Vitamin deficiency, congenital malformations

In mammals, the first report of induction of congenital malformations attributed to extrinsic factors is a single observation in 1921. This report linked a dietary deficiency of a fat soluble factor with rudimentary limb development in pigs, subsequently determined to be vitamin A. It was not until 1929 that X-rays were shown to affect embryonic development. 

Warkany J, Schraffenberger E (1946) Congenital malformations induced in rats by maternal vitamin A deficiency. I. Defects of the eye. Arch Ophthalmol 35 150-169... 

Hale (95) questioned whether congenital blindness due to maternal vitamin A deficiency could be induced in rats. Cannon (97) enumerates a number of authors who investigated reproduction in vitamin-A-depleted rats and failed to discover congenital malformations in the offspring. He also reported failure to induce congenital anomalies by maternal vitamin A depletion in the young of rats. 

A typical RA-receptor is the receptor fiar vitamin A (all-mtws retinol). Vitamin A is essential for pre-and postnatal development. Congenital vitamin A deficiencies are accompanied by a broad spectrum of malformations. In adult life, vitamin A is indispensable for growth, maintenance, and survival of many tissues. It is necessary for vision and reproduction. A lack of vitamin A in the adult causes night blindness and photoreceptor degeneration. But the devel-... 

Vitamin A-deficient pigs have severe congenital anomalies, such as hair lip, cleft palate, accessory ears, subcutaneous cysts, and various malformations of the eyes. 

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