ß-Carotene and other carotenoids appear to be absorbed by some animal species but not others. Individuals and species that do not circulate carotenoids in plasma, even though they are present in the diet, might convert dietary carotenoids to vitamin A in the intestine more efficiently than the ones that do circulate carotenoids (Olson, J.A., 1999). Although the efficiency of the conversion has not been specifically studied in nonhuman primates, serum or plasma concentrations of total carotenoids or of ß-carotene, a-carotene, a-cryptoxanthin, ß-cryptoxanthin, lutein plus zeaxanthin, or lycopene (both provitamin A and non-provitamin A compounds) have been measured in several species (de La Pena et al., 1972; Cornwell and Boots, 1981; Boots et al., 1983; Sabrah et al., 1990; Snodderly et al., 1990; Crissey et al., 1999; Slifka et al., 1999, 2000). Attempts were made in some studies to estimate carotenoid concentrations in the average diet, but individual primates were able to self-select preferred foods, so it was difficult to measure carotenoid intakes precisely.

Very low or nonmeasurable concentrations of serum carotenoids have been found in tamarins (Saguinus oedipus) and capuchins (Cebus albifrons), whereas high concentrations were found in serum of the sooty mangabey (Cerocebus torquatus) and the orangutan (Pongo pygmaeus). Rhesus (Macaca mulatta), cynomolgus (Macaca fascicularis), and squirrel (Saimiri sciureus) monkeys did not have significant concentrations of non-polar carotenoids, such as ß-carotene, in their plasma, but appreciable concentrations of polar carotenoids, such as lutein and zeaxanthin, were found if they were in the diet (Krinsky et al., 1990; Snodderly et al., 1990). It is not clear whether the variability in plasma carotenoid concentration results from differences in carotenoid metabolism among primate species or from the presence of different dietary carotenoids or of different dietary carotenoid concentrations.


Vitamin A and carotene concentrations in feedstuffs vary with origin—including species and growing conditions of plant feedstuffs, species and vitamin A and carotene intakes of animals used as food, and feedstuff processing and storage. To ensure an adequate vitamin A supply, primates in captivity are usually provided diets to which synthetic vitamin A has been added. Synthetic retinyl palmitate and retinyl acetate are the usual supplemental forms, and these are commonly microencapsulated with antioxidants to improve their stability. Nevertheless, if unaccounted for, heat, moisture, manufacturing procedures, and extended storage times can lead to lower than expected dietary vitamin A activity (Camire et al., 1990; Baker, 1995).


Retinyl esters are hydrolyzed in the gut by pancreatic and intestinal brush-border ester hydrolases and the released retinol emulsified with bile salts and lipid. Retinol is absorbed rapidly by the intestinal villi, esterified primarily with palmitic and stearic acids in the mucosal cell, and transported to the liver as retinyl esters in the lipid core of chylomicra. The liver stores much of the retinol, mostly in ester form, and regulates its secretion into the plasma for transport to other tissues in association with retinol-binding protein (RBP) and a cotransport prealbumin, transthyretin (Olson, 1991, 1996; Ross, 1999). In humans, when vitamin A intake is adequate, 50-85% or more of body vitamin A is stored in the liver. Thus, liver levels of the vitamin are good indicators of vitamin A status.

Plasma retinol has proved useful in assessing vitamin A status in humans when plasma concentrations were very low (under 10 µg·dl-1) or very high (over 100 µg·dl-1). Very low concentrations were associated with depletion of vitamin A reserves, whereas very high concentrations were associated with vitamin A intakes exceeding need. When liver reserves (expressed as retinol) are adequate but not excessive (20-520 µg·g-1 of wet liver tissue), plasma vitamin A concentration tended to be homeostatically controlled at a point in each person that was largely independent of total body reserves (Olson, 1991). Although normally it is a small fraction (2-20%) of total plasma vitamin A, retinyl ester was highly concentrated relative to free retinol in humans with vitamin A intakes exceeding the storage capacity of the liver; this phenomenon might reflect conversion of excess vitamin A to a less toxic form (Lee and Nieman, 1993). A transient increase in plasma retinyl esters also occurs after consumption of a vitamin A-rich meal, so fasting blood samples should be used for status-assessment (Olson, 1996).

Plasma or serum vitamin A concentrations have been measured in captive rhesus monkeys (Macaca mulatta), cynomolgus monkeys (Macaca fascicularis), African green monkeys (Cercopithecus aethiops), capuchins (Cebus spp.), marmosets (Callithrix jacchus), tamarins (Saguinus fuscicolis), squirrel monkeys (Saimiri sciureus), owl monkeys (Aotus trigatus), spider monkeys (Ateles geoffroyi), colobus monkeys (Colobus guereza), sooty mangabeys (Cercocebus torquatus), Schmidt’s monkeys (Cercopithecus ascanius), baboons (Papio cynocephalus), mandrills (Papio sphinx), chimpanzees (Pan troglodytes), orangutans (Pongo pygmaeus), and gorillas (Gorilla gorrilla) (O’Toole et al., 1974; Cornwell and Boots, 1981; Meydani et al., 1983; McGuire et al., 1989; Flurer and Schweigert, 1990; Rogers et al., 1993; Crissey et al., 1999). Circulating vitamin A concentrations varied between species and between studies. In one study, tamarins, squirrel monkeys, capuchins, and owl monkeys had plasma vitamin A concentrations that were

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