450
0. B. COWEY AND J. R. SAROENT
recent summary of existing knowledge on these diseases as well as
information on daily requirements is contained in a paper by
Hashimoto and Okaichi (1969).
The mode of action of vitamins received little attention in the early
decades of the present century. Even so the view was current that they
functioned as catalysts because of the small amount required by healthy
animals. The coincident isolation in 1926 of the enzyme urease and the
vitamin thiamine may intuitively have encouraged this view but it was
not until the mid-thirties that the connection was Snally realized;
riboflavin was then identified as & component of Warburg’s yellow
enzyme. I n the next twelve years or so it became evident that many
vitamins (biotin, pyridoxal, pantothenate and so on) act as essential
co-factors in enzyme systems functioning in various aspects of carbohydrate, fat and protein metabolism.
All enzymes are protein in nature but many require an additional
co-factor for their catalytic action. Frequently the co-factor is a metal
(Mg+ +, Zn+ +) but it may also be a vitamin derivative and some enzymes require both organic and inorganic co-factors. At the present
time phosphorylated derivatives of thiamine, pyridoxal and riboflavin are known to function as co-enzymes in addition to the
nucleotide derivatives of nicotinamide (nicotinamide adenine dinucleotides) and riboflavin (flavine-adenine dinucleotide).
The development of a vitamin deficiency syndrome occurs in
several stages (Brin, 1967). First the body is gradually depleted of the
vitamin or co-enzyme due to dietary lack, malabsorption or abnormal
metabolism. Secondly there is a fall in activity of those enzymes
dependent on the particular vitamin as a co-enzyme. Thirdly as enzyme
activity is depressed a general decline in the well-being of the animal
is apparent with loss of appetite and hyperirritability. Finally the
deficiency syndrome is manifest with, perhaps, diagnostic tissue
pathology, permanent damage and death.
Some animals must absorb appreciable quantities of certain vitamins
that are formed by the bacterial flora present in their digestive tract.
Such animals are not totally dependent on a dietary supply of these
vitamins. It is frequently difficult to demonstrate a vitamin deficiency
syndrome in them since the vitamins obtained from intestinal bacteria
may mask the inability of the animal to synthesize the vitamins in
question.
The designation of vitamins by letters began in a fairly orderly
fashion but because of the rapidity with which vitamin research
proceeded from about 1920 onwards considerable overlapping and some
confusion occurred in the naming of these compounds. This situation
0. B. COWEY AND J. R. SAROENT
recent summary of existing knowledge on these diseases as well as
information on daily requirements is contained in a paper by
Hashimoto and Okaichi (1969).
The mode of action of vitamins received little attention in the early
decades of the present century. Even so the view was current that they
functioned as catalysts because of the small amount required by healthy
animals. The coincident isolation in 1926 of the enzyme urease and the
vitamin thiamine may intuitively have encouraged this view but it was
not until the mid-thirties that the connection was Snally realized;
riboflavin was then identified as & component of Warburg’s yellow
enzyme. I n the next twelve years or so it became evident that many
vitamins (biotin, pyridoxal, pantothenate and so on) act as essential
co-factors in enzyme systems functioning in various aspects of carbohydrate, fat and protein metabolism.
All enzymes are protein in nature but many require an additional
co-factor for their catalytic action. Frequently the co-factor is a metal
(Mg+ +, Zn+ +) but it may also be a vitamin derivative and some enzymes require both organic and inorganic co-factors. At the present
time phosphorylated derivatives of thiamine, pyridoxal and riboflavin are known to function as co-enzymes in addition to the
nucleotide derivatives of nicotinamide (nicotinamide adenine dinucleotides) and riboflavin (flavine-adenine dinucleotide).
The development of a vitamin deficiency syndrome occurs in
several stages (Brin, 1967). First the body is gradually depleted of the
vitamin or co-enzyme due to dietary lack, malabsorption or abnormal
metabolism. Secondly there is a fall in activity of those enzymes
dependent on the particular vitamin as a co-enzyme. Thirdly as enzyme
activity is depressed a general decline in the well-being of the animal
is apparent with loss of appetite and hyperirritability. Finally the
deficiency syndrome is manifest with, perhaps, diagnostic tissue
pathology, permanent damage and death.
Some animals must absorb appreciable quantities of certain vitamins
that are formed by the bacterial flora present in their digestive tract.
Such animals are not totally dependent on a dietary supply of these
vitamins. It is frequently difficult to demonstrate a vitamin deficiency
syndrome in them since the vitamins obtained from intestinal bacteria
may mask the inability of the animal to synthesize the vitamins in
question.
The designation of vitamins by letters began in a fairly orderly
fashion but because of the rapidity with which vitamin research
proceeded from about 1920 onwards considerable overlapping and some
confusion occurred in the naming of these compounds. This situation