National Academies Press: OpenBook

Vitamin Tolerance of Animals (1987)

Chapter: Summary

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Suggested Citation:"Summary." National Research Council. 1987. Vitamin Tolerance of Animals. Washington, DC: The National Academies Press. doi: 10.17226/949.
Page 85
Suggested Citation:"Summary." National Research Council. 1987. Vitamin Tolerance of Animals. Washington, DC: The National Academies Press. doi: 10.17226/949.
Page 86

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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

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.

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Many feedstuffs and forages do not provide the dietary vitamins necessary for optimum growth and development, making supplementation necessary. This volume offers a practical, well-organized guide to safe levels of vitamin supplementation in all major domestic species, including poultry, cattle, sheep, and fishes. Fourteen essential vitamins are discussed with information on requirements in various species, deficiency symptoms, metabolism, indications of hypervitaminosis, and safe dosages.

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