Abstract
The essential role of the trace element zinc in both the prenatal and post-natal periods of mammalian development has been well documented (Underwood, 1977; Hurley, 1980; Prasad, 1976). Zinc is important in many ways: it is required for the activity of numerous enzymes (Parisi and Yallee, 1969), and is important for stability of biological membranes (Chvapil, 1973), for integrity and synthesis of nucleic acids (Dreosti et al., 1972; Dreosti and Hurley, 1975; Eckhert and Hurley, 1977; Eichhorn et al., 1973), and for synthesis of proteins and lipids (Underwood, 1977). Based on the large number of important reactions that involve zinc, it is reasonable to suppose that metabolism of this element is under some regulation. It has been suggested that the primary site of zinc homeostasis is the intestine (Cotzias et al., 1962; Cousins, 1979a, 1979b; Weigand and Kirchgessner, 1976a, 1976b, 1980). Currently, most investigators think that zinc homeostasis in the intestine, occurring through absorption or excretion of the element (or both), is mediated in part by low molecular weight (LMW) ligands. This area of nutrition research has been the subject of considerable recent interest, especially because of reports of dietary zinc deficiency in various age groups of several human populations (Prasad, 1976; Hambidge et al., 1972, 1976; Jameson, 1976, 1981). Zinc deficiency in humans has been correlated with a number of disorders, including congenital malformations and complications of pregnancy, poor growth and development during infancy, childhood, and adolescence, and impaired immunocompetence.
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Lönnerdal, B., Keen, C.L., Hurley, L.S. (1984). Zinc Binding Ligands and Complexes in Zinc Metabolism. In: Draper, H.H. (eds) Advances in Nutritional Research. Advances in Nutritional Research, vol 110. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2801-8_6
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