Abstract
The gross and microscopic pathological changes induced by a relatively acute vitamin A deficiency have been thoroughly studied 1 and the mechanism of the process of repair described. 2 , 3 On the other hand, a mild chronic deficiency of the vitamin, such as is more likely to occur in man, has received less attention. The production of such a borderline condition in animals is attended by many difficulties; chief among these is the fact that an excess of the vitamin is readily stored and external evidence of the deficiency removed whereas too small a supply results in the more acute type of the deficiency and in death. The following procedure, however, was found satisfactory for the production of a chronic deficiency of long duration.
Albino rats were specially prepared by withdrawing vitamin A from the mother's diet before the young were 13 days old. At weaning (21 days) the animals were caged individually and fed a purified, vitamin A-free ration adequate in all other respects. When either beginning decline in weight, the first stages of xerophthalmia, or continued excess cornification of the vaginal epithelium of the females appeared (at an average age of 52 days), a small but known quantity of vitamin A in the form of cod liver oil† was administered by mouth. Thereafter, the amount of vitamin A to be given each day was determined for each individual rat from its clinical state (body weight, appearance of eyes, snuffles, and vaginal smear). Thus, the quantity of the vitamin was so adjusted that the animals were maintained in a state of incipient vitamin A deficiency for periods up to one year. The average daily dose of vitamin A required varied from 0.7 to 6.0 (range 0.7–8.0) International Units.
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