FISH NUTRITION
459
phosphate; the biocatalytically active form of the vitamin is
pyridoxal phosphate (VII).
A large array of enzymes concerned in the intermediary metabolism
of amino acids require pyridoxal phosphate as a coenzyme. The variety
of the reactions involved is quite striking, including transaminations,
amino acid decarboxylations, and amino acid dehydrations. Of these
the most important are transaminations, because, when linked to the
synthesis and transformations of glutamate by specific enzymes they
form reaction sequences which are crucial to the assimilation and
excretion of nitrogen.
As many enzymes require pyridoxal phosphate many biochemical
lesions occur in vitamin Be deficiency. However different enzymes are
affected differently, some being more sensitive than others to vitamin
Be deficiency, a situation possibly reflecting their cellular localization
and distribution. As fish have a high protein requirement the sequence
of biochemical lesions at the enzyme level in their tissues might provide
a fruitful study.
Gross pathological symptoms of vitamin B, deficiency show some
similarities in most animals, the areas affected being skin, blood and
nervous tissue. Thus in mammals, skin lesions, several types of anaemia,
epileptiform fits and retarded growth commonly occur. In chinook
salmon, Halver (1957) mentions among other things, anaemia, nervous
disorders, epileptiform fits and hyper-irritability. Among vitamin B
deficiency symptoms in the yellowtail are nervous disorders, skin lesions
around the mouth and rostrum, and retarded growth (Sakaguchi et al.,
1969). Sakaguchi and his colleagues also observed a decrease in the
fat content of the liver of vitamin Be deficient yellowtails. Whether
this decrease occurred in particular lipid components was not
ascertained. Impaired synthesis of nitrogen bases (affecting phospholipid formation) may have resulted from vitamin Be deficiency. Another
possibility is that glyceroneogenesis from amino acids was lowered
because of transaminase malfunction.
The effects of dietary pyridoxine deficiency on liver transaminase
activity were demonstrated by Ogino (1965). The livers of carp
receiving diets with high levels of pyridoxine (4*04mg/100g diet)
contained 2-3 times as much transaminase activity (both glutamatepyruvate and glutamate-oxaloacetate) as those of fish having low
pyridoxine levels (0=04mg/lOOg diet). Fish had been eating the
low pyridoxine diet for about five weeks. At the same time the
pyridoxine content of the livers of fish consuming the low pyridoxine
diet was about half that of those receiving higher amounts of
pyridoxine (3.5 pg/g liver compared with 6.3 pg/g liver).
459
phosphate; the biocatalytically active form of the vitamin is
pyridoxal phosphate (VII).
A large array of enzymes concerned in the intermediary metabolism
of amino acids require pyridoxal phosphate as a coenzyme. The variety
of the reactions involved is quite striking, including transaminations,
amino acid decarboxylations, and amino acid dehydrations. Of these
the most important are transaminations, because, when linked to the
synthesis and transformations of glutamate by specific enzymes they
form reaction sequences which are crucial to the assimilation and
excretion of nitrogen.
As many enzymes require pyridoxal phosphate many biochemical
lesions occur in vitamin Be deficiency. However different enzymes are
affected differently, some being more sensitive than others to vitamin
Be deficiency, a situation possibly reflecting their cellular localization
and distribution. As fish have a high protein requirement the sequence
of biochemical lesions at the enzyme level in their tissues might provide
a fruitful study.
Gross pathological symptoms of vitamin B, deficiency show some
similarities in most animals, the areas affected being skin, blood and
nervous tissue. Thus in mammals, skin lesions, several types of anaemia,
epileptiform fits and retarded growth commonly occur. In chinook
salmon, Halver (1957) mentions among other things, anaemia, nervous
disorders, epileptiform fits and hyper-irritability. Among vitamin B
deficiency symptoms in the yellowtail are nervous disorders, skin lesions
around the mouth and rostrum, and retarded growth (Sakaguchi et al.,
1969). Sakaguchi and his colleagues also observed a decrease in the
fat content of the liver of vitamin Be deficient yellowtails. Whether
this decrease occurred in particular lipid components was not
ascertained. Impaired synthesis of nitrogen bases (affecting phospholipid formation) may have resulted from vitamin Be deficiency. Another
possibility is that glyceroneogenesis from amino acids was lowered
because of transaminase malfunction.
The effects of dietary pyridoxine deficiency on liver transaminase
activity were demonstrated by Ogino (1965). The livers of carp
receiving diets with high levels of pyridoxine (4*04mg/100g diet)
contained 2-3 times as much transaminase activity (both glutamatepyruvate and glutamate-oxaloacetate) as those of fish having low
pyridoxine levels (0=04mg/lOOg diet). Fish had been eating the
low pyridoxine diet for about five weeks. At the same time the
pyridoxine content of the livers of fish consuming the low pyridoxine
diet was about half that of those receiving higher amounts of
pyridoxine (3.5 pg/g liver compared with 6.3 pg/g liver).