FISH NUTRITION
431
the alga, mostly 016, appeared in the brine shrimp but the latter
also contained 20 : 6 acids not present in the alga. When guppies were
reared on the brine shrimp, fatty acids reflecting those of the shrimp
were found in the fish, but the latter contained a much higher proportion
of 22 : 6 acids than the shrimp.
The interplay between dietary fatty acids and biosynthetic activities
is especially important in considering the " essential fatty acids "
(EFA) of fish. It is now very well established in the rat that the
linoleic, w6 series acids have full EFA activity while the linolenic,
03, series have partial EFA activity. The former group includes
arachidonic acid, 20 : 4w6. Recent reviews of EFA in mammals have
been compiled by Alfin-Slater and Aftergood (1968) and Guarneri and
Johnson (1970). The fist major sign of EFA deficiency in the rat is
that the animal stops growing after some three months. Examination of
phospholipids in tissues shows the presence of high levels of polyenoic
acids derived from oleic acid (w9) and palmitoleic acid ( w 7 ) . This is
in contrast to the usual situation where polyenoic acids derived from
linolenic ( w 3 ) and especially linoleic (w6) acids predominate. As discussed earlier, most biomembranes have a high content of polyenoic
acids but membranous sub-cellular organelles from EFA deficient rats
appear normal a t first sight. It is only when such organelles, e.g.
mitochondria, are stressed, e.g. by osmotic shock, ageing or phospholipase activity, that metabolic abnormalities appear. No other
obvious metabolic symptoms are apparent in the absence of EFA and
growth is resumed when EFA are administered. It is now known that
EFA are the precursors of prostaglandins in animals (but prostaglandins do not reverse EFA deficiency) and EFA also serve as the
endogenous substrates for the microsomal lipid peroxidase system in
liver (Guarneri and Johnson, 1970).
It has already been noted that fish maintained on a low fat diet
become deficient in polyenoic acids, which implies that fish cannot
synthesize these acids, Direct biochemical studies fully confirm this
conclusion. Thus Klenk and Kramer (1960) demonstrated that slices
of fish liver cannot synthesize polyunsaturated fatty acids from acetate
de novo. Radioactive acetate was incorporated largely into the
carboxyl group of the polyunsaturated acids, indicating that the latter
had been formed by chain elongation of an existing structure. Mead
et al. (1960) also showed that linoleic acid (18:2w6) could not be
synthesized by fish from acetate, but arachidonic acid (20 : 4w6) was
apparently formed from linoleic acid by chain elongation and
desaturation as in the rat. The latter studies involved pooled lipids
isolated after injecting both freshwater and marine Tilapia mossambica
431
the alga, mostly 016, appeared in the brine shrimp but the latter
also contained 20 : 6 acids not present in the alga. When guppies were
reared on the brine shrimp, fatty acids reflecting those of the shrimp
were found in the fish, but the latter contained a much higher proportion
of 22 : 6 acids than the shrimp.
The interplay between dietary fatty acids and biosynthetic activities
is especially important in considering the " essential fatty acids "
(EFA) of fish. It is now very well established in the rat that the
linoleic, w6 series acids have full EFA activity while the linolenic,
03, series have partial EFA activity. The former group includes
arachidonic acid, 20 : 4w6. Recent reviews of EFA in mammals have
been compiled by Alfin-Slater and Aftergood (1968) and Guarneri and
Johnson (1970). The fist major sign of EFA deficiency in the rat is
that the animal stops growing after some three months. Examination of
phospholipids in tissues shows the presence of high levels of polyenoic
acids derived from oleic acid (w9) and palmitoleic acid ( w 7 ) . This is
in contrast to the usual situation where polyenoic acids derived from
linolenic ( w 3 ) and especially linoleic (w6) acids predominate. As discussed earlier, most biomembranes have a high content of polyenoic
acids but membranous sub-cellular organelles from EFA deficient rats
appear normal a t first sight. It is only when such organelles, e.g.
mitochondria, are stressed, e.g. by osmotic shock, ageing or phospholipase activity, that metabolic abnormalities appear. No other
obvious metabolic symptoms are apparent in the absence of EFA and
growth is resumed when EFA are administered. It is now known that
EFA are the precursors of prostaglandins in animals (but prostaglandins do not reverse EFA deficiency) and EFA also serve as the
endogenous substrates for the microsomal lipid peroxidase system in
liver (Guarneri and Johnson, 1970).
It has already been noted that fish maintained on a low fat diet
become deficient in polyenoic acids, which implies that fish cannot
synthesize these acids, Direct biochemical studies fully confirm this
conclusion. Thus Klenk and Kramer (1960) demonstrated that slices
of fish liver cannot synthesize polyunsaturated fatty acids from acetate
de novo. Radioactive acetate was incorporated largely into the
carboxyl group of the polyunsaturated acids, indicating that the latter
had been formed by chain elongation of an existing structure. Mead
et al. (1960) also showed that linoleic acid (18:2w6) could not be
synthesized by fish from acetate, but arachidonic acid (20 : 4w6) was
apparently formed from linoleic acid by chain elongation and
desaturation as in the rat. The latter studies involved pooled lipids
isolated after injecting both freshwater and marine Tilapia mossambica