Vitamin A

In ancient Egypt the occurrences of an eye disorder and night blindness were resolved by the topical treatment of liver juices or consuming cooked liver. The condition existed for centuries and was reported in the Confederate Army during the American Civil War.[1] The active component in liver extract was identified as fat-soluble (1914), but was not structurally elucidated until 1930, when it was called vitamin A.

The family of compounds that exert vitamin A activity includes over 600 carotenoids 50 are active) and various natural and synthetic vitamin A compounds.[2] The term vitamin A generically describes compounds that exhibit the biological activity of retinol (alcohol form) involved in the vision process, although the acidic form (retinoic acid) seems to perform specific functions in growth and tissue differentiation.[6] Each form shares structural similarities with retinol and its corresponding aldehyde (retinal), thus collectively referred to as reti-noids. For comparative purposes, an international standard is used (1 IU=0.3 mg all-trans retinol). Some carote-noids have high antioxidant properties, while the retinoids do not.

Colostrum and milk provide vitamin A to the nursing animal, while synthetic vitamin A or provitamin A compounds are fed to growing and adult animals. The amount of carotenoids in forage is plentiful, but highly variable, declining with season length and plant maturity. Processing forages lowers its provitamin concentration.

Carotenoids are poorly converted to vitamin A in the intestine of domestic livestock.[3] Consequently, animals grazing pastures only have a small (< 4-month) reser-

Because the chemical structure of retinol has five double bonds and a hydroxyl group, it is readily oxidized. Commercial vitamin A is emulsified in gelatin and sugar, and is subsequently processed into a beadlet containing an antioxidant. Unprotected vitamin A is rapidly oxidized under acidic or moisture conditions when prooxidant minerals (e.g., Cu, Fe, Zn) or PUFAs or elevated nitrates are in the diet, or when feed-processing methods (friction, pressure, extrusion, steam) abuse the gelatin-coated beadlet.[5] Mycotoxins oxidize the vitamin and have produced vitamin A deficiencies in livestock.

The fat-soluble vitamin A compounds aggregate in the small intestine with other lipids from the action of pancreatic esterases and bile salts. They are transported in micellular form across the epithelial cell of the intestinal villi.[1] The absorption efficiency of synthetic vitamin A is 80 to 90%, whereas that of the carotenoids is <50%. Absorption efficiency depends largely on factors influencing lipid digestion. Retinoids are mainly retained by the liver (parenchyma and stellate) cells and, to a smaller degree, by other body cells. The major circulating form of vitamin A and carotenoids is bound to a retinol-binding protein (synthesized in liver). Lipoprotein lipase hydrolyzes the retinyl ester and facilitates its movement into cells. Only when vitamin A liver reserves are depleted does plasma retinol concentration decline.[1]

The main function ascribed to vitamin A involves the vision process, where binding proteins on the rods permit the conversion of retinol to retinal.[1-3] Its association with the membrane-bound protein opsin triggers conforma-tional changes to rhodopsin. A series of isomerizations change the retina to light or dark sensations. Vitamin A also affects the uterine environment by promoting embryo development and enhancing their survival. The uterine endometrium secretes a retinol-binding protein that transfers up to 390 times more vitamin A between days 10 to 13 of gestation. Retinal can be irreversibly converted to retinoic acid and has been implicated in the expression of genes that determine the sequential development of the embryo.[1] The carotenoids are effective antioxidants and function by reducing free radical formation. Both retinoids and carotenoids are immunomodulators by affecting both T cells and B-cell function.[2]

Signs of vitamin A deficiency include neonatal blindness (due to in utero constriction of the optic nerve), other skeletal abnormalities, poor growth, and reproductive failure (e.g., low conception, abortion, small litters in swine, stillbirths, poor semen quality). Although some of these signs are not specific for vitamin A, responses to vitamin A supplementation provide evidence for a deficiency.

The animal's ability to store vitamin A in the liver prevents a large, single ingestion from being toxic, but prolonged consumption can produce clinical symptoms of hypervitaminosis A. These include spontaneous fractures, internal hemorrhages, appetite and weight loss, thickened epithelial tissue, and increased clotting time.[2]

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