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OCR for page 36
Ascorbic Acid
Ascorbic acid was recognized as early as 1734 as the
factor in fresh fruit and vegetables that prevents the
development of scurvy (Chick, 19531. Despite this early
recognition, it was not until 1932 that two different re-
search groups isolated and identified this compound
from mammalian adrenal glands and citrus fruits (Svir-
bely and Szent-Gyorgyi, 1932a,b; Waugh and King,
1932~. Ascorbic acid is a white crystalline compound,
classified as a carbohydrate, with a molecular weight of
176 and a melting point of 190 to 192°C (Bauernfeind,
1982~. It is readily soluble in water, slightly soluble in
alcohol and glycerol, and virtually insoluble in ether and
chloroform. Ascorbic acid is relatively stable in air. In
aqueous solutions, however, ascorbic acid is attacked by
oxygen and other oxidizing agents that convert the re-
duced form of the vitamin first to dehydroascorbic acid
and then on to further oxidation products in irreversible
reactions.
NUTRITIONAL ROLE
Dietary Requirements of Various Species
Ascorbic acid can be synthesized from glucose
through the intermediate formation of glucuronic acid
and gulonic acid (Burns, 1975~. Ascorbic acid appears to
be ubiquitous in all plants (Loewus et al., 1975~. It is
synthesized in all animal species studied with the excep-
tion of humans, several primates, the Indian fruit bat,
the guinea pig, a few birds, fish, and invertebrates
(Burns, 1957; Ray Chauduri and Chatterjee, 1969; Chat-
terjee et al., 1975~. Therefore, ascorbic acid is not con-
sidered to be an essential dietary nutrient for most
domestic animals and laboratory animals; however, it is
physiologically essential for all of them.
Biochemical Functions
The basic functional property of ascorbic acid is its
redox potential ~ + 0.08 mV) whereby the compound can
reduce transition metals, thus allowing the vitamin to
participate in a number of metabolically important hy-
droxylation reactions. For example, a major function of
ascorbic acid is as a cofactor in the biosynthesis of colla-
gen. Research has indicated that the function of ascor-
bic acid in domestic animals is essentially the same as
that in humans or guinea pigs. Furthermore, it would
appear that there are certain circumstances or periods
during which the biosynthesis of ascorbic acid in domes-
tic animals may not be sufficient to meet metabolic de-
mands. During such periods, such as those of disease or
high environmental temperature, exogenous supplies of
ascorbic acid have been shown to be beneficial to the
health and survival of these animals (Cole et al., 1944;
Rydell, 1948; Scott, 1975; Teare et al., 1979; Vaananen
and Wekman, 1979; Bauernfeind, 1982~.
FORMS OF THE VITAMIN
Vitamin C is available as ascorbic acid, ascorbate-2-
sulphate, ascorbyl palmitate, and sodium ascorbate.
However, for most animals requiring a dietary source of
the vitamin, only ascorbic acid (see Figure 9 for reduced
and oxidized forms) has significant antiscorbutic prop-
erties. For fish such as the catfish, salmon, and trout,
there are reports that ascorbate-2-sulphate and ascorbyl
palmitate also have antiscorbutic properties (Halver et
al., 1975; Brandt et al., 1985~.
ABSORPTION AND METABOLISM
The site and mechanism of absorption of ascorbic acid
may differ between those animals capable of synthesiz
36
OCR for page 37
o
l
c
1
OH-C
11
OH C
1
H-C- O
OH-C- H
C H2 OH
L,Ascorbic
acid
0-~ ~
o=c 1
H-C- O
OH- C H
C H2 OH
L,Dehydroascorbic
acid
FIGURE 9 The reduced and oxidized forms of ascorbic acid.
ing the vitamin and those requiring it as dietary source
(Hornig, 1975~. In humans and guinea pigs, maximal
absorption occurs in the duodenum (Nicholsen and
Chornock, 1942; Hornig et al., 1973) by a Na+-
dependent, active, carrier-mediated system (Stevenson
and Brush, 1969; Stevenson, 1974~. In contrast, ascor-
bic acid absorption in the rat, for which it is not a dietary
essential, is a passive process that occurs primarily in
the ileum (Hornig et al., 1973~. It is assumed that the
absorption mechanism of ascorbic acid in domestic ani-
mals is similar to that of the rat (Spencer et al., 1963~;
however, there is very little information available on this
subject. Research on ruminants (Knight et al., 1941;
Cappa, 1958) and horses (Errington et al., 1954; Her-
rick,1972; laeschke and Keller, 1982) indicates that the
efficiency of ascorbic acid absorption by the oral route is
low in these species due to ascorbic acid destruction by
microbial action or other unknown factors.
The efficiency of enteric absorption of ascorbic acid in
domestic animals has not been investigated. However,
research on humans indicates that the efficiency of as-
corbic acid absorption declines as the dosage levels are
increased (Kubler and Gehler, 1970; Kallner et al., 1977;
Hornig et al., 1980~. More than 70 percent of intakes
less than 1 g are absorbed, while intakes greater than 5 g
have less than 20 percent absorption. In addition, recent
research also indicates that the efficiency of absorption
may decline with age (Davies et al., 1984~. Women with
an average age of 82.6 years appeared to have approxi-
mately one-tenth the absorptive capacity for ascorbic
acid of women with an average age of 21.8 years.
Studies on the tissue distribution of ascorbic acid in
domestic animals have not been extensive, with the ex-
ception of the chicken and the trout. In the trout, radio-
autographs of intubated trout indicated a heavy
Ascorbic Acid 37
concentration of labeled ascorbic acid in the liver, the
anterior kidney (which is also known as the head kidney
or adrenal gland), the renal kidney, and, particularly, the
skin and scales (Halver et al., 1975~. Hilton et al. (1979)
found the concentrations of ascorbic acid to be highest
in the brain and gonads. In the chicken, the highest
concentration of labeled ascorbic acid was observed in
the liver with smaller amounts in the kidney, lung, and
spleen (Hornig and Frigg, 19791. White muscle ascorbic
acid concentrations were not affected by differences in
the dietary level of ascorbic acid (Dorr and Nockels,
19711.
The metabolism of ascorbic acid in domestic animals
has not been extensively studied. Presently, there is
very little information available. The known metabolic
fate of ascorbic acid varies with species and depends
upon the route of introduction and the quantity taken in
by the animal (Tolbert et al., 19751. In all species, initial
metabolism involves the reversible conversion of ascor-
bic acid to dehydroascorbic acid; species' differences in
the metabolism of ascorbic acid would appear to occur
after this step. In the guinea pig and the rat, there is
enzymatic delactonization of dehydroascorbic acid to
diketogulonic acid (Kagawa et al., 1960, 1962), which
can then be decarboxylated to form carbon dioxide and a
number of other compounds (Hornig, 1975~. Carbon di-
oxide exhalation is the major route of elimination of
ascorbic acid by the guinea pig and the rat. In contrast,
no enzymatic delactonization of dehydroascorbic acid
has been found to occur in humans (Baker et al., 1966~.
Humans eliminate ascorbic acid and a number of its
metabolites primarily by way of the urine (Hornig,
1975~.
HYPERVITAMINOSIS
Despite the claims that ascorbic acid is nontoxic to
humans (Pauling, 1970), a number of toxicity symptoms
or signs in humans and a number of laboratory animals
have been attributed to intakes of large doses of ascor-
bic acid. These include oxaluria (Keith et al., 1974),
uricosuria (Stein et al., 1976), hypoglycemia (Lewin,
1974), excessive absorption of iron (Cook and Monsen,
1977), diarrhea, allergic responses, and increased activ-
ity of degradative enzymes of ascorbic acid (Schrauzer
and Rhead, 1973), destruction of vitamin Bl2 (Herbert
and Jacob, 1974), and interference with mixed-function
oxidase systems in the liver (Peterson et al., 1982; Sut-
ton et al., 1982~. However, some of these abnormalities
have been incidental and have been noted in uncon-
trolled experiments. There are a number of contradic-
tory reports as well. For example, studies indicating the
destruction of vitamin B~2 by ascorbic acid (Herbert and
OCR for page 38
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OCR for page 40
40 Vitamin Tolerance of Animals
Jacob, 1974) have been questioned, and the potentiation
of a vitamin By deficiency by high levels of ascorbic acid
appears to be unlikely (Hogenkamp, 1980~. Neverthe-
less, there seem to be some negative side effects to ex-
cessive amounts of ascorbic acid intakes, although there
is no information indicating lethality. An LD50 value has
not been determined for any laboratory animal species.
There is very little information on any toxicity signs
associated with excess ascorbic acid intake in domestic
animals. In studies conducted on dogs, Leveque (1969)
reported allergic types of reaction in the mouth. These
signs disappeared when the level of ascorbic acid intake
by the dogs was reduced. However, this observation
was incidental, and the study was not controlled. The
only study conducted on mink suggested that these ani-
mals may be very sensitive to high levels of ascorbic acid
(Ender and Helgebostad, 19721. Intakes of 100 to 200
mg of ascorbic acid/kg of BW per day produced a pro-
nounced anemia in pregnant females with a subsequent
significant reduction in the number and size of kits. Vir-
tually no studies have been conducted on other species
of domestic animals to determine the levels of ascorbic
acid that may be toxic or the symptoms or signs of ascor-
bic acid toxicity.
Concentrations in Tissues
Ascorbic acid has a wide distribution in animal tissues.
In laboratory animals, high concentrations of ascorbic
acid are normally found in glandular tissues such as the
pituitary, salivary, and adrenal glands with the adrenal
glands having the greatest concentration (Kirk, 1962;
Hammarstroem, 1966; Hornig, 1975~. The brain, liver,
lungs, pancreas, and spleen normally have intermediate
to high concentrations. Because these organs are larger
than glandular tissues, their contribution of ascorbic acid
to the total amount in the body is far greater.
With the exception of fish, very few studies with do-
mestic animal species have been concerned with the
effect of excessive levels of ascorbic acid on tissue. In
studies on catfish, salmon, and trout, the ascorbic acid
concentrations in the liver and head kidney increased in
relation to dietary levels of the vitamin, eventually
showing a plateau beyond which there were no further
increases (Halver et al., 1969; Hilton et al., 1978; Lim
and Lovell,1978~. In contrast, muscle ascorbic acid con-
centrations were not affected by increases in the dietary
intakes of the vitamin (Hilton et al., 1979~. Similarly,
studies on chickens have indicated that muscle ascorbic
acid concentrations remained constant when the dietary
level of ascorbic acid was varied (Dorr and Nockels,
1971~. In virtually all other domestic animal studies,
only plasma ascorbic acid levels have been reported.
They seldom have been related to differences in ascor-
bic acid intake levels.
PRESUMED UPPER SAFE LEVELS
As indicated in Table 10, there is insufficient informa-
tion to determine maximum tolerance levels of ascorbic
acid for most domestic animals species. At this time, the
most complete information is available only for the
chicken. Dietary intakes up to 3,300 mg of ascorbic acid/
kg of feed do not appear to affect the chicken adversely
in prolonged growth studies of more than 60 days (Her-
rick and Nockels, 1969; Chen and Nockels, 1973; Nock-
els, 1973; Schmeling and Nockels, 1978~. Similarly,
research on swine (Brown et al., 1971, 1975; Sandholm
et al., 1979; Chavez, 1983) and fish (Lanno et al., 1985)
has indicated that dietary intakes of as much as 10 g of
ascorbic acid/kg of feed do not adversely affect growth.
However, studies on swine have been of much shorter
duration (less than 60 days) than studies on chickens or
trout. In addition, intakes of 0.5 and 3.0 g ascorbic acid/
day in cats and dogs, respectively, do not appear to af-
fect these animals adversely in short-term studies
(Belfield, 1967; Edwards, 1968; Leveque, 1969;
Vaananen and Wekman, 19791. Long-term studies are
required.
There is much more information concerning the safe
and apparently toxic ascorbic acid intake levels in labo-
ratory animal species (Table 10~. Some of the results,
such as those with rats and guinea pigs, are contradic-
tory, however. Nevertheless, it appears that levels up to
1 g of ascorbic acid/kg of feed in rat and guinea pig diets
do not adversely affect the animals' growth. Further
studies are warranted.
SUMMARY
1. Excess ascorbic acid intakes in humans and labora-
tory animals have been reported to produce a variety of
toxic signs or symptoms including allergic responses,
oxaluria, uricosuria, and interference with mixed-
function oxidase systems.
2. Despite the variety of toxic signs in laboratory ani-
mals due to excessive intakes of ascorbic acid, there has
been no associated lethality reported.
3. There is insufficient information on the tolerance
and toxicity of ascorbic acid in most domestic animals.
4. In growth studies of varying lengths, ascorbic acid
intakes of 3.3 g/kg of feed for chickens and 10 g/kg of
feed for swine and trout do not appear to affect ad-
versely the growth of these animals. Studies on other
domestic animals are needed.
OCR for page 41
Ascorbic Acid 41
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Kirk, J. E. 1962. Variations in the tissue contents of vitamins and
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Kubler, W., and J. Gehler. 1970. Fur Kinetik der enteralen Ascorbin
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Representative terms from entire chapter:
domestic animals
