There are three vitamins– A, D, and E-which dissolve readily in fats and are found only in certain fats which our foods contain. They do not, in general, occur together. Vitamin A is abundant in cod liver oil, butter fat, and milk fat; in the glandular organs of animals, such as the liver, kidney, sweetbread, etc.; and in all yellow pigmented vegetables. It never occurs in white vegetables, such as the potato, white turnip, apple.
This substance is now identified with the yellow pigment of vegetable foods, a compound known as carotin, from its abundance in carrots; or at least it seems to be demonstrated that carotin is the mother substance of the vitamin into which it is readily converted in the body. The latter seems the more probable, since the liver of an animal may be nearly freed from vitamin A by feeding a diet free from it, and become rich in the vitamin when an abundance of carotin is provided. Such a liver is still nearly free from yellow pigment. This is interpreted as meaning that the yellow pigment is converted into the vitamin, and is not itself the vitamin A.
It has recently been stated, on experimental evidence, that plants are all practically free from the vitamin A, but that they furnish carotin from which it is made in the body. Liver fats, egg yolk fats, and cod liver oil contain the vitamin instead of carotin. Little is known about the chemical nature of carotin and less about that of vitamin A. The former is a highly unsaturated hydrocarbon containing 40 carbon and 56 hydrogen atoms in its molecule. It is an unsaturated molecule and takes on oxygen readily, losing in the process its yellow color and its value as the mother substance of the vitamin.
Effects of Deficiency of Vitamin A
Much research has been done on the effects of deprivation of animals of this vitamin. The injury to the body which results from this kind of specific starvation is limited to the epithelial tissues. Since these line the ducts of the tear glands, salivary glands, and other digestive glands, and constitute other glandular tissues of major importance, vitamin A deficiency quickly undermines health.
The epithelial cells keratinize, becoming like the outer layers of the skin, and lose their normal functions. Plaques of these cells desquamate and tend to plug the ducts of glands. In vitamin A deficiency the earliest symptoms are deficiency of tears, dryness of the eyes, and dryness of the mouth. The skin becomes dry and scaly, the germinal epithelium in the testes degenerates, and the animals become sterile.
Attention has repeatedly been called to the occurrence of large numbers of calculi in the kidneys and bladders of rats suffering from deficiency of vitamin A. Rats develop deposits of phosphates and oxalates in the urinary tract very rapidly, and almost invariably when fed diets deficient in this vitamin. When chickens are fed an A-deficient diet, there accumulate in the kidneys great numbers of crystals of urates, or salts of uric acid, so that the kidneys feel sandy between the fingers. There is also some evidence that gall stones are more likely to develop under conditions of vitamin A insufficiency than otherwise. Plaques of epithelial cells desquamate and form nuclei upon which cholesterol deposits.
One of the earliest observed effects of vitamin A deficiency was the appearance of an ophthalmia characterized by drying of the cornea followed by ulceration and perforation of the eyeball. This has been shown to be a secondary result of injury to the tear glands. The gland atrophies and loses its power to secrete tears; the eyeball thereupon becomes dry, and cornification of the cornea soon develops.
A number of papers have been published which refer to the incidence of a similar ophthalmia in human subjects subsisting upon diets of poor quality. There is much reason to believe that the occurrence of night blindness is sometimes attributable to chronic deficiency of vitamin A. In the intestinal tract there may be impaired absorption due to injury to the epithelial cells of the wall.
In rats, when the diet is impoverished in vitamin A, the vaginal mucosa forms cornified epithelial cells continuously. Under normal nutrition there is a similar cornification limited to a brief period during which there is growth, maturation, and rupture of Graafian follicles, after which it disappears; but in A-deficient rats the desquamation of cornified cells is continuous and obscures all ovarian cycles that may be present.
Vitamin A deficiency does not create a malfunction of the ovaries, for they continue to secrete hormones similar to those in estrus. This effect on the vaginal mucosa of the rat is so pronounced that Evans and Bishop report their ability to detect vitamin A deficiency in otherwise apparently healthy animals receiving enough A to prevent ophthalmia. Raising the level of A in the diet may abolish the persistent cornification of the vaginal epithelium and restore normal conditions.
In vitamin A deficiency this transformation of epithelium into stratified, squamous keratinizing epithelium is especially pronounced in the upper respiratory tract, and in the renal pelvis, urinary bladder, seminal vesicles, epididymis, prostate, salivary glands, and pancreas.
When there is deficiency of vitamin A, the intestinal flora is markedly changed as respects gram-negative and gram-positive bacteria in the faeces. The faeces of rats on the deficient diet are dry and hard, which may account for the disappearance of streptococci; otherwise there is no change in the proportion of bacteria which ferment glucose, lactose, and sucrose. The proportion of hydrogensulphide-forming bacteria remains constant.
Under deficiency of vitamin A, rats frequently die of bacterial invasion of the ear and nasal cavities before the appearance of ophthalmia. As the infection advances, it leads to nutritional disaster in which the animal is not restored to a normal condition by feeding rations containing vitamin A. Werkman has reported that a deficiency of vitamin A in the diet increased the susceptibility of rats to anthrax and pneumonia.
An interesting observation reported by Howe is the reversion of the odontoblasts to osteoblasts when animals are deprived of vitamin A. The odontoblastic membrane surrounds the pulp of the tooth and lies in apposition to the under surface of the dentine. From each odontoblast a fiber extends through a tubule in the dentine to the base of the enamel.
The odontoblast forms dentine. Howe states that when animals are deprived of vitamin A, the odontoblasts revert to osteoblasts, or bone-forming cells, and that subsequently bone deposits may be formed by these cells. The frequent occurrence of pulp stones in the teeth of animals deprived of vitamin A supports this view. The importance of this vitamin for the health of the teeth appears, therefore, to be very great.