concentrations. Oral supplementation with Zn rapidly reversed the signs of Zn deficiency, but Zn concentrations in hair remained low for some time (Swenerton and Hurley, 1980). Although the Zn-deficient diet was fed only during the third trimester of pregnancy, behavioral effects on the infants born to these mothers were noted: they played and explored less, associated more with their mothers, and were less active (Sandstead et al., 1978).
Most of the studies cited above used diets very low in Zn (less than 1 mg·kg-1) to induce Zn deficiency. In a series of studies on rhesus monkeys, moderate or marginal Zn deficiency was produced by feeding a purified diet with Zn at 2 or 4 mg·kg-1 of diet (air dry), respectively (Golub et al., 1982, 1984a,b,c, 1990a,b, 1992, 1994, 1995, 1996a,b; Baly et al., 1984; Leek et al., 1984; Haynes et al., 1985, 1987; Keen et al., 1989, 1993; Lonnerdal et al., 1990a,b). The marginal Zn deficiency resulted in changes in activity level, taste sensitivity, and immune function but not in the more severe signs of Zn deficiency, such as anorexia, alopecia, diarrhea, and dermatitis. The Zn requirement of nonpregnant female monkeys was not determined; but when a diet with Zn at 12 mg·kg-1 air-dry diet was fed, plasma Zn remained normal, whereas it decreased when the diet contained 8 mg·kg-1 or less (Golub et al., 1982).
When the diet containing Zn at 4 mg·kg-1 (air dry) was fed to pregnant females, the more severe signs of dermatitis, anorexia, and low plasma Zn were observed and suggested that the Zn requirement is higher during pregnancy. Stillbirths, abortions, and delivery complications were more frequent in the group fed the low-Zn diet. Frequent observations of reduced plasma vitamin A and iron-deficiency anemia (Golub et al., 1984b; Baly et al. 1984) indicated that impaired Zn status can affect the metabolism of other essential nutrients. Effects of the low-Zn diet were observed not only in pregnant females, but also in infants born to them, which had slower than normal growth, taste dysfunction, and reduced food intake (Golub et al, 1984b). Delayed skeletal maturation and defective bone mineralization were also observed in the infants (Leek et al., 1984). Monkeys fed the marginal-Zn diet appeared to increase Zn absorption homeostatically. Pregnant and lactating dams fed the low-Zn diet showed about 25% higher Zn absorption than control dams (Lonnerdal et al., 1990a). A similar increase in Zn absorption was found in infants born to dams fed the low-Zn diet; that suggests that the Zn status was also compromised in the offspring.
The Zn requirement of infant rhesus monkeys can be estimated from the study of long-term feeding with formulas that had different concentrations of Zn (Polberger et al., 1996). Although formula containing Zn at 1 mg·L-1 resulted in signs of Zn deficiency, infants consuming formula containing 4 mg·L-1 did not show any of the signs. A Zn intake of 1.6-2 mg·d-1 or 1-1.5 mg·BWkg-1·d-1 appears to meet the Zn requirement of growing rhesus infants. Rhesus milk contains Zn at about 2-5 mg·L-1 during the first month of lactation and slightly lower concentrations (1-2 mg·L-1) after that (Lonnerdal et al., 1984). Thus, inasmuch as Zn bioavailability is high in monkey milk, lower Zn intakes than from formula are adequate for nursed infants.
The complexity of assessing Zn status contributes to difficulties in establishing Zn requirements. Plasma or serum Zn concentrations are often used to diagnose Zn deficiency, but substantial decreases in those concentrations often occur only in severe deficiency (King and Keen, 1999). The “normal” mean Zn concentration in cerebrospinal fluid of rhesus monkeys (Macaca mulatta) has been reported to be 1.0 µg·dl-1 (Hambleton et al., 1981). In many of the studies of marginal or moderate Zn deficiency discussed above, plasma or serum Zn concentrations were not markedly affected. Furthermore, the use of galvanized cages has been shown to increase plasma Zn (Stevens et al., 1977) and hair Zn (Marriott et al., 1996). Thus, “normal” plasma Zn concentrations cannot be used to rule out impaired Zn status. Measurement of concentrations of Zn and metallothionein in liver biopsies might be useful in assessment of long-term Zn deprivation (Keen et al., 1988). In a study with rhesus monkeys, infants fed formula with a somewhat lower than usual Zn concentration (1 vs 4 mg·L-1) had “normal” plasma Zn concentrations, but growth and neutrophil chemotaxis were significantly reduced, and a marked increase in Zn absorption indicated impaired Zn status (Polberger et al., 1996).
Zn deficiency has been produced in the squirrel monkey (Saimiri sciureus) (Macapinlac et al., 1967; Barney et al., 1967). The animals were fed a semipurified diet in which low-Zn casein was the protein source. Growth was retarded, the hair coat appeared unkempt, and some alopecia occurred. Hematologic measurements in deficient animals were unchanged. Blood albumin was moderately decreased. Zn in serum and hair was decreased in deficient animals. Thickening of the mucosa of the tongue, particularly over the anterior dorsal surface, occurred within 60 days. Parakeratosis of the tongue developed and appeared to be a unique characteristic of Zn deficiency in this species. The deficiency signs were prevented with Zn at 15 mg·kg-1 of air-dry diet.
The minimal dietary requirement of Zn for squirrel monkeys has not been determined, but Zn at 17 mg·kg-1 of dietary dry matter seems to be adequate for weanling animals in the absence of dietary phytate (Barney et al., 1967).
Zn deficiency also has been observed in the moustached tamarin (Saguinus mystax) (Chadwick et al., 1979). Animals were fed a commercial diet containing Zn at 150 mg·kg-1 of diet, according to the manufacturer, although this value was not confirmed by analysis. The diet was supplemented with apples and oranges. The marmosets developed alopecia on the tail, thinness of hair, open sores about the anus