2.1 Dietary essential amino acid (EAA) deficiency
2.2 Toxic non-essential amino acids
Although all fish examined to date display reduced growth when fed EAA deficient diets, the following additional gross anatomical deficiency signs have been observed under experimental conditions with juvenile fish fed synthetic rations deficient in one or more EAAs:
|
Limiting EAA |
Fish |
Deficiency signs1/ |
|
Lysine |
Salmo gairdneri |
Dorsal/caudal fin erosion (1, 2); increased mortality (2) |
|
Cyprinus carpio |
Increased mortality (3) |
|
|
Methionine |
S. gairdneri |
Cataract (4, 5) |
|
Salmo salar |
Cataract (6) |
|
|
Tryptophan |
S. gairdneri |
Scoliosis2/ (7-10); lordosis2/ (7,10); renal calcinosis (8); cataract (7, 9); caudal fin erosion; decreased carcass lipid content (9); elevated Ca, Mg, Na and K carcass concentration (7) |
|
Oncophynchus nerka |
Scoliosis (11) |
|
|
Miscellaneous |
C. carpio |
Increased mortality and incidence of lordosis observed with dietary deficiencies of leucine, isoleucine, lysine, arginine and histidine (3) |
1/ 1-Walton, Cowey and Adron (1984); 2-Ketola (1983); 3-Mazid et al. (1978); 4-Walton, Cowey and Adron (1982); 5-Poston et al. (1977); 6-Barash, Poston and Rumsey (1982); 7-Walton et al. (1984); 8-Kloppel and Post (1975); 9-Poston and Rumsey (1983); 10-Shanks, Gahimer and Halver (1962); 11-Halver and Shanks (1960)2/ Curvature of the vertebral column
Under practical farming conditions dietary EAA deficiencies may arise from one of four possible routes:
- Poor feed formulation arising from the use of disproportionate amounts of feed proteins with natural specific EAA deficiencies. Table 1 presents the chemical score and limiting EAAs of some selected food proteins available to the fish feed compounder. For the sake of comparison chemical scores have been calculated for individual protein sources with reference to the mean dietary EAA requirements of rainbow trout and common carp (Ogino, 1980). Compared to fish meal, which has a well balanced EAA profile, the majority of protein sources presented have amino acid imbalances which render them unsuitable as a sole source of dietary protein for fish. For example, the deficiency of methionine in plant proteins, yeast, meat and bone meal, blood meal, and hydrolysed feather meal; the deficiency of lysine in oilseeds, hydrolysed feather meal and algae; the deficiency of threonine in some oilseeds and pulses; and the deficiency of tryptophan in fish silage. It is clear that during feed formulation special care must be given to the choice of feed-stuffs used so that the desired overall dietary EAA profile is obtained.Dietary imbalances may also arise from the presence of disproportionate levels of specific amino acids; including leucine/isoleucine antagonisms, and to a lesser extent arginine/lysine and cystine/methionine antagonisms. For example, blood meal is a rich source of valine, leucine and histidine, but is a very poor source of methionine and isoleucine. However, in view of the antagonistic effect of excess leucine on isoleucine, animals fed high dietary levels of blood meal suffer from an isoleucine deficiency caused by an excess of dietary leucine (Taylor, Cole and Lewis, 1977). Although similar antagonisms have also been reported for cystine/methionine (use of hydrolysed feather meal; Ichhponani and Lodhi, 1976) and arginine/lysine (Harper, Benevenga and Wohlhueter, 1970) in terrestrial farm animals, they have not been found to occur in fish fed synthetic amino acid diet combinations (Robinson, Wilson and Poe, 1981).
- Dietary EAA deficiencies may arise from excessive heat treatment of feed proteins during feed/diet manufacture. For example, under conditions of excessive heat treatment proteins become more resistant to digestion due to peptide bond formation occurring between the side chains of lysine and dicarboxylic acid. The free epsilon amino groups of lysine are particularly susceptible to heat damage, forming addition compounds with non-protein molecules (reducing sugars) present in the foodstuff (Cockerell, Francis and Halliday, 1972). An estimate of the biological value of the feed protein can be made by chemically measuring the free or available lysine content (epsilon amino group availability; Cowey, 1979).
- Dietary EAA deficiencies may arise from the chemical treatment of feed proteins with acids (silage production) or alkalies, due to the loss of free tryptophan and lysine/cystine respectively (Kies, 1981).
- Dietary EAA deficiencies may arise from the leaching of free and protein bound amino acids into the water. For example, Grabner, Wieser and Lackner (1981), reported the loss, through leaching, of almost all the free and about one-third of the free plus protein bound amino acids from frozen or freeze-dried zooplankton (Artemia salina and Moina spp.) after a 10 min. water immersion period at 9°C.
Although not documented, nutritional pathologies may arise from the ingestion of feed proteins containing toxic amino acids. Feed proteins known to contain toxic amino acids include alkali-treated soybean (toxic amino acid - lysinoalanine), the legume Leucaena leucocephala (toxic amino acid - mimosine) and the faba bean Vicia faba (toxic amino acid - dihydroxyphenylalanine).
