Factors affecting dietary requirement and deficiency signs of L-tryptophan in rainbow trout.

Two experiments were conducted to determine the concentration of dietary tryptophan needed for optimal growth and survival of fingerling rainbow trout (Salmo gairdneri), to characterize signs of tryptophan deficiency, and to ascertain the effects of niacin on deficiency signs. Test diets containing either hydrolyzed or intact casein were fed with graded levels of added L-tryptophan (0.0, 0.25, 0.50, 0.75 and 1.0 g/100 g protein). Maximum growth occurred at 0.75 and 0.50 g tryptophan in fish fed hydrolyzed and intact casein, respectively. Changes in mineral and amino acid mixtures in the intact casein diet yielded a cation-anion (Na + K - Cl) balance of +15.3 meq/100 g diet and pH of 6.44, compared with a balance of -21.3 and -25 meq, and pH 5.8 and 4.4 for unmodified hydrolyzed and intact casein diets, respectively. Analysis of growth by the polynomial regression function; Y = 0.16 + 0.429X - 0.26X2, where Y = mean daily gain in grams, and X = grams of added tryptophan/100 g protein, predicted that at least 0.58 g of tryptophan was needed for maximum weight gain. Analysis of apparent pathology-free fish by the function; Y = 34.33 + 147.33X -83.87X2, where Y = percentage with no signs of deficiency, and X = grams of added tryptophan, predicted that 0.63 g tryptophan/100 g protein was needed for optimum health scores. Deletion of supplemental niacin did not affect fish response to tryptophan.

The effect of supplemental dietary amino acids, minerals and vitamins on salmonids fed cataractogenic diets.

Three nutritional experiments were conducted to determine the effects of various nutrients on the development of ocular lesions in brook trout, Salvelinus fontinalis, lake trout, Salvelinus namaycush, and rainbow trout, Salmo gairdneri. Supplemental methionine prevented development of cataracts and stimulated growth in trout fed diets containing soy protein isolate as the sole protein. Supplemental riboflavin prevented high mortality, cataracts, and other lens-corneal lesions shown in trout fed a semipurified diet containing casein and gelatin. Swim-up fry which were fed a vitamin A-deficient semipurified diet from first feeding grew slowly, developed edema, corneal lesions, and retinal degeneration, but not lens cataracts. In contrast, feeding the same vitamin A-deficient diet to older trout previously fed vitamin A did not cause ocular lesions or other signs of deficiency. Supplemental beta-carotene prevented ocular lesions in swim-up trout held in warm (12.4 degrees C), but not in cold (9 degrees C) water.

Vitamin E and selenium interrelations in the diet of Atlantic salmon (Salmo salar): gross, histological and biochemical deficiency signs.

Either simultaneous or separate dietary deficiencies of vitamin E and selenium in Atlantic salmon during first 4 weeks of feeding caused twice the mortality shown in fish fed both supplemental vitamin E (0.5 IU/g dry diet) and selenium (0.1 mug/g). Subsequent dietary repletion with both vitamin E and selenium significantly reduced mortality during the following 2 weeks. Larger salmon (0.9 g initial mean weight), with vitamin E deficiency with or without selenium resulted in the following deficiency signs: extreme anemia, pale gills, anisocytosis, poikilocytosis, elevated plasma protein, exudative diathesis, dermal depigmentation, in vitro ascorbic acid-stimulated peroxidation in hepatic microsomes, yellow-orange liver color, yellow-brown intestinal contents, enlarged gall bladder distended with dark green bile, low vitamin E in carcass and hepatic tissue, muscular dystrophy, increased carcass fat and water, and a response to handling characterized by a transitory fainting with interruption in swimming. A deficiency of dietary selenium suppressed plasma glutathione peroxidase activity. Supplemental selenium with vitamin E significantly increased tocopherol activity in hepatic, but not carcass tissues. Supplements of both vitamin E and selenium were necessary to prevent muscular dystrophy.