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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc 12 Zinc SUMMARY Zinc functions as a component of various enzymes in the maintenance of the structural integrity of proteins and in the regulation of gene expression. Overt human zinc deficiency in North America is not common, and the symptoms of a mild deficiency are diverse due to zinc’s ubiquitous involvement in metabolic processes. Factorial analysis was used to set the Estimated Average Requirement (EAR). The Recommended Dietary Allowance (RDA) for adults is 8 mg/ day for women and 11 mg/day for men. Recently, the median intake from food in the United States was approximately 9 mg/day for women and 14 mg/day for men. The Tolerable Upper Intake Level (UL) for adults is 40 mg/day, a value based on reduction in erythrocyte copper-zinc superoxide dismutase activity. BACKGROUND INFORMATION Function Zinc has been shown to be essential for microorganisms, plants, and animals. Deprivation of zinc arrests growth and development and produces system dysfunction in these organisms. The biological functions of zinc can be divided into three categories: catalytic, structural, and regulatory (Cousins, 1996). There is extensive evidence in support of each of these functions, and there may be some overlap.
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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Nearly 100 specific enzymes (e.g., EC 126.96.36.199 alcohol dehydrogenase) depend on zinc for catalytic activity. Zinc removal results in loss of activity, and reconstitution of the holoenzyme with zinc usually restores activity. Examples of zinc metalloenzymes can be found in all six enzyme classes (Vallee and Galdes, 1984). Well-studied zinc metalloenzymes include the ribonucleic acid (RNA) polymerases, alcohol dehydrogenase, carbonic anhydrase, and alkaline phosphatase. Zinc is defined as a Lewis acid, and its action as an electron acceptor contributes to its catalytic activity in many of these enzymes. Changes in activity of zinc metalloenzymes during dietary zinc restriction or excess have not been consistent in experimental studies with humans or animals. The structural role of zinc involves proteins that form domains capable of zinc coordination, which facilitates protein folding to produce biologically active molecules. The vast majority of such proteins form a “zinc finger-like” structure created by chelation centers, including cysteine and histidine residues (Klug and Schwabe, 1995). Some of these proteins have roles in gene regulation as dioxyribonucleic acid binding transcription factors. Examples include nonspecific factors such as Sp1 and specific factors such as retinoic acid receptors and vitamin D receptors. These structural motifs are found throughout biology and include the zinc-containing nucleocapside proteins of viruses such as the human immunodeficiency virus (Berg and Shi, 1996). The relationship of zinc finger protein bioactivity to zinc in the diet has not received extensive study. Zinc also provides a structural function for some enzymes; copper-zinc superoxide dismutase is the most notable example. In this instance, copper provides catalytic activity, whereas zinc’s role is structural. Also of potential relevance as a structural role is the essentiality of zinc for intracellular binding of tyrosine kinase to T-cell receptors, CD4 and CD8α, which are required for T-lymphocyte development and activation (Huse et al., 1998; Lin et al., 1998). The role of zinc as a regulator of gene expression has received less attention than its other functions. Metallothionein expression is regulated by a mechanism that involves zinc’s binding to the transcription factor, metal response element transcription factor (MTF1), which activates gene transcription (Cousins, 1994; Dalton et al., 1997). The number of genes that are activated by this type of mechanism is not known, however, because a null mutation for MTF1 is lethal during fetal development of mice, suggesting some critical genes must be regulated by MTF1 (Günes et al., 1998). Zinc transporter proteins associated with cellular zinc accumulation and release may be among the metal response element-regulated family
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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc of genes (McMahon and Cousins, 1998). Zinc has been shown to influence both apoptosis and protein kinase C activity (McCabe et al., 1993; Telford and Fraker, 1995; Zalewski et al., 1994), which is within the regulatory function. The relationship of zinc to normal synaptic signaling processes also falls within the regulatory role (Cole et al., 1999). The most widely studied MTF-regulated gene is the metallothionein gene. An unequivocal function has not been established, but this metalloprotein appears to act as a zinc trafficking molecule for maintaining cellular zinc concentrations (Cousins, 1996) and perhaps as part of a cellular redox system for zinc donation to zinc finger proteins (Jacob et al., 1998; Roesijadi et al., 1998). Upregulation of metallothionein by specific cytokines and some hormones suggests a function that is critical to a stress response. Induction of metallothionein by changes in dietary zinc intake has received considerable attention in experiments with both animals and humans (reviewed in Chesters, 1997; Cousins, 1994). Erythrocyte metallothionein concentrations decreased rapidly in humans fed a phytate-containing diet of very low zinc content (Grider et al., 1990). Erythrocyte metallothionein concentration appears to be a measure of severe zinc depletion, and the extent of a change in concentration can distinguish between low and adequate levels of zinc intake under experimental conditions (Thomas et al., 1992). Erythrocyte metallothionein and monocyte metallothionein messenger RNA concentrations increase with elevated zinc intake levels such as those encountered with dietary supplements (Grider et al., 1990; Sullivan et al., 1998). Studies of metallothionein concentration in blood cells or plasma during large human dietary trials have not been undertaken. Consequently, the use of metallothionein as a static or functional indicator of zinc status needs further study. While knowledge of the biochemical and molecular genetics of zinc function is well developed and expanding, neither the relationship of these genetics to zinc deficiency or toxicity nor the function(s) for which zinc is particularly critical have been established. For example, explanations for depressed growth, immune dysfunction, diarrhea, altered cognition, host defense properties, defects in carbohydrate utilization, reproductive teratogenesis, and numerous other clinical outcomes of mild and severe zinc deficiency (Hambidge, 1989; King and Keen, 1999) have not been conclusively established. Physiology of Absorption, Metabolism, and Excretion Zinc is widely distributed in foods. Because virtually none of it is present as the free ion, bioavailability is a function of the extent of
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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc digestion. Digestion produces the opportunity for zinc to bind to exogenous and endogenous constituents in the intestinal lumen, including peptides, amino acids, nucleic acids, and other organic acids and inorganic anions such as phosphate. The vast majority of zinc is absorbed by the small intestine through a transcellular process with the jejunum being the site with the greatest transport rate (Cousins, 1989b; Lee et al., 1989; Lonnerdal, 1989). Absorption kinetics appear to be saturable, and there is an increase in transport velocity with zinc depletion. Paracellular transport may occur at high zinc intakes. Transit time also influences the extent of absorption to an extent that, in malabsorption syndromes, zinc absorption is reduced. Transfer from the intestine is via the portal system with most newly absorbed zinc bound to albumin. Considerable amounts of zinc enter the intestine from endogenous sources. Homeostatic regulation of zinc metabolism is achieved principally through a balance of absorption and secretion of endogenous reserves involving adaptive mechanisms programmed by dietary zinc intake (King and Keen, 1999). Zinc depletion in humans is accompanied by reduced endogenous zinc loss on the order of 1.3 to 4.6 mg/day, derived from both pancreatic and intestinal cell secretions. Strong evidence suggests zinc transporter proteins in the various tissues act in concert to obtain such adaptation, but evidence is lacking in humans (McMahon and Cousins, 1998). Measurement of true absorption, which eliminates the contribution of endogenous zinc from calculations, shows that zinc depletion increases the efficiency of intestinal zinc absorption. Regulation of absorption may provide a “coarse control” of body zinc, whereas endogenous zinc release provides “fine control” to maintain balance (King and Keen, 1999). An autosomal recessive trait, acrodermatitis enteropathica, is a zinc malabsorption problem of undetermined genetic basis. The mutation causes severe skin lesions and cognitive dysfunction (Aggett, 1989). The genetic defect suggests that one gene has a major influence on zinc absorption. Tracer studies have shown that zinc is metabolically very active with initial uptake by liver representing a rapid phase of zinc turnover. Over 85 percent of the total body zinc is found in skeletal muscle and bone (King and Keen, 1999). While plasma zinc is only 0.1 percent of this total, its concentration is tightly regulated at about 10 to 15 μmol/L. Stress, acute trauma, and infection cause changes in hormones (e.g., cortisol) and cytokines (e.g., interleukin 6) that lower plasma concentration. Small changes in tissue pools could cause the decrease. In humans, plasma zinc concentrations are maintained without notable change when zinc intake is restricted
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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc or increased unless these changes in intake are severe and prolonged (Cousins, 1989a). Preliminary kinetic data indicate that the combined size of readily exchangeable zinc pools (i.e., those that exchange with zinc in plasma within 72 hours) decreases with dietary zinc restriction (Miller et al., 1994). Fasting results in increased plasma zinc concentration, an outcome that possibly reflects catabolic changes in muscle protein. Cyclic postprandial changes in plasma zinc concentration have been documented (King et al., 1994). In both cases, hormonally regulated events are the biochemical basis for the changes. Albumin is the principal zinc-binding protein in plasma from which most metabolic zinc flux occurs. Functional aspects of zinc tightly bound to α-2-macroglobulin have not been described. Plasma amino acids bind some zinc and could be an important source of zinc excretion. Zinc secretion into and excretion from the intestine provides the major route of endogenous zinc excretion. It is derived partially from pancreatic secretions, which are stimulated after a meal. Biliary secretion of zinc is limited, but intestinal cell secretions also contribute to fecal loss (Lonnerdal, 1989). These losses may range from less than 1 mg/day with a zinc-poor diet to greater than 5 mg/day with a zinc-rich diet, a difference that reflects the regulatory role that the intestinal tract serves in zinc homeostasis. Urinary zinc losses are only a fraction (less than 10 percent) of normal fecal losses (King and Keen, 1999). Zinc transporter activity may account for renal zinc reabsorption (McMahon and Cousins, 1998), and glucagon may help regulate it. Increases in urinary losses are concomitant with increases in muscle protein catabolism due to starvation or trauma. The increase in plasma amino acids, which constitute a potentially filterable zinc pool, is at least partially responsible. Zinc loss from the body is also attributed to epithelial cell desquamation, sweat, semen, hair, and the menstrual cycle. Clinical Effects of Inadequate Intake Individuals with malabsorption syndromes including sprue, Crohn’s disease, and short bowel syndrome are at risk of zinc deficiency due to malabsorption of zinc and increased urinary zinc losses (Pironi et al., 1987; Valberg et al., 1986). In mild human zinc deficiency states, the detectable features and laboratory/functional abnormalities of mild zinc deficiency are diverse. This diversity is not altogether surprising in view of the biochemistry of zinc and the ubiquity of this metal in biology with its participation in an extra-ordinarily wide range of vital metabolic processes. Impaired growth
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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc velocity is a primary clinical feature of mild zinc deficiency and can be corrected with zinc supplementation (Hambidge et al., 1979b; Walravens et al., 1989). Other functions that respond to zinc supplementation include pregnancy outcome (Goldenberg et al., 1995) and immune function (Bogden et al., 1987). Evidence of the efficacy of zinc lozenges in reducing the duration of common colds is still unclear (Jackson et al., 2000). Severe zinc deficiency has been documented in patients fed intravenously without the addition of adequate zinc to the infusates (Chen et al., 1991) and in cases of the autosomal recessively inherited disease acrodermatitis enteropathica (Walling et al., 1989). Because of the ubiquity of zinc and the involvement of this micronutrient in so many core areas of metabolism, it is not surprising that the features of zinc deficiency are frequently quite basic and nonspecific, including growth retardation, alopecia, diarrhea, delayed sexual maturation and impotence, eye and skin lesions, and impaired appetite. Clinical features and laboratory criteria are not always consistent. This inconsistency poses a major difficulty in the quest to validate reliable, sensitive clinical or functional indicators of zinc status that apply to a range of otherwise potentially useful laboratory indicators such as alkaline phosphatase activity. A further major conundrum is posed by the impressive, yet apparently imperfect, homeostatic mechanisms that maintain a narrow range of zinc concentrations within the body in spite of widely diverse dietary intakes of this metal and in spite of differences in bioavailability. This situation applies, for example, to circulating zinc in the plasma, which consequently provides only an insensitive index of zinc status (King, 1990). Therefore, it has become increasingly apparent that homeostatic mechanisms fall short of perfection and that clinically important features of zinc deficiency can occur with only modest degrees of dietary zinc restriction while circulating zinc concentrations are indistinguishable from normal. SELECTION OF INDICATORS FOR ESTIMATING THE REQUIREMENT FOR ZINC Principal Indicator The selection of zinc absorption (more specifically, the minimal quantity of absorbed zinc necessary to match total daily excretion of endogenous zinc) as the principal indicator for adult Estimated Average Requirements (EAR) has been based on the evaluation of a factorial approach to determining zinc requirements. Details of this
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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc approach are discussed under “Findings by Life Stage and Gender Group—Adults Ages 19 Years and Older”. A sufficient number of metabolic studies of zinc homeostasis have been reported to permit an estimation of dietary zinc requirements in adults. The first step in this approach is to calculate nonintestinal losses of endogenous zinc, that is, losses via the kidney and integument with smaller quantities in semen and menstrual losses. Although urinary zinc excretion decreases markedly with severe dietary zinc restriction (Baer and King, 1984), extensive data indicate that excretion by this route is unrelated to dietary zinc intake over a wide range (4 to 25 mg/day) that is certain to encompass the dietary zinc requirements for adults. Data regarding this lack of relation between intake and integumental and semen losses of zinc are more limited. Therefore, nonintestinal losses of endogenous zinc have been treated as a constant in response to varied zinc intake. In contrast to excretion of zinc via other routes, excretion of endogenous zinc via the intestine is a major variable in the maintenance of zinc homeostasis and is strongly correlated with absorbed zinc. The second step in estimating dietary zinc requirements is to define this relationship (Figure 12-1). After it has been defined and adjusted by the constant for other endogenous losses, one can calculate the minimum quantity of absorbed zinc necessary to offset endogenous zinc losses (Figure 12-1). The dietary zinc intake corresponding to this average minimum quantity of absorbed zinc is the EAR. This value has been determined from the plot of the asymptotic regression analysis of absorbed zinc versus ingested zinc (Figure 12-2). Theoretically, given the results described in detail for adults below, balance could also be used as an indicator. However, review of all published data on zinc balance (and net [apparent] absorption) studies in young adult men (excluding those studies that have included tracer data and are being utilized for the current factorial calculations) collectively revealed no correlation with dietary zinc. Presumably this lack of correlation reflects the vagaries of balance studies. The factorial calculations for adults are based on tracer/ metabolic studies in which participants were fed diets from which the bioavailability of zinc was likely to be representative of typical diets in North America or, in some instances, possibly greater than average.
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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc FIGURE 12-1 The relationship between endogenous zinc excretion and absorbed zinc. Heavy line represents the linear regression of intestinal excretion of endogenous zinc (mg/day) versus absorbed zinc (mg/day) from means of ten data sets for healthy men ages 19 through 50 years. The bold dashed lines above and parallel to the regression line represent the total endogenous zinc losses for men and women in relation to zinc absorption. The faint dashed line is the line of perfect agreement or equality of endogenous zinc and absorbed zinc. The intersect of this line with that of total endogenous zinc excretion indicates the average minimum quantity of absorbed zinc necessary to match endogenous losses for men and women. SOURCE: Hunt JR et al. (1992), Jackson et al. (1984), Lee et al. (1993), Taylor et al. (1991), Turnlund et al. (1984, 1986), Wada et al. (1985). Secondary Indicators Physical Growth Response to Zinc Supplementation In contrast to studies on the effects of low-dose zinc supplements on clinical features (e.g., pneumonia, diarrhea [Bhutta et al., 1999]) and on nonspecific laboratory functional tests of zinc status (e.g., tests of neuro-cognitive function [Sandstead et al., 1998]) or immune status (Shankar and Prasad, 1998), studies of the effects of zinc supplementation on physical growth velocity in children are useful in evaluating dietary zinc requirements for several reasons.
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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc FIGURE 12-2 Asymptotic regression of absorbed zinc and ingested zinc. Individual points are means for the same data sets in Figure 12-1. SOURCE: Hunt JR et al. (1992), Jackson et al. (1984), Lee et al. (1993), Taylor et al. (1991), Turnlund et al. (1984, 1986), Wada et al. (1985). First, confirmation of the effect of zinc supplements on growth velocity (linear growth and weight) in children with varying degrees of growth retardation has been shown in a number of studies from many countries (Brown et al., 1998; Umeta et al., 2000). Second, because a sufficient number of these studies have been undertaken in North America, growth is applicable as a functional/clinical indicator of zinc requirement in North American children (Gibson et al., 1989; Walravens and Hambidge, 1976; Walravens et al., 1983, 1989). Third, baseline dietary data typically included in these studies are adequate to use for group analyses. Size and Turnover Rates of Zinc Pools Strong positive correlations have been observed between dietary zinc content, especially the amount of absorbed zinc, and estimates of the size of the combined pools of zinc that exchange with zinc in
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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc plasma (Miller et al., 1994; Sian et al., 1996). Once links to clinical, biochemical, or molecular effects of zinc deficiency have been achieved and appropriate cut-off levels for different age groups and gender have been defined, pool size and turnover measurements may be of value in future refinements of EARs. Even simpler models involving the measurement of plasma zinc clearance may be useful in assessing zinc deficiency, but dietary data derived by such a method are not available at this time (Kaji et al., 1998; Nakamura et al., 1993; Yokoi et al., 1994). More detailed model-based compartmental analyses, when specifically applied to the evaluation of dietary requirements, also have the potential to contribute to a more precise understanding of zinc requirements (Miller et al., 1998; Wastney et al., 1986). Plasma and Serum Zinc Concentration While both plasma zinc concentration and serum zinc concentration are used as indicators of zinc status, plasma zinc concentration is preferable because of the lack of contamination of zinc from the erythrocyte. Homeostatic mechanisms are effective in maintaining plasma zinc concentrations for many weeks of even severe dietary zinc restriction (Johnson et al., 1993; Wada et al., 1985). A number of studies have reported no association between dietary zinc intake and plasma or serum zinc concentration (Artacho et al., 1997; Kant et al., 1989; Neggers et al., 1997; Thomas et al., 1988). Payette and Gray-Donald (1991) did observe a significant correlation between dietary zinc intake and serum zinc concentration in noninstitutionalized elderly; however, the correlation was positive for men and negative for women. Discernible relationships have been reported between plasma zinc concentration and habitual dietary zinc intake, even within the range typically occurring in North America. These relationships are of some utility in providing a supportive indicator of zinc requirements. For example, serum zinc concentrations of Canadian adolescent girls aged 14 to 19 years vary inversely with phytate:zinc molar ratios, and a greater percentage of lactoovo-vegetarians have serum zinc values below 70 μg/dL than do omnivores (Donovan and Gibson, 1995). Cut-off concentrations for lower limits have been established and depend on the time of day at which collections are made because of the substantial and cumulative effects of meals in lowering concentrations (King et al., 1994). The cut-off concentrations for prebreakfast samples is 70 μg/dL. Different cut-off concentrations are not considered necessary for different age groups or genders.
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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Insufficient and inconsistent data exist for plasma or serum zinc concentrations in apparently normal subjects whose habitual dietary zinc intakes straddle the vicinity of the average requirement, and therefore use of those concentrations for estimating an average requirement is limited. Furthermore, plasma and serum zinc concentrations do not seem to be sufficiently sensitive to serve as a subsidiary indicator. Zinc Concentration in Erythrocytes Erythrocyte zinc concentration is depressed at moderately severe levels of dietary zinc restriction (Thomas et al., 1992), but the sensitivity of this assay is inadequate to provide more than a secondary supportive indicator of dietary zinc requirements. Sample preparation may account for some of the lack of sensitivity. Results from experimental depletion studies (Baer and King, 1984; Bales et al., 1994; Grider et al., 1990; Ruz et al., 1992; Thomas et al., 1992) have been mixed, and the value of erythrocyte zinc concentrations as an indicator of zinc nutritional status is not well defined. Zinc Concentration in Hair Associations between low zinc concentration in hair and poor growth have been documented (Ferguson et al., 1993; Gibson et al., 1989; Hambidge et al., 1972; Walravens et al., 1983). In three of these studies, low zinc concentration in hair was used as a criterion for zinc supplementation in children and resulted in increased growth velocity. Low zinc concentrations in hair have been reported in Canadian children with low meat consumption (Smit-Vanderkooy and Gibson, 1987). Subjects whose habitual diets are high in phytate or who have very high phytate:zinc molar ratios have also been noted to have relatively low zinc concentrations in hair. However, there is a lack of uniformity in apparently low zinc concentrations in hair, and no lower cut-off values have been defined clearly for any age group or either gender. The use of zinc in hair as a supportive indicator for establishing zinc requirements needs further research. Activity of Zinc-Dependent Enzymes With the large number of zinc-dependent enzymes that have been identified, it is perhaps remarkable that no single zinc-dependent enzyme has found broad acceptance as an indicator of zinc status or
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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Cakman I, Kirchner H, Rink L. 1997. Zinc supplementation reconstitutes the production of interferon-α by leukocytes from elderly persons. J Interferon Cytokine Res 17:469–472. Casey CE, Hambidge KM, Neville MC. 1985. Studies in human lactation: Zinc, copper, manganese and chromium in human milk in the first month of lactation. Am J Clin Nutr 41:1193–1200. Casey CE, Neville MC, Hambidge KM. 1989. Studies in human lactation: Secretion of zinc, copper, and manganese in human milk. Am J Clin Nutr 49:773–785. Caulfield LE, Zavaleta N, Figueroa A. 1999a. Adding zinc to prenatal iron and folate supplements improves maternal and neonatal zinc status in a Peruvian population. Am J Clin Nutr 69:1257–1263. Caulfield LE, Zavaleta N, Figueroa A, Leon Z. 1999b. Maternal zinc supplementation does not affect size at birth or pregnancy duration in Peru. J Nutr 129:1563–1568. Chandra RK. 1984. Excessive intake of zinc impairs immune responses. J Am Med Assoc 252:1443–1446. Cheek DB, Reba RC, Woodward K. 1968. Cell growth and the possible role of trace minerals. In: Cheek DB, ed. Human Growth; Body Composition, Cell Growth, Energy, and Intelligence. Philadelphia: Lea and Febiger. Pp. 424–439. Chen W, Chiang TP, Chen TC. 1991. Serum zinc and copper during long-term total parenteral nutrition. J Formos Med Assoc 90:1075–1080. Chesters JK. 1997. Zinc. In: O’Dell BL, Sunde RA, eds. Handbook of Nutritionally Essential Mineral Elements. New York: Marcel Dekker. Pp. 185–230. Cole TB, Wenzel HJ, Kafer KE, Schwartzkroin PA, Palmiter RD. 1999. Elimination of zinc from synaptic vesicles in the intact mouse brain by disruption of the ZnT3 gene. Proc Natl Acad Sci USA 96:1716–1721. Colin MA, Taper LJ, Ritchey SJ. 1983. Effect of dietary zinc and protein levels on the utilization of zinc and copper by adult females. J Nutr 113:1480–1488. Coudray C, Bellanger J, Castiglia-Delavaud C, Remesy C, Vermorel M, Rayssignuier Y. 1997. Effect of soluble or partly soluble dietary fibres supplementation on absorption and balance of calcium, magnesium, iron and zinc in healthy young men. Eur J Clin Nutr 51:375–380. Cousins RJ. 1985. Absorption, transport, and hepatic metabolism of copper and zinc: Special reference to metallothionein and ceruloplasmin. Physiol Rev 65:238–309. Cousins RJ. 1989a. Systemic transport of zinc. In: Mills CF, ed. Zinc in Human Biology. New York: Springer-Verlag. Pp. 79–93. Cousins RJ. 1989b. Theoretical and practical aspects of zinc uptake and absorption. Adv Exp Med Biol 249:3–12. Cousins RJ. 1994. Metal elements and gene expression. Ann Rev Nutr 14:449–469. Cousins RJ. 1996. Zinc. In: Filer LJ, Ziegler EE, eds. Present Knowledge in Nutrition, 7th ed. Washington, DC: International Life Science Institute-Nutrition Foundation. Pp. 293–306. Couzy F, Kastenmayer P, Mansourian R, Guinchard S, Munoz-Box R, Dirren H. 1993. Zinc absorption in healthy elderly humans and the effect of diet. Am J Clin Nutr 58:690–694. Dalton TP, Bittel D, Andrews GK. 1997. Reversible activation of mouse metal response element-binding transcription factor 1 DNA binding involves zinc interaction with the zinc finger domain. Molec Cell Biol 17:2781–2789.
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