FISH NUTRITION
433
interconversions of polyunsaturated acids has been proposed by
Kayama and Tsuchiya (1962) (see also Mead and Kayama, 1967). A
similar scheme is shown in Fig. 7.
Deficiency symptoms caused by a dietary absence of 18 : 2 and 18 : 3
acids in fish were first observed by Nicolaides and Woodall (1962) who
demonstrated that salmon fry maintained on a fat-free diet since
hatching lacked normal pigmentation in the skin. A similar depigmentation was observed with fish kept on a diet containing triolein
or linolenic acid (fed as the free acid), but feeding trilinolein largely
prevented depigmentation. Trilinolein or linolenic acid, or both,
elicited a positive growth response in salmon fry when substituted
isocalorifically for sucrose in a fat-free ration, but triolein did not.
Higashi et al. (1966) showed that trout kept on a fat-free diet for three
months developed even more striking symptoms, including erosion of
the posterior fin and in extreme cases the spinal column was exposed.
These symptoms disappeared on feeding mixtures of linoleic and linolenic acids as ethyl esters. Sinnhuber (1969) describes a strikingly
abnormal symptom in trout fed a diet deficient in polyenoic acids which
he refers to as a " shock syndrome ". I n this condition a sudden stimulus
e.g. netting or even turning on a light, causes a rapid swimming motion
followed by a comatose state. Dietary linolenic acid prevented this
syndrome.
Reiser et al. (1963) demonstrated that growth of goldfish eating a
fat-free diet was increased when the diet was supplemented with either
linoleic or linolenic acid ; the latter acid was the more effective. Chain
lengthening occurred significantly with both fatty acids. In the same
work it was shown that depletion of higher polyenoic acids in salt-water
fish (the mullet, Mu&! cephalus and the fundulus, ~undulus grandie)
could not be reversed by feeding diets containing 30% corn oil (rich in
linoleic acid), 30% linseed oil (rich in both linoleic and linolenic acids)
or even by diets containing 6% linoleic acid or 6% linolenic acid. A
pronounced reappearance of higher polyunsaturated fatty acids
occurred, however, on a diet containing 0.9% linolenic acid together
with 0.08% linoleic acid (the latter as an impurity). While no growth
rates are quoted, the important conclusion emerges that marine fish
will chain elongate dietary linolenic acid only when it is present at relatively low dietary levels. It is of significance that the ratio of dietary
linolenic acid to linoleic acid (w3/w6) in these conditions was 11. Lee
et al. (1967) later showed that growth rates in fingerling trout reared on
10% corn oil diets were at least doubled when the diet was supplemented
with 1% linolenic acid. In this case the ratio of dietary linolenic acid
to linoleic acid was 0.2. That chain elongation had occurred in these
433
interconversions of polyunsaturated acids has been proposed by
Kayama and Tsuchiya (1962) (see also Mead and Kayama, 1967). A
similar scheme is shown in Fig. 7.
Deficiency symptoms caused by a dietary absence of 18 : 2 and 18 : 3
acids in fish were first observed by Nicolaides and Woodall (1962) who
demonstrated that salmon fry maintained on a fat-free diet since
hatching lacked normal pigmentation in the skin. A similar depigmentation was observed with fish kept on a diet containing triolein
or linolenic acid (fed as the free acid), but feeding trilinolein largely
prevented depigmentation. Trilinolein or linolenic acid, or both,
elicited a positive growth response in salmon fry when substituted
isocalorifically for sucrose in a fat-free ration, but triolein did not.
Higashi et al. (1966) showed that trout kept on a fat-free diet for three
months developed even more striking symptoms, including erosion of
the posterior fin and in extreme cases the spinal column was exposed.
These symptoms disappeared on feeding mixtures of linoleic and linolenic acids as ethyl esters. Sinnhuber (1969) describes a strikingly
abnormal symptom in trout fed a diet deficient in polyenoic acids which
he refers to as a " shock syndrome ". I n this condition a sudden stimulus
e.g. netting or even turning on a light, causes a rapid swimming motion
followed by a comatose state. Dietary linolenic acid prevented this
syndrome.
Reiser et al. (1963) demonstrated that growth of goldfish eating a
fat-free diet was increased when the diet was supplemented with either
linoleic or linolenic acid ; the latter acid was the more effective. Chain
lengthening occurred significantly with both fatty acids. In the same
work it was shown that depletion of higher polyenoic acids in salt-water
fish (the mullet, Mu&! cephalus and the fundulus, ~undulus grandie)
could not be reversed by feeding diets containing 30% corn oil (rich in
linoleic acid), 30% linseed oil (rich in both linoleic and linolenic acids)
or even by diets containing 6% linoleic acid or 6% linolenic acid. A
pronounced reappearance of higher polyunsaturated fatty acids
occurred, however, on a diet containing 0.9% linolenic acid together
with 0.08% linoleic acid (the latter as an impurity). While no growth
rates are quoted, the important conclusion emerges that marine fish
will chain elongate dietary linolenic acid only when it is present at relatively low dietary levels. It is of significance that the ratio of dietary
linolenic acid to linoleic acid (w3/w6) in these conditions was 11. Lee
et al. (1967) later showed that growth rates in fingerling trout reared on
10% corn oil diets were at least doubled when the diet was supplemented
with 1% linolenic acid. In this case the ratio of dietary linolenic acid
to linoleic acid was 0.2. That chain elongation had occurred in these