Abstract
Although selenium is a pollutant released by several industries, it is also an essential nutrient that protects mammals against mercury intoxication. When added to aquatic ecosystems, selenium is bioaccumulated readily and can reduce mercury accumulation in some biota. Using a predator–prey experimental model, we investigated both the route of selenium uptake and the mechanism of reduction in mercury accumulation. Young northern pike (Esox lucius) and yellow perch (Perca flavescens) were caged in situ in mercury-contaminated Clay Lake, northwestern Ontario. Pike were held in water containing trace (< 0.2 μg Se/L) or elevated (4.5–6.4 μg Se/L) concentrations of selenium and were able to accumulate 203Hg and 75Se from food (yellow perch) only, water only, or from food and water. Control pike accumulated as much as 20 times more 73Se from food than from water, assimilating ~30% of selenium in food. With increased levels of selenium in water (around 5 μg Se/L), food and water were of similar importance as sources. Waterborne selenium did not alter either the amount of 203Hg accumulated from water or its subsequent partitioning among the pike tissues sampled. When elevated in food, selenium decreased both the body burden of 203Hg in pike and the proportion in muscle. It is inferred that selenium added to aquatic ecosystems, and incorporated subsequently in the food web, would interfere with biomagnification of mercury. Furthermore, future studies of selenium toxicity in fish should emphasize its accumulation from food.

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