and tail, and were generally debilitated. The lesions were reversed by adding ZnSO4·7H2O to provide Zn at 40 mg·L-1 in drinking water. The alopecia returned when the animals were given Zn at 80 mg·L-1 of drinking water, and some hair regrowth occurred when Zn in the water was returned to 40 mg·L-1. The reason for the adverse effect of the higher concentration of Zn was not apparent.
Increased serum Zn has been found in Senegalese baboons (Papio papio) that were moderately sensitive to light-induced seizures. Chronic oral administration of the chelating agent, D-penicillamine, lowered serum Zn and protected against the seizures (Alley et al., 1981).
Iodine (I) is a part of the thyroid hormones thyroxine (3,5,3'5'-tetraiodothyronine) and 3,5,3'-triiodothyronine (Stanbury, 1996). Thus, I plays a major role in the regulation of growth and of metabolic rate. Although it is found in generous amounts in oceans, much of the I originally present in soil has been leached from surface layers by glaciers, snow, and rain. Ocean winds carry I-bearing moisture to near-shore areas, but ancient interior soils and the plants growing on them are often I-deficient.
Potassium iodide, calcium iodate, ethylenediamine dihydriodide, and pentacalcium orthoperiodate are sources of I commonly added to animal diets to prevent deficiency. All four have high bioavailability. Calcium iodate, ethylenediamine dihydriodide, and pentacalcium orthoperiodate have greater physical stability (Miller and Ammerman, 1995).
Schultz et al. (1965) and Pickering (1968) reported on the uptake of radioiodine by the thyroid glands of pregnant rhesus monkeys (Macaca mulatta) and their fetuses. Fetal thyroids incorporated radioiodine more rapidly than maternal thyroids. Both maternal and fetal thyroids contained substantial I-containing thyroid hormones. Thyroidectomized infant rhesus monkeys exhibited nearly all the signs of cretinism seen in humans (Pickering and Fisher, 1953a, 1953b), but frank deficiency signs were not produced by feeding I-deficient diets. It is noteworthy that low protein concentrations (2%) in the diet of Macaca nemestrina resulted in thyroidal ultrastructural changes mimicking thyroid hypofunction induced by hypophysectomy or thyroxine administration (Worthington and Enwonwu, 1975). However, the thyroidal changes may be a consequence of tyrosine deficiency associated with low protein intake and have little relationship to the I supply.
Iodine deficiency has been produced in the common marmoset (Callithrix jacchus) by feeding a diet composed of natural ingredients selected for their low I content (Mano et al., 1985). The diet furnished I at about 0.36 g·d-1. On the basis of DMintake of about 12-13 g·d-1, dietary I concentration was 0.03 g·g-1 of DM. Body weights were maintained, and there were no clinical signs of ill health. However, mean plasma thyroxine concentration declined from an original value of 140.1 nmol·L-1 to 22.4 nmol·L-1, and mean plasma thyroid-stimulating hormone concentration increased from 1.8 ng·ml-1 to 9.0 ng·ml-1. Compared with newborn offspring of control marmosets receiving a potassium iodate supplement providing I at 7.9 µg·d-1 (0.65 µg·g-1 of dietary DM), the young of I-deficient females had heavier thyroid glands and lower thyroidal I concentrations. On histologic examination, their thyroid glands exhibited hypertrophy and hyperplasia; follicular colloid was absent.
The infants from first and second pregnancies were evaluated in further studies. Those of mothers fed the low-I diet had sparse hair coats but were not different from controls in body weight or skeletal development. The brain weights of deficient newborns from the second pregnancies were reduced, particularly those of the cerebellum, where brain-cell numbers were reduced. Brain-stem cell size was reduced in the cerebrum. Offspring from the second pregnancies were more severely affected than those from the first (Mano et al., 1987).
Young marmosets born of mothers fed an I-deficient diet in the studies of Mano et al. (1985) were fed a deficient or a normal diet (Goss et al., 1988). They were compared with animals born of mothers fed a normal diet and themselves fed a normal diet. Marmosets from I-deficient mothers and fed the deficient diet were smaller at birth and grew more slowly; whereas those fed the normal diet were smaller at birth but exhibited compensatory growth and were of nearly normal size by the age of 1 year. The I-deficient animals did not have a typical cretin face.
Specific quantitative requirements for I have not been determined. The studies with marmosets indicate that 0.03 mg·kg-1 of dietary DMis insufficient but that 0.65 mg·kg-1 is sufficient. Diets containing I at about 2.2 mg·kg-1 of dietary DM were previously deemed adequate for most growing and adult nonhuman primates (National Research Council, 1978), but this concentration appears not to have been judged a minimum requirement. Estimates of I requirements for other species reported in the National Research Council nutrient requirement series do not exceed 0.35 mg·kg-1 of dietary DM.
Most of the selenium (Se) in biologic systems is in amino acid constituents of proteins. Proteins that contain Se in stoichiometric amounts are called selenoproteins; selenocysteine is the primary reactive structure in the animal selenoproteins that have been identified (Burk and Levander, 1999). A number of proteins contain Se in nonstoichiometric amounts and are called simply Se-containing proteins; this Se is often found in selenomethionine, and