cupric oxide, CuO, is absorbed very poorly by most species (Baker and Ammerman, 1995a). However, no studies on the biologic availability of Cu in these compounds have been conducted with nonhuman primates.

Excessive dietary zinc can lead to Cu deficiency in a number of mammalian species (Baker and Ammerman, 1995a). That could be important in infant primates raised with their mothers in breeding colonies in galvanized cages, such as corncribs. Under such circumstances, depigmentation of the hair (achromotrichia), alopecia, weakness, and microcytic anemia were observed in infants of rhesus (Macaca mulatta) mothers fed commercial diets but not in the adults. The achromotrichia was described as development of a steel-gray hair coat. Serum zinc was increased, and serum Cu decreased. Animals raised in stainless-steel cages and fed the same diet did not develop the syndrome. High intakes of zinc from the galvanized caging apparently induced a Cu deficiency in the infant animals (Stevens et al. 1977; Obeck, 1978; Wagner et al., 1985). Stevens et al. (1977) and Wagner et al. (1985) gave no details on diet composition. Obeck (1978) reported that the commercial diet contained zinc at 34 mg·kg-1 and Cu at 10 mg·kg-1, an insufficient amount of Cu to prevent the syndrome. Higher concentrations were not evaluated, so it is not known whether the effect of galvanized caging on infant rhesus can be overcome by increasing the Cu in rations consumed mostly by the mothers. Hypocupremia, sider-oblastic anemia, leukopenia, and neutropenia were observed in an adolescent human who ingested excessive amounts of zinc (Porea et al., 2000).

Low Cu status in infant rhesus monkeys also has been induced by feeding a commercial canned infant liquid formula designed for human infants (Lonnerdal et al., 2001). Information on the form of Cu in the liquid formula and the heat treatment to which it was subjected were not revealed by the manufacturer of the product. However, the Cu concentration was described to be comparable to that in other commercial products tested at the same time. The researchers speculated that the conditions of heat processing might have reduced Cu availability, thereby inducing a Cu deficiency. Besides hypocupremia, low serum ceruloplasmin, and low erythrocyte Cu, Zn-superoxide dismutase activity, the monkeys became anemic and had a change in hair color.

Fischer and Giroux (1987) fed a specially formulated commercial type of monkey diet containing zinc at 30 mg·kg-1and Cu at 6 mg·kg-1to cynomolgus (Macaca fascicularis) monkeys. The diet was supplemented with 10 or 24 mg of zinc each day. The 10-mg zinc supplement was given to the control group to meet the nutritional requirement and compensate for zinc bound to dietary phytate. The male and female animals weighed about 3.5 and 2.7 kg and ate 120 and 90 g·d-1, respectively. Monkeys that received the 24-mg zinc supplement had higher plasma zinc, lower plasma Cu, and somewhat increased plasma cholesterol. Plasma ceruloplasmin, hematocrit, and hemoglobin were not affected. Increased plasma cholesterol is a sign of Cu deficiency in rats and humans. In this experiment, zinc supplementation appeared to impair Cu status.

Adult cynomolgus monkeys weighing 4.2-4.8 kg were fed purified liquid diets containing Cu at about 0.4 mg·kg-1 of DMfor 28 weeks (Milne et al., 1981). High concentrations of ascorbic acid are known to reduce Cu use in several species (Baker and Ammerman, 1995a), so the effect of ascorbic acid was evaluated by giving animals a supplement of 1 or 25 mg of ascorbic acid per kilogram of body weight. There was relatively little change in serum Cu or ceruloplasmin (a Cu-containing enzyme) concentrations, but there was a significant increase in serum cholesterol rising from 80 mg·dl-1 to 108 mg·dl-1. At the end of 28 weeks, approximately 2 mg of Cu·kg-1 of DMwere added to the diet, furnishing a total Cu concentration of about 2.5 mg·kg-1 of dietary DM. After 4 weeks on this Cu-supplemented diet, serum cholesterol concentrations of animals receiving the higher amounts of ascorbic acid were elevated above those of animals receiving the lower amounts of ascorbic acid, suggesting that ascorbic acid may have interfered with Cu absorption.

Available data are not sufficient to establish a Cu requirement. Cu at 12-20 mg·kg-1 in commercial diets seems to be sufficient under most conditions (Knapka et al., 1995). However, it might not be sufficient for breeding colonies exposed to high concentrations of zinc from galvanized caging. Cu from CuSO4 at about 2 mg·kg-1 of diet was sufficient to reverse an increase in cholesterol in adult cynomolgus monkeys (Milne et al., 1981). Cu at 15 mg·kg-1 of dietary DMshould be sufficient to meet the dietary needs of animals not exposed to excessive dietary zinc.


Manganese (Mn) is a constituent of several metalloenzymes, such as arginase, pyruvate carboxylase, glutamine synthetase, and Mn-superoxide dismutase. Such enzymes as oxidoreductases, lyases, ligases, hydrolases, kinases, decarboxylases, and transferases can be activated by Mn, but most of these can also be activated by other cations, particularly magnesium (Nielsen, 1999).

Manganous sulfate and manganous oxide are the most common supplemental forms of Mn used in animal feeds. Compared with manganous sulfate, the bioavailability of manganese oxide in chicks was 60-77%, and that of manganous carbonate was 32-36% (McDowell, 1992).

Mn deficiency has been demonstrated in a number of avian and mammalian species. Female rhesus (Macaca mulatta) monkeys fed a semisynthetic diet containing Mn at 0.5 were mated and maintained on this low-Mn diet throughout their pregnancy. Their infants were

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