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Effect of Increased Dietary Carbohydrate on Selenium Metabolism and Toxicity in Rainbow Trout (Salmo gairdneri)¹

Department of Nutrition, University of Guelph, Guelph, Ontario N1G 2W1 ^* Canada Centre for Inland Waters, Department of Fisheries and Oceans Canada, Box 5050, Burlington, Ontario L7R 4A1 Canada

Juvenile trout were reared on either a high available carbohydrate (HC) or low available carbohydrate (LC) diet supplemented with from 0 to 10 µg selenium per gram of diet for 16 weeks, to determine if excess liver glycogen deposition affected the metabolism and toxicity of dietary selenium. Trout reared on the HC diet with 10 µg selenium per gram diet first demonstrated signs of selenosis and had significantly higher (P < 0.05) liver selenium levels than trout reared on the LC diet with 10 µg selenium per gram diet after 16 weeks, indicating that excess dietary carbohydrate enhances dietary selenium toxicity in trout. The mechanism of the interaction is unclear since neither selenium elimination rates nor carcass and kidney selenium levels were affected by the dietary carbohydrate level. Trout reared on high dietary selenium diets (10 µg/g) had an increased incidence of renal calcinosis. In addition, liver copper levels were significantly affected by both dietary selenium and liver glycogen content indicating a significant copper-selenium and copper-glycogen interaction in trout. The development of renal calcinosis and the copper interactions suggest a variety of toxic effects of selenium on trout that may all be responsible for the observed changes in growth and feed efficiency.

KEY WORDS: • selenium metabolism • selenium toxicity • trout • carbohydrate • liver glycogen • liver copper • renal calcinosis

¹ Supported by grants from the Natural Science and Engineering Research Council, the Ontario Ministry of Agriculture and Food and the Ontario Ministry of Natural Resources.

Manuscript received 14 December 1982.