Vitamin A

Vitamin nomenclature policy[1-3] dictates that the term ''vitamin A'' be used for all B-ionone derivatives, other than provitamin A carotenoids, exhibiting the biological activity of all-trans retinol (i.e., vitamin A alcohol or vitamin A1). Esters of all-trans retinol should be referred to as retinyl esters.

Vitamin A is present in animal tissues, whereas most plant materials contain only provitamin A carotenoids, which must be split in the intestinal tract to form vitamin A. In blood, vitamin A is transported as retinol, but it is stored, primarily in the liver, as retinyl palmitate. Absorption efficiency of vitamin A is relatively constant over a wide range of doses, but higher doses of carotenoids are absorbed much less efficiently than lower doses.[4]

Vitamin A esters are more stable in feeds and premixes than retinol. The hydroxyl group as well as the four double bonds on the retinol side chain are subject to oxidative losses. Thus, esterification of vitamin A alcohol does not totally protect this vitamin from oxidative losses. Current commercial sources of vitamin A are generally ''coated'' esters (e.g., acetate or palmitate) that contain an added antioxidant such as ethoxyquin or butylated hyroxytol-uene (BHT).

The water content of premixes and feedstuffs has a negative effect on vitamin A stability. Moisture causes vitamin A beadlets to soften and become more permeable to oxygen. Thus, both high humidity and the presence of free choline chloride (hygroscopic) enhance vitamin A destruction. Trace minerals also exacerbate vitamin A losses in premixes exposed to moisture. For maximum retention of vitamin A activity, premixes should be as moisture-free as possible and should be made to have a pH above 5. Low pH causes isomerization of all-trans vitamin A to less potent cis forms and also results in de-esterification of vitamin A esters to retinol. Likewise, heat processing, especially extrusion, can reduce vitamin A bioavailability.

Crystalline b-carotene is absorbed from the gut more efficiently than b-carotene existing in foods and feeds. Some of the b-carotene in foods is complexed with protein. Fiber components of feeds, especially pectins, have been shown to reduce b-carotene absorption from the gut in chicks.

Ullrey[5] reviewed the bioavailability aspects of vitamin A precursor materials for swine and reported that pigs were far less efficient than rats or chicks in converting carotenoid precursors to active vitamin A. Thus, bioefficacies (wt/wt) ranging from 7 to 14% were observed for corn carotenes in pigs relative to all-trans retinyl palmitate. Hence, carotenoid precursors in corn (also corn gluten meal) have no more than 261 IU/mg vitamin A activity when consumed by swine. This is decidedly less than the theoretical potency of 1667 IU/mg (assuming all the carotenoids are all-trans-b carotene), which is assumed for the rat.[3] Corn carotenoids consist of about 50% cryptoxanthin, 25% b-zeacarotene, and 25% b-carotene.

Quantification of vitamin A bioavailability is difficult. Accumulation of vitamin A in the liver may be the most acceptable method.[4]

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