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1. Duplicate groups of rainbow trout (Salrno gairdnerz] (mean weight 11 g) were given for 40 weeks one of four partially purified diets that were either adequate or low in selenium or vitamin E or both.2. Weight gains of trout given the dually deficient diet were significantly lower than those of trout given a complete diet or a diet deficient in Se. No mortalities occurred and the only pathology seen was exudative diathesis in the dually deficient trout.3. There was significant interaction between the two nutrients both with respect to packed cell volume and to malondialdehyde formation in the in vitro NADPH-dependent microsomal lipid peroxidation system. 4. Tissue levels of vitamin E and Se decreased to very low levels in trout given diets lacking these nutrients. For plasma there was a significant effect of dietary vitamin E on Se concentration.5. Glutathione (GSH) peroxidase (EC 1 . 1 1 . 1 .9) activity in liver and plasma was significantly lower in trout receiving low dietary Se but was independent of vitamin E intake. The ratios of hepatic GSH peroxidase activity measured with cumene hydroperoxide and hydrogen peroxide were the same for all treatments. This confirms the absence of a Se-independent GSH peroxidase activity in trout liver.6. Se deficiency did not lead to any compensatory increase in hepatic GSH transferase (EC 2 . 5 . 1 . 18) activity; values were essentially the same in all treatments.7. Plasma pyruvate kinase (EC 2 . 7 . 1 .40) activity increased significantly in the trout deficient in both nutrients. This was thought to be due to leakage of the enzyme from the muscle and may be indicative of incipient (subclinical) muscle damage.The essentiality of dietary selenium for mammals and its close metabolic relation with vitamin E has been recognized since Schwarz & Folz (1957) first demonstrated that Se could replace vitamin E in the prevention of dietary liver necrosis. Results on this interrelation in fish are limited. Poston et al. (1976), using Atlantic salmon (Salmo salar) during the first six weeks after yolk sac absorption (mean weight 0.1 g), demonstrated that dietary supplements of both vitamin E and Se were necessary to reduce mortality significantly. In larger fish (0.9 g live weight) both vitamin E and Se were necessary to prevent muscular dystrophy. Hilton et al. (1980), using rainbow trout (Salmo gairdneri) of 1.28 g mean initial weight, could find no deficiency symptoms at dietary Se levels of 0.07 pg/g with 0.4 pg Se/l of rearing water and in the presence of a dietary vitamin E concentration of 0-4 IU/g. Both experiments were carried out at a water temperature of 14-15'.

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Turbot and rainbow trout, which had previously recieved diets free of fat, were fed [1-14C] fatty acids. The distribution of radioactivity in the tissue fatty acids was examined 6 days later. In rainbow trout fed [1-14C] 18:3omega3, 70% of the radioactivity was present in 22:6omega3 fatty acid. In contrast, turbot fed [1-14C] 18:1omega9, 18:2omega6, or 18:3omega3 converted only small amounts of labeled fatty acids (3-15%) into fatty acids of longer chain length. The major product of the limited modification found in turbot was the dietary acid elongated by 2 carbon atoms.

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