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Vitamin A Deficiency in the Mouse¹

Two Figures

Department of Biochemistry, Fordham University, New York, New York

A study of vitamin A deficiency was made in three strains of white mice.

1. Rats and mice depleted of tissue stores of vitamin A under identical conditions differ markedly in their susceptibility to the development of a deficiency state, mice exhibiting greater resistance with respect to weight gains, life spans, and time of appearance of symptoms.

2. A set of conditions was developed which led to the production of a clear-cut vitamin A deficiency syndrome in 80% of the mice within 45 to 50 days. Both the dietary components and the nutritional background of the weanling with respect to vitamin A were all-important in determining the susceptibility of the mouse to an avitaminosis.

3. The small amount of vitamin A transmitted to the embryo by the mother for storage purposes, and the importance of the lactation period as a prime factor in conditioning the mouse's response to vitamin A-deficient diets, were shown.

4. Vitamin E-free and fat-free diets decreased the time required for the appearance of deficiency symptoms on vitamin A-free diets by increasing the rate of depletion of liver stores of vitamin A.

5. Pathologic and histologic changes associated with vitamin A deficiency in the white mouse are described. Abnormalities in the eye were noted only in those animals with an advanced avitaminosis. Eye changes occurred much later than the marked degeneration of the epithelium of the genito-urinary tract.

6. The reproductive function in the vitamin A-deficient male is virtually destroyed, but sterility can be reversed by the addition of vitamin A to the diet. The reproductive function in the vitamin A-deficient female is somewhat impaired but not completely destroyed. Manifestations of this impaired function are listed.

This investigation was supported (in part) by a research grant from the National Cancer Institute, of the National Institutes of Health, Public Health Service.

Manuscript received 10 October 1951.

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