Miller et al 1993;Kamunde et al 2001Kamunde et al , 2002b and Cd (Szebedinszky et al 2001) can sometimes accumulate in fish gills. Concentrations of Cu accumulated from dietary sources may exceed those associated with toxicity during waterborne exposures (MacRae et al 1999), possibly because metal accumulated via diet (from blood) is protein bound by the time it reaches the gill and therefore is not toxic.…”

“…In some cases dietary exposures including ingestion of particles can be predominant, water only bioassays can be misleading (Farag et al 1994(Farag et al , 1999Lee et al 2000a, b;Fisher 2001b, 2002;Szebedinszky et al 2001;Hare et al 2003). Unique potential exposure pathways such as biofilm in rivers (Clements 2002) must be considered.…”