Retinol preformed

Recently we published data that even in countries with excellent food sources and availability, insufficient vitamin A supply will occur (Schulz et ah, 2007). The aim of this trial was to analyze vitamin A and p-carotene status and investigate the contribution of nutrition to vitamin A and p-carotene supply in mother-infant pairs of multiparous births or births within short birth rates. Twenty-nine volimteers aged between 21 and 36 years were evaluated for 48 hours after delivery. In order to establish overall supply, retinol and p-carotene were determined in maternal plasma, cord blood, and colostrum via HPLC analysis. A food frequency protocol was obtained from all participants. Regardless of the high-to-moderate socioeconomic background, 27.6% of participants showed plasma retinol levels below 1.4 pmol/liter, which can be taken as borderline deficiency. In addition, 46.4% showed retinol intake <66% of RDA and 50.0% did not consume liver at all, although liver contributes as a main source for preformed retinol. Despite a high total carotenoid intake of 6.9 3.9mg/day, 20.7% of mothers showed plasma levels <0.5 pmol/liter p-carotene. 

Vitamin A (retinol, 6.1) is the parent of a range of compounds known as retinoids, which possess the biological activity of vitamin A. In general, animal foods provide preformed vitamin A as retinyl esters (e.g. 6.5, which are easily hydrolysed in the gastrointestinal tract) while plant foods provide precursors of vitamin A, i.e. carotenoids. Only carotenoids with a /3-ionone ring (e.g. /1-carotene) can serve as vitamin A precursors. /3-Carotene (6.6)... 

In food, vitamin A exits in two forms preformed vitamin A (retinol and retinyl esters) in animal products and pro-vitamin A carotenoids... 

Preformed vitamin A is found only in animals and a small number of bacteria. A number of the carotenoid pigments in plants can be cleaved oxidatively to yield retinol /S-carotene is quantitatively the most important of these provitamin A carotenoids. Although preformed retinol is both acutely and chronically toxic in excess, carotene is not, because there is only a limited capacity to cleave it to retinol. 

Q s-retinol has 75% of the biological activity of aU-trans-retinol, and reti-naldehyde has 90%. Food composition tables give total preformed vitamin A as the sum of aU-trans-retinol -i- 0.75 x 13-c/s-retinol - - 0.9 x retinaldehyde (Holland et al., 1991). 

During the development of vitamin A deficiency in experimental animals, the plasma concentration of RBP falls, while the liver content rises. The administration of retinol to deficient animals results in a considerable release of holo-RBP from the liver. This is a rapid effect on the release of preformed apo-RBP in response to the availability of retinol, rather than an increase in the synthesis of the protein. There is no evidence that retinol controls the synthesis of RB P (Soprano et al., 1982). This provides the basis of the relative dose response (RDR) test for liver stores of vitamin A (Section 2.4.1.3) administration of a test dose of retinol gives a considerably greater increase in plasma retinol, bound to RBP, in deficient subjects than in those with adequate liver reserves, because of the accumulation of apo-RBP in the liver. 

Preformed vitamin A, most often in the form of retinyi ester, or carotenoids are subject to emulsification and mised micelle formation by the action of bile salts before being transported into the intestinal cell. Here the retinyi esters are moved across the mucosal membrane and hydrolyzed to retinol within the cell to then be reesterified by cellular retinol-binding protein II and packaged into chylomicra, which then enter the mesenteric lymphatic system and pass mto the systemic circulation. A small amount of the ingested retinoid is also converted into retinoic acid in the intestinal cell. The efficiency of absorption of preformed vitamin A is high at between 70% and 90%. ... 

Supplements. The principal forms of preformed vitamin A (retinol) in suppl ents are retinyl palmitate and retinyl acetate. P-Carotene is also a common source of vitamin A in suppl ents, and many supplements provide a combination of retinol and P-carotene. ... 

As retinol activity equivalents (RAEs). 1 RAE = 1 pg retinol, 12 pg p-carotene, 24 pg a-carotene, or 24 pg p-cryptoxanthin. The RAE for dietary provitamin A carotenoids is twofold greater than retinol equivalents (RE), whereas the RAE for preformed vitamin A is the same as RE As cholecalciferol. 1 pg cholecalciferol = 40 lU vitamin D Under the assumption of minimal sunlight... 

Vitamin A is a generic term that includes preformed vitamin A , namely retinol (alcohol), retinal (aldehyde) and retinoic acid (carboxylic acid) , and the provitamin A carotenoids, which are those carotenoids capable of metabolism to retinol, e.g. 3-carotene (Fig. 51.1). 

Vitamin A is available either from (i) preformed retinol (present in animal foods as retinyl esters), or (ii) metabolised from provitamin A precursors. The recommended dietary allowance for preformed vitamin A is 0.9 mg/day for men and 0.7 mg/day for women. Provitamin A somces are graded according to their retinol activity equivalence (RAE), e.g. since 12mg of 3-carotene in food 5delds Img retinol, its RAE is 12. 

Animals are not capable of de novo synthesis of vitamin A-active substances, neither preformed retinol and its derivatives nor the carotenoid precursor forms. The preformed retinoids are defined and their chemical and structural characteristics are given in other chapters in this volume and in the appendix. 

Two approaches have been used to evaluate the vitamin A value of diets a biological assay and a chemical assay. Biological assays in animals measure the total physiologically available vitamin A activity of the diet, i.e., not only retinol but also its active isomers. Biological assays, therefore, account for variable efficiencies in absorption, conversion, and utilization of preformed and precursor vitamin A sources. These assays were the standard technique for dietary evaluation in the older literature and continue to be used as the ultimate test even today. However, biological assays are time-consuming and expensive. 

As already noted, because of the variation in the food sources of vitamin A activity in diets, i.e., preformed and precursor, a common mode of expressing their vitamin A value is needed. Before pure crystalline retinol and p-carotene... 

Zinc deficiency accompanied by a depression in plasma retinol has been noted in several studies. Some investigators have reported an increased liver vitamin A in several species of zinc-deficient animals (Stevenson and Earle, 1956 Saraswat and Arora, 1972 J. C. Smith et aL, 1973, 1976 Brown et aL, 1976 Jacobs et al., 1978 Carney et aL, 1976). There are also reports in humans in an association between lowered zinc, retinol, and RBP (Jacobs et a/., 1978 Solomons and Russell, 1980). J. C. Smith et al, (1973) suggested that hepatic mobilization of vitamin A was impaired by zinc deficiency and their follow-up studies demonstrated a depression in liver and plasma RBP in the zinc-deficient rat compared to pair-fed controls (Brown et al., 1976 Smith et al., 1974). The depression was hypothesized to be the result of a depressed synthesis rather than an increased turnover of RBP. That preformed RBP is present in zinc-deficient rats was demonstrated by Carney et al. (1976) using labeled vitamin A. Zinc-deficient rats, whether or not they were also vitamin A-deficient, were able to mobilize over a short time span a small oral dose of vitamin A as well as could their pair-fed controls. Those animals deficient only in zinc excreted metabolites of the labeled vitamin in a similar quantitative manner as the pair-fed controls for 6 days postdosing. These data suggest that the release of retinol from retinyl ester stores, as well as a depressed RBP synthetic rate, contributed to low plasma levels of vitamin A in zinc deficiency. 

At the other end of the spectrum of serum values, populations with high mean serum carotenoids often are reported to have lower or no different mean retinol levels than found among populations with normal or low carotenoid values. This is illustrated in Table X by comparing data from surveys conducted in Senegal where 98% of the dietary vitamin A activity comes from carotenoids with surveys from the United States where about 50% is from preformed sources. It is difficult to determine if the high blood carotenoids are causally related to a real shift downward in the retinol distribution curve or if this is a methodologic artifact. Several of the colorimetric and fluorometric analytical methods for... 

Effect of Dietary Source of Retinol Equivalents (RE), Preformed versus Precursor, on Plasma Levels of Vitamin A and Carotenoids in Senegal" and the United States ... 

Epidemiologic evidence indicates that an inverse relationship exists between cancer risk and vitamin A consumption. In most epidemiologic investigations, estimates of vitamin A intake have been based on the frequency of ingestion of foods known to have a high content of p-caiotene (e.g., green and yellow vegetables) or a few foodstuffs that contain preformed retinol (e.g., liver or whole milk). 

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