Abstract
Two groups of Atlantic salmon ( Salmo salar), mean weight 6 g, were given diets of differing selenium content (deficient 0.017 mg Se/kg; supplemented 0.944 mg Se/kg) and adequate vitamin E content (40 mg α-tocopheryl acetate/kg) for 28 weeks. The final weight and packed cell volume of salmon given the Se-supplemented diet were significantly greater than those of the Se-deprived fish. Blood vitamin E concentrations, and liver, blood and brain Se concentrations were all significantly lowered in Se-deficient salmon. No gross pathologies were observed but pathology was evident in pancreatic tissue (loss of integrity in endoplasmic reticulum and increased vacuolation) from Se-deficient salmon. Glutathione peroxidase (EC.1.11.1.9) activity was greatly reduced in liver of the Se-deficient salmon although there was no indication of any compensatory non Se-dependent glutathione peroxidase activity. Hepatic glutathione S-transferase (EC.2.5.1.18) activity, plasma pyruvate kinase (EC.2.7.1.40) activity, erythrocyte fragility and kidney reduced glutathione were all increased in Se deficiency.
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