captured rhesus monkeys (Macaca mulatta), patas monkeys (Erythrocebus patas), baboons (Papio anubis), and owl monkeys (Aotus trivirgatus) decreased over time in captivity. During captivity, the primates were fed a vegetarian stock diet consisting of potatoes, bread, carrots, root vegetables, and green vegetables supplemented with ascorbic acid and halibut liver oil (Oxnard, 1964). A condition called “cage paralysis” in captive monkeys is similar to “subacute degeneration” of the spinal cord in humans and might be due to vitamin B12 deficiency. Animals with cage paralysis had lowered serum vitamin B12 concentrations, degeneration of the spinal cord, and patchy demyelination of peripheral nerves (Oxnard and Smith, 1966; Torres et al., 1971). Visual impairment with histologic changes in the visual pathway also were described (Hind, 1970).
Manifestations of vitamin B12 deficiency seem to be similar in rhesus and patas monkeys (Oxnard et al., 1970; Torres et al., 1971; Hind, 1970). In controlled deficiency studies in baboons (Papio cynocephalus), serum and liver vitamin B12 decreased to very low concentrations, and urinary excretion of methylmalonic acid increased after a loading dose of valine. Growth of the deficient animals decreased in the second year. No frank deficiency signs were seen, perhaps because the study was only 24 months long (Siddons, 1974b; Verjee et al., 1975). Siddons and Jacob (1975) found that vitamin B12 concentrations in baboon tissues were highest in the liver, followed by the pituitary, kidney, heart, spleen, and pancreas. The main site of vitamin B12 absorption appeared to be the distal half of the small intestine. Satisfactory body stores were maintained by dietary intakes of 1 to 2 µg per day. Because gastric intrinsic factor is considered important for absorption of vitamin B12, cobalamin absorption was measured in normal baboons and after total gastrectomy (Green et al., 1982). Cobalamin absorption was diminished but not completely abolished by gastrectomy. Provision of intrinsic factor enhanced absorption of orally administered cyanocobalamin, but physiologically significant amounts of cobalamin were still absorbed in its absence. Evidence also was obtained that the form of cobalamin excreted in the bile was more readily absorbed than oral cyanocobalamin, or bile itself may have enhanced cobalamin absorption. The absorption of cobalamin in bile was enhanced further by provision of gastric intrinsic factor, and these studies suggest that the enterohepatic circulation of cobalamin may be an important vitamin B12 conservation measure.
Kark et al. (1974) injected 20 µg of vitamin B12 every 14 days into control animals that weighed about 4.4 kg at the beginning of the study but eventually weighed about 10 kg. All measures of vitamin B12 status were normal. Siddon (1974b), working with baboons fed purified diets, supplemented control animals with vitamin B12 at 1 µg·d-1 for 9 months and 2 µg·d-1 for the next 15 months. The 2-µg dosage promoted a slightly higher body weight gain and a more satisfactory serum vitamin B12 concentration. The baboons weighed about 7.5 kg at the beginning of the study and about 12.3 kg at the beginning of the second year. Wilson and Pitney (1955) found that rhesus monkeys required more than 2 µg but less than 10 µg daily to maintain serum concentrations of vitamin B12. The weights of the animals were not given.
The requirement of nonhuman primates for vitamin B12 has been estimated to be 11 µg·kg-1 of dietary DM; this is adequate to prevent deficiency signs and should provide a reasonably normal serum concentration.
Vitamin C, also known as ascorbic acid or ascorbate, is required as a cofactor in numerous enzymatic reactions. Some of them concern the hydroxylation of proline or lysine, steps in the formation of collagen. Other metabolic reactions involving ascorbic acid are carnitine biosynthesis, catecholamine synthesis, peptide amidation, and tyrosine metabolism (Levine et al., 1996; Jacob, 1999). Vitamin C enhances the absorption of nonheme iron and decreases copper absorption (Moser and Bendich, 1991). It is added to primate diets in the form of ascorbic acid or L-ascorbyl-2-polyphosphate. L-ascorbyl-2-polyphosphate is a form of ascorbic acid that is less susceptible to oxidation and yet is biologically available to nonhuman primates. Presumably, the phosphate ester is hydrolyzed by intestinal phosphatase before absorption (Machlin et al., 1979). Another form, L-ascorbyl-2-sulfate, although resistant to oxidation and used in fish diets, has no vitamin C activity in primates (Machlin et al., 1976; Kotze and Menne, 1978).
Many mammals have the ability to synthesize ascorbic acid from glucose, but most primates, including humans, lack gulonolactone oxidase, the enzyme required for ascorbic acid synthesis. Many, perhaps most, prosimians possess this enzyme and presumably do not require a dietary source of vitamin C. Fifteen species of prosimians—including sifakas (Propithecus verreauxi), pottos (Perodicticus potto), and a number of species of lemurs, bushbabies, and lorises—have substantial liver concentrations of gulonolactone oxidase; these species might be able to synthesize ascorbic acid (Elliot et al., 1966; Nakajima et al., 1969; Pollock and Mullen, 1987). However, the enzyme is not found in the liver of western tarsiers (Tarsius bancanus), so perhaps prosimians are not all alike in their ability to synthesize this vitamin (Pullock and Mullin, 1987). Confirmatory studies in which diets devoid of vitamin C have been fed to prosimians for extended periods have not been conducted. The ability to synthesize vitamin C is clearly lacking in all other higher primates that have been studied to date.
Effects of vitamin C deficiency in the macaque species include weakness, lethargy, anorexia, weight loss, and mus-