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OCR for page 85
Summary
The scientific literature provides information con-
cerning the adverse effects of high-level exposures to
most of the vitamins. Unfortunately, this information
base is limited with respect to the species investigated,
the forms of vitamins studied, and the types of experi-
mental design used. Therefore, the maximum tolerable
levels of animals for several of the vitamins were esti-
mated only from a limited base of information.
It is apparent that toxicity in animals is greatest for
high-level oral exposures to vitamin A, vitamin D, and
choline (in the form of choline chIoride). For each, about
10-fold the dietary level required to prevent deficiency
diseases can depress growth and adversely affect par-
ticular organ systems. Signs of Hypervitaminosis A can
be observed among animals fed 10 to 30 times the vita-
min levels required to prevent deficiency diseases. Hy-
pervitaminosis A is characterized by disturbances of
nervous function, such as hyperirritabiity, twitching,
convulsions, and paralysis. It is also characterized by
liver dysfunction and skin disorders. Nonruminants ap-
pear to be able to tolerate dietary levels of at least 30-
fold their vitamin A requirements. Ruminants may be
able to tolerate only 10-fold their required levels. Signs
of Hypervitaminosis D can be observed among animals
fed 4- to 10-fold their nutritional requirements for more
than 60 days. For less than 60 days, however, animals
can tolerate as much as 1,000-fold the required levels
without adverse effects. Hypervitaminosis D is charac-
terized by anorexia, gastrointestinal distress, lameness,
polyuria, hypercalcemia, and calcinosis (particularly
cardiovascular and renal calcification). It is not known
whether calcinosis involves specific tissue lesions in-
duced by high levels of the vitamin, or whether it is
simply a consequence of the induced hypercalcemia.
Depressed growth has been observed in response to
dietary supplements of choline at 2 to 4 times the re-
quirements. Most, if not all, of this toxicity may be due
to disturbances in acid-base relations in the use of the
chloride salt of this vitamin, however.
Niacin, riboflavin, and pantothenic acid are generally
tolerated by animals at dietary levels as great as 10- to
20-fold their respective nutritional requirements. Nia-
cin Hypervitaminosis is characterized by reduced
growth and by disturbances in the metabolism of lipo-
proteins and foreign compounds. Niacin can also affect
nervous function. Nicotinic acid appears to be less toxic
than nicotinamide. The pathology of riboflavin hypervi-
taminosis is not well described. It is clear, however, that
its toxicity is greater when administered parenterally
than when administered orally. High levels of pan-
tothenic acid can cause liver damage characterized by
hepatic steatitis and elevated serum transaminase activ-
ities.
Vitamin E is generally tolerated at dietary intakes as
great as 100-fold nutritional required levels of animals.
Hypervitaminosis E is characterized by reduced
growth, reduced hematocrit, reticulocytosis, hepatic
dysfunction, and hypoprothrombinemia. The last effect
is apparently due to an antagonism of the utilization of
vitamin K.
Vitamins K and C, thiamin, and folic acid are gener-
ally tolerated at oral intake levels of at least 1,000-fold
animals' respective nutritional requirements. Mena-
dione has been shown to be nephrotoxic; however, other
forms of vitamin K are essentially innocuous. In labora-
tory animals, high levels of ascorbic acid (vitamin C) can
produce oxaluria, uricosuria, hypoglycemia, excessive
absorption of iron, gastrointestinal disturbances, aller-
gic reactions, and anemia. These effects have not been
extensively studied in domestic animals, few of which
require this factor in their diets. Thiamin hypervitamin-
osis is characterized by impaired nervous function (for
example, epileptiform convulsions and respiratory pa-
ralysis). The mechanism by which high levels of thiamin
85
OCR for page 86
86 Vitamin Tolerance of Animals
interfere with nervous function remains to be made
clear. Pyridoxine excess can result in ataxia and periph-
eral neuropathy involving demyelination of nervous tis-
sue. This condition has only been studied in dogs and
rats. Folic acid hypervitaminosis due to oral exposure
has not been reported. Parenteral administration of
massive amounts of the vitamin has been found to pro-
duce epileptiform convulsion and renal hypertrophy in
rats, however.
Very little information is available concerning the pa-
thologies of biotin and vitamin BE hypervitaminoses.
Poultry and swine can easily tolerate biotin dietary lev-
els 4 times their nutritional requirements. It is probable
that much greater levels may be tolerated. The present
scientific literature is unclear and most incomplete con-
cerning animal tolerance of vitamin B12. It is likely, how-
ever, that even high levels of this vitamin are essentially
Innocuous.
Representative terms from entire chapter:
nervous function
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