Does dietary Ca protect against toxicity of a low dietborne Cd exposure to the rainbow trout?
We examined the toxicity of Cd, provided in a natural diet and at an environmentally relevant concentration ( approximately 12microgg(-1) dry wt.), to the juvenile rainbow trout (Oncorhynchus mykiss). In addition, we tested the protection by elevated dietary Ca against both the accumulation and toxicity of dietary Cd from this natural diet (background Ca approximately 1mgg(-1) dry wt.). Food pellets were made from blackworms (Lumbriculus variegatus), and spiked with Cd and either no additional Ca or elevated ( approximately 60mgg(-1) dry wt.) concentrations for each of the treatment diets. Survival was unaffected for trout fed diet with 12microgg(-1) dry wt. Cd for a month, but growth was potentially reduced. Tissue burden analysis revealed that the stomach, liver and kidney accumulated the most Cd, with concentrations progressively increasing in the liver and kidney over the whole exposure period. Cd concentrations in the plasma and red blood cells were unaffected by the different treatments, but subcellular fractionation analysis indicated that a higher concentration of Cd was associated with the metal-sensitive fractions of red blood cells of the fish that were exposed to the dietborne Cd. Dietary Cd exposure also caused potential toxicity to cells of the stomach in that they bound more Cd to heat-denaturable proteins. However, detoxification appeared to take place in the Cd-exposed fish because more Cd was bound to metallothionein-like proteins by week 4 of exposure. Elevated Ca in the Cd diet generally protected against accumulation and toxicity of dietborne Cd. The protection against Cd accumulation was almost complete at the gills, robust in the stomach and whole body (> or =50% reductions), but not significant in the liver, kidney, carcass, plasma, or red blood cells. Elevated dietary Ca also reduced Cd accumulation in the organelles of the fish stomach and red blood cells. In addition, dietborne Ca not only reduced the uptake of Cd by the cells, but also altered how the cells handled Cd intracellularly. In general, our results have demonstrated the need to use diets with natural compositions for dietary toxicity studies.
Ng
Tania Y-T
TY
Department of Biology, McMaster University, 1280 Main Street West, Hamilton, ON L8S 4K1, Canada. taniang@mcmaster.ca
Klinck
Joel S
JS
Wood
Chris M
CM
D000818:Animals; D002104:Cadmium / Q000097:blood / Q000633:toxicity*; D002118:Calcium / Q000097:blood / Q000494:pharmacology*; D004032:Diet / Q000662:veterinary; D004781:Environmental Exposure; D004912:Erythrocytes / Q000737:chemistry / Q000187:drug effects*; D006128:Growth / Q000187:drug effects; D017686:Oncorhynchus mykiss / Q000254:growth & development / Q000378:metabolism / Q000502:physiology*; D013270:Stomach / Q000737:chemistry / Q000187:drug effects; D016019:Survival Analysis; D014874:Water Pollutants, Chemical / Q000633:toxicity*
D014874:Water Pollutants, Chemical; D002104:Cadmium; D002118:Calcium