Abstract

The present study investigated the interactive effects of dietary cadmium (Cd) and selenium (Se) on the tissue-specific (liver, kidney, and muscle) accumulation of these two elements, hepatic oxidative stress response, and morphometrics in rainbow trout (Oncorhynchus mykiss) during chronic exposure. Fish were exposed to elevated dietary Cd (45 μg g−1 dry wt.), and medium (10 μg g−1 dry wt.) or high (45 μg g−1 dry wt.) dietary selenium (added as selenomethionine), both alone and in combination, for 30 days. Exposure to dietary Cd alone caused oxidative stress in fish as reflected by reduced thiol redox (GSH:GSSG), increased lipid peroxidation, and induction of anti-oxidative enzymes (catalase, superoxide dismutase, and glutathione peroxidase) in the liver. Also, an increase in tissue-specific Cd burden and impaired morphometrics (hepato-somatic index and condition factor) were also recorded in fish following exposure to dietary Cd. In contrast, the dietary co-exposure to Cd and Se (at both medium and high doses) resulted in a decrease in Cd burden in the liver and kidney of fish. However, co-exposure to medium, but not high, dose of dietary Se completely alleviated Cd-induced oxidative stress and impaired morphometrics in fish, indicating that the reduced Cd tissue burden might not have been the primary factor behind the amelioration of Cd toxicity by Se. Overall, our study demonstrated that the protective effect of Se against the chronic Cd toxicity in fish is mainly mediated by the anti-oxidative properties of Se, but this protective effect is dose-specific and occurs only at a moderate exposure dose.

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