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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 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 1.1.1.1 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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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Davidsson L, Mackenzie J, Kastenmayer P, Aggett PJ, Hurrell RF. 1996. Zinc and calcium apparent absorption from an infant cereal: A stable isotope study in healthy infants. Br J Nutr 75:291–300. Davis CD, Milne DB, Nielsen FH. 2000. Changes in dietary zinc and copper affect zinc-status indicators of postmenopausal women, notably extracellular superoxide dismutase and amyloid precursor proteins. Am J Clin Nutr 71:781–788. Devine A, Rosen C, Mohan S, Baylink D, Prince RL. 1998. Effects of zinc and other nutritional factors on insulin-like growth factor I and insulin-like growth factor binding proteins in postmenopausal women. Am J Clin Nutr 68:200–206. Dewey KG, Cohen RJ, Brown KH, Rivera LL. 1999. Age of introduction of complementary foods and growth of term, low-birth-weight, breast-fed infants: A randomized intervention study in Honduras. Am J Clin Nutr 69:679–686. Donovan UM, Gibson RS. 1995. Iron and zinc status of young women aged 14 to 19 years consuming vegetarian and omnivorous diets. J Am Coll Nutr 14:463–472. Donovan UM, Gibson RS. 1996. Dietary intakes of adolescent females consuming vegetarian, semi-vegetarian, and omnivorous diets. J Adolesc Health 18:292–300. Duchateau J, Delepesse G, Vrijens R, Collet H. 1981. Beneficial effects of oral zinc supplementation on the immune response of old people. Am J Med 70:1001–1004. Ellis R, Kelsay JL, Reynolds RD, Morris ER, Moser PB, Frazier CW. 1987. Phytate:zinc and phytate x calcium:zinc millimolar ratios in self-selected diets of Americans, Asian Indians, and Nepalese. J Am Diet Assoc 87:1043–1047. Faber M, Gouws E, Spinnler Benade AJ, Labadarios D. 1986. Anthropometric measurements, dietary intake and biochemical data of South African lactoovovegetarians. S Afr Med J 69:733–738. Failla ML. 1999. Considerations for determining “optimal nutrition” for copper, zinc, manganese and molybdenum. Proc Nutr Soc 58:497–505. Fairweather-Tait SJ, Wharf SG, Fox TE. 1995. Zinc absorption in infants fed iron-fortified weaning food. Am J Clin Nutr 62:785–789. Ferguson EL, Gibson RS, Opare-Obisaw C, Ounpuu S, Thompson LU, Lehrfeld J. 1993. The zinc nutriture of preschool children living in two African countries. J Nutr 123:1487–1496. Festa MD, Anderson HL, Dowdy RP, Ellersieck MR. 1985. Effect of zinc intake on copper excretion and retention in men. Am J Clin Nutr 41:285–292. Fischer PWF, Giroux A, L’Abbe MR. 1984. Effect of zinc supplementation on copper status in adult man. Am J Clin Nutr 40:743–746. Fortes C, Forastiere F, Agabiti N, Fano V, Pacifici R, Virgili F, Piras G, Guidi L, Bartoloni C, Tricerri A, Zuccaro P, Ebrahim S, Perucci CA. 1998. The effect of zinc and vitamin A supplementation on immune response in an older population. J Am Geriatr Soc 46:19–26. Fosmire GJ. 1990. Zinc toxicity. Am J Clin Nutr 51:225–227. Fransson GB, Lonnerdal B. 1982. Zinc, copper, calcium, and magnesium in human milk. J Pediatr 101:504–508. Freeland-Graves JH, Bodzy PW, Eppright MA. 1980a. Zinc status of vegetarians. J Am Diet Assoc 77:655–661. Freeland-Graves JH, Ebangit ML, Hendrikson PJ. 1980b. Alterations in zinc absorption and salivary sediment zinc after a lacto-ovo-vegetarian diet. Am J Clin Nutr 33:1757–1766. Freeland-Graves JH, Friedman BJ, Han WH, Shorey RL, Young R. 1982. Effect of zinc supplementation on plasma high-density lipoprotein cholesterol and zinc. Am J Clin Nutr 35:988–992.

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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 Fung EB, Ritchie LD, Woodhouse LR, Roehl R, King JC. 1997. Zinc absorption in women during pregnancy and lactation: A longitudinal study. Am J Clin Nutr 66:80–88. Ganapathy SN, Booker LK, Craven R, Edwards CH. 1981. Trace minerals, amino acids, and plasma proteins in adult men fed wheat diets. J Am Diet Assoc 78:490–497. Gibson RS. 1994. Content and bioavailability of trace elements in vegetarian diets. Am J Clin Nutr 59:1223S–1232S. Gibson RS, Vanderkooy PD, MacDonald AC, Goldman A, Ryan BA, Berry M. 1989. A growth-limiting, mild zinc-deficiency syndrome in some southern Ontario boys with low height percentiles. Am J Clin Nutr 49:1266–1273. Gibson RS, Donovan UM, Heath AL. 1997. Dietary strategies to improve the iron and zinc nutriture of young women following a vegetarian diet. Plant Foods Hum Nutr 51:1–16. Gibson RS, Heath AL, Prosser N, Parnell W, Donovan UM, Green T, McLaughlin KE, O’Connor DL, Bettger W, Skeaff CM. 2000. Are young women with low iron stores at risk of zinc as well as iron deficiency? In: Roussel AM, Anderson RA, Favrier A, eds. Trace Elements in Man and Animals 10. New York: Kluwer Academic. Pp. 323–328. Goldenberg RL, Tamura T, Neggers Y, Copper RL, Johnston KE, DuBard MB, Hauth JC. 1995. The effect of zinc supplementation on preganancy outcome. J Am Med Assoc 274:463–468. Greger JL, Snedeker SM. 1980. Effect of dietary protein and phosphorus levels on the utilization of zinc, copper and manganese by adult males. J Nutr 110:2243–2253. Greger JL, Baligar P, Abernathy RP, Bennett OA, Peterson T. 1978. Calcium, magnesium, phosphorus, copper, and manganese balance in adolescent females. Am J Clin Nutr 31:117–121. Grider A, Bailey LB, Cousins RJ. 1990. Erythrocyte metallothionein as an index of zinc status in humans. Proc Natl Acad Sci USA 87:1259–1262. Günes C, Heuchel R, Georgiev O, Müller K-H, Lichtlen P, Blüthmann H, Marino S, Aguzzi A, Schaffner W. 1998. Embryonic lethality and liver degeneration in mice lacking the metal-responsive transcriptional activator MTF-1. Embo J 17:2846–2854. Gunshin H, Mackenzie B, Berger UV, Gunshin Y, Romero MF, Boron WF, Nussberger S, Gollan JL, Hediger MA. 1997. Cloning and characterization of a mammalian proton-coupled metal-ion transporter. Nature 388:482–488. Hallfrisch J, Powell A, Carafelli C, Reiser S, Prather ES. 1987. Mineral balances of men and women consuming high fiber diets with complex or simple carbohydrate. J Nutr 117:48–55. Hambidge KM. 1989. Mild zinc deficiency in human subjects. In: Mills CF, ed. Zinc in Human Biology. New York: Springer-Verlag. Pp. 281–296. Hambidge KM, Hambidge C, Jacobs M, Baum JD. 1972. Low levels of zinc in hair, anorexia, poor growth, and hypogeusia in children. Pediatr Res 6:868–874. Hambidge KM, Chavez MN, Brown RM, Walravens PA. 1979a. Zinc nutritional status of young middle-income children and effects of consuming zinc-fortified breakfast cereals. Am J Clin Nutr 32:2532–2539. Hambidge KM, Walravens PA, Casey CE, Brown RM, Bender C. 1979b. Plasma zinc concentrations of breast-fed infants. J Pediatr 94:607–608.

OCR for page 442
Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Hambidge KM, Krebs NF, Jacobs MA, Favier A, Guyette L, Ikle DN. 1983. Zinc nutritional status during pregnancy: A longitudinal study. Am J Clin Nutr 37:429–442. Han O, Failla ML, Hill AD, Morris ER, Smith JC Jr. 1994. Inositol phosphates inhibit uptake and transport of iron and zinc by a human intestinal cell line. J Nutr 124:580–587. Harland BF, Peterson M. 1978. Nutritional status of lacto-ovo vegetarian Trappist monks. J Am Diet Assoc 72:259–264. Harland BF, Smith SA, Howard MP, Ellis R, Smith JC Jr. 1988. Nutritional status and phytate:zinc and phytate x calcium:zinc dietary molar ratios of lacto-ovo vegetarian Trappist monks: 10 years later. J Am Diet Assoc 88:1562–1566. Heinig MJ, Nommsen LA, Peerson JM, Lonnerdal B, Dewey KG. 1993. Energy and protein intakes of breast-fed and formula-fed infants during the first year of life and their association with growth velocity: The DARLING Study. Am J Clin Nutr 58:152–161. Hess FM, King JC, Margen S. 1977. Zinc excretion in young women on low zinc intakes and oral contraceptive agents. J Nutr 107:1610–1620. Holbrook JT, Smith JC Jr, Reiser S. 1989. Dietary fructose or starch: Effects on copper, zinc, iron, manganese, calcium, and magnesium balances in humans. Am J Clin Nutr 49:1290–1294. Hooper PL, Visconti L, Garry PJ, Johnson GE. 1980. Zinc lowers high-density lipoprotein-cholesterol levels. J Am Med Assoc 244:1960–1961. Hunt CD, Johnson PE, Herbel J, Mullen LK. 1992. Effects of dietary zinc depletion on seminal volume and zinc loss, serum testosterone concentrations, and sperm morphology in young men. Am J Clin Nutr 56:148–157. Hunt IF, Murphy NJ, Henderson C. 1988. Food and nutrient intake of Seventh-day Adventist women. Am J Clin Nutr 48:850–851. Hunt JR. 1996. Bioavailability algorithms in setting recommended dietary allowances: Lessons from iron, applications to zinc. J Nutr 126:2345S–2353S. Hunt JR, Mullen LK, Lykken GI. 1992. Zinc retention from an experimental diet based on the US FDA Total Diet Study. Nutr Res 12:1335–1344. Hunt JR, Gallagher SK, Johnson LK, Lykken GI. 1995. High- versus low-meat diets: Effects on zinc absorption, iron status, and calcium, copper, iron, magnesium, manganese, nitrogen, phosphorus, and zinc balance in postmenopausal women. Am J Clin Nutr 62:621–632. Hunt JR, Matthys LA, Johnson LK. 1998. Zinc absorption, mineral balance, and blood lipids in women consuming controlled lactoovovegetarian and omnivorous diets for 8 weeks. Am J Clin Nutr 67:421–430. Huse M, Eck MJ, Harrison SC. 1998. A Zn2+ ion links the cytoplasmic tail of CD4 and the N-terminal region of Lck. J Biol Chem 273:18729–18733. Jackson JL, Lesho E, Peterson C. 2000. Zinc and the common cold: A meta-analysis revisted. J Nutr 130:1512S-1515S. Jackson MJ, Jones DA, Edwards RH, Swainbank IG, Coleman ML. 1984. Zinc homeostasis in man: Studies using a new stable isotope-dilution technique. Br J Nutr 51:199–208. Jacob C, Maret W, Vallee BL. 1998. Control of zinc transfer between thionein, metallothionein, and zinc proteins. Proc Natl Acad Sci USA 95:3489–3494. Janelle KC, Barr SI. 1995. Nutrient intakes and eating behavior scores of vegetarian and nonvegetarian women. J Am Diet Assoc 95:180–186, 189. Johansson G, Widerstrom L. 1994. Change from mixed diet to lactovegetarian diet: Influence on IgA levels in blood and saliva. Scand J Dent Res 102:350–354.

OCR for page 442
Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Johnson MA, Baier MJ, Greger JL. 1982. Effects of dietary tin on zinc, copper, iron, manganese, and magnesium metabolism of adult males. Am J Clin Nutr 35:1332–1338. Johnson PE, Evans GW. 1978. Relative zinc availability in human breast milk, infant formulas, and cow’s milk. Am J Clin Nutr 31:416–421. Johnson PE, Hunt CD, Milne DB, Mullen LK. 1993. Homeostatic control of zinc metabolism in men: Zinc excretion and balance in men fed diets low in zinc. Am J Clin Nutr 57:557–565. Kadrabova J, Madaric A, Kovacikova Z, Ginter E. 1995. Selenium status, plasma zinc, copper, and magnesium in vegetarians. Biol Trace Elem Res 50:13–24. Kaji M, Gotoh M, Takagi Y, Masuda H, Kimura Y, Uenoyama Y. 1998. Studies to determine the usefulness of the zinc clearance test to diagnose marginal zinc deficiency and the effects of oral zinc supplementation for short children. J Am Coll Nutr 17:388–391. Kant AK, Moser-Veillon PB, Reynolds RD. 1989. Dietary intakes and plasma concentrations of zinc, copper, iron, magnesium, and selenium of young, middle aged, and older men. Nutr Res 9:717–724. Kauwell GP, Bailey LB, Gregory JF 3rd, Bowling DW, Cousins RJ. 1995. Zinc status is not adversely affected by folic acid supplementation and zinc intake does not impair folate utilization in human subjects. J Nutr 125:66–72. Kelsay JL, Frazier CW, Prather ES, Canary JJ, Clark WM, Powell AS. 1988. Impact of variation in carbohydrate intake on mineral utilization by vegetarians. Am J Clin Nutr 48:875–879. Kies CV. 1988. Mineral utilization of vegetarians: Impact of variation in fat intake. Am J Clin Nutr 48: 884–887. King JC. 1990. Assessment of zinc status. J Nutr 120:1474–1479. King JC, Keen CL. 1999. Zinc. In: Shils ME, Olson JA, Shike M, Ross AC, eds. Modern Nutrition in Health and Disease, 9th ed. Baltimore: Williams & Wilkins. Pp. 223–239. King JC, Turnlund JR. 1989. Human zinc requirements. In: Mills CF, ed. Zinc in Human Biology. London: Springer-Verlag. Pp. 335–350. King JC, Stein T, Doyle M. 1981. Effect of vegetarianism on the zinc status of pregnant women. Am J Clin Nutr 34:1049–1055. King JC, Hambidge KM, Westcott JL, Kern DL, Marshall G. 1994. Daily variation in plasma zinc concentrations in women fed meals at six-hour intervals. J Nutr 124:508–516. Kirksey A, Ernst JA, Roepke JL, Tsai TL. 1979. Influence of mineral intake and use of oral contraceptives before pregnancy on the mineral content of human colostrum and of more mature milk. Am J Clin Nutr 32:30–39. Klug A, Schwabe JWR. 1995. Zinc fingers. FASEB J 9:597–604. Krajcovicova-Kudlackova M, Simoncic R, Babinska K, Bederova A, Brtkova A, Magalova T, Grancicova E. 1995. Selected vitamins and trace elements in blood of vegetarians. Ann Nutr Metab 39:334–339. Krebs NF, Hambidge KM. 1986. Zinc requirements and zinc intakes of breast-fed infants. Am J Clin Nutr 43:288–292. Krebs NF, Hambidge KM, Jacobs MA, Rasbach JO. 1985. The effects of a dietary zinc supplement during lactation on longitudinal changes in maternal zinc status and milk zinc concentrations. Am J Clin Nutr 41:560–570. Krebs NF, Reidinger CJ, Robertson AD, Hambidge KM. 1994. Growth and intakes of energy and zinc in infants fed human milk. J Pediatr 124:32–39.

OCR for page 442
Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Krebs NF, Reidinger CJ, Hartley S, Robertson AD, Hambidge KM. 1995. Zinc supplementation during lactation: Effects on maternal status and milk zinc concentrations. Am J Clin Nutr 61:1030–1036. Krebs NF, Reidinger CJ, Miller LV, Hambidge KM. 1996. Zinc homeostasis in breast-fed infants. Pediatr Res 39:661–665. Kuczmarski RJ, Ogden CL, Grummer-Strawn LM, Flegal KM, Guo SS, Wei R, Mei Z, Curtin LR, Roche AF, Johnson CL. 2000. CDC Growth Charts: United States. Advance data from vital health statistics. No. 314. Hyattesville, MD: National Center for Health Statistics. Kumar S. 1976. Effect of zinc supplementation on rats during pregnancy. Nutr Rpts Intl 13:33–36. Lee DY, Prasad AS, Hydrick-Adair C, Brewer G, Johnson PE. 1993. Homeostasis of zinc in marginal human zinc deficiency: Role of absorption and endogenous excretion of zinc. J Lab Clin Med 122:549–556. Lee HH, Prasad AS, Brewer GJ, Owyang C. 1989. Zinc absorption in human small intestine. Am J Physiol 256:G87–G91. Levin N, Rattan J, Gilat T. 1986. Mineral intake and blood levels in vegetarians. Isr J Med Sci 22:105–108. Lin RS, Rodriguez C, Veillette A, Lodish HF. 1998. Zinc is essential for binding of p56lck to CD4 and CD8α. J Biol Chem 273:32878–32882. Lonnerdal B. 1989. Intestinal absorption of zinc. In: Mills CF, ed. Zinc in Human Biology. New York: Springer-Verlag. Pp. 33–55. Lonnerdal B, Keen CL, Hurley LS. 1981. Iron, copper, zinc and manganese in milk. Ann Rev Nutr 1:149–174. Lonnerdal B, Bell JG, Hendrickx AG, Burns RA, Keen CL. 1988. Effect of phytate removal on zinc absorption from soy formula. Am J Clin Nutr 48:1301–1306. Lowik MR, Schrijver J, Odink J, van den Berg H, Wedel M. 1990. Long-term effects of a vegetarian diet on the nutritional status of elderly people (Dutch Nutrition Surveillance System). J Am Coll Nutr 9:600–609. Mahalko JR, Sandstead HH, Johnson LK, Milne DB. 1983. Effect of a moderate increase in dietary protein on the retention and excretion of Ca, Cu, Fe, Mg, P, and Zn by adult males. Am J Clin Nutr 37:8–14. Mares-Perlman JA, Subar AF, Block G, Greger JL, Luby MH. 1995. Zinc intake and sources in the US adult population: 1976–1980. J Am Coll Nutr 14:349–357. McCabe MJ Jr, Jiang SA, Orrenius S. 1993. Chelation of intracellular zinc triggers apoptosis in mature thymocytes. Lab Invest 69:101–110. McKenna AA, Ilich JZ, Andon MB, Wang C, Matkovic V. 1997. Zinc balance in adolescent females consuming a low- or high-calcium diet. Am J Clin Nutr 65:1460–1464. McMahon RJ, Cousins RJ. 1998. Mammalian zinc transporters. J Nutr 128:667–670. Merialdi M, Caulfield LE, Zavaleta N, Figueroa A, DiPietro JA. 1998. Adding zinc to prenatal iron and folate tablets improves fetal neurobehavioral development. Am J Obstet Gynecol 180:483–490. Miller LV, Hambidge KM, Naake VL, Hong Z, Westcott JL, Fennessey PV. 1994. Size of the zinc pools that exchange rapidly with plasma zinc in humans: Alternative techniques for measuring and relation to dietary zinc intake. J Nutr 124:268–276. Miller LV, Krebs NF, Hambidge KM. 1998. Human zinc metabolism: Advances in the modeling of stable isotope data. Adv Exp Med Biol 445:253–269.

OCR for page 442
Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Milne DB, Canfield WK, Mahalko JR, Sandstead HH. 1983. Effect of dietary zinc on whole body surface loss of zinc: Impact on estimation of zinc retention by balance method. Am J Clin Nutr 38:181–186. Milne DB, Canfield WK, Mahalko JR, Sandstead HH. 1984. Effect of oral folic acid supplements on zinc, copper, and iron absorption and excretion. Am J Clin Nutr 39:535–539. Milne DB, Canfield WK, Gallagher SK, Hunt JR, Klevay LM. 1987. Ethanol metabolism in postmenopausal women fed a diet marginal in zinc. Am J Clin Nutr 46:688–693. Moser PB, Reynolds RD. 1983. Dietary zinc intake and zinc concentrations of plasma, erythrocytes, and breast milk in antepartum and postpartum lactating and nonlactating women: A longitudinal study. Am J Clin Nutr 38:101–108. Moser-Veillon PB, Reynolds RD. 1990. A longitudinal study of pyridoxine and zinc supplementation of lactating women. Am J Clin Nutr 52:135–141. Moss AJ, Levy AS, Kim I, Park YK. 1989. Use of Vitamin and Mineral Supplements in the United States: Current Users, Types of Products, and Nutrients. Advance Data, Vital and Health Statistics of the National Center for Health Statistics, Number 174. Hyattsville, MD: National Center for Health Statistics. Nakamura T, Nishiyama S, Futagoishi-Suginohara Y, Matsuda I, Higashi A. 1993. Mild to moderate zinc deficiency in short children: Effect of zinc supplementation on linear growth velocity. J Pediatr 123:65–69. Neggers YH, Goldenberg RL, Tamura T, Johnston KE, Copper RL, DuBard M. 1997. Plasma and erythrocyte zinc concentrations and their relationship to dietary zinc intake and zinc supplementation during pregnancy in low-income African-American women. J Am Diet Assoc 97:1269–1274. Ninh NX, Thissen JP, Collette L, Gerard G, Khoi HH, Ketelslegers JM. 1996. Zinc supplementation increases growth and circulating insulin-like growth factor I (IGF-I) in growth-retarded Vietnamese children. Am J Clin Nutr 63:514–519. Oberleas D, Muhrer ME, O’Dell BL. 1966. Dietary metal-complexing agents and zinc availability in the rat. J Nutr 90:56–62. O’Brien KO, Zavaleta N, Caulfield LE, Wen J, Abrams SA. 2000. Prenatal iron supplements impair zinc absorption in pregnant Peruvian women. J Nutr 130:2251–2255. Ortega RM, Andres P, Martinez RM, Lopez-Sobaler AM, Quintas ME. 1997. Zinc levels in maternal milk: The influence of nutritional status with respect to zinc during the third trimester of pregnancy. Eur J Clin Nutr 51:253–258. Paik HY, Joung H, Lee JY, Lee HK, King JC, Keen CL. 1999. Serum extracellular superoxide dismutase activity as an indicator of zinc status in humans. Biol Trace Elem Res 69:45–57. Payette H, Gray-Donald K. 1991. Dietary intake and biochemical indices of nutritional status in an elderly population, with estimates of the precision of the 7-d food record. Am J Clin Nutr 54:478–488. Picciano MF, Guthrie HA. 1976. Copper, iron, and zinc contents of mature human milk. Am J Clin Nutr 29:242–254. Pironi L, Miglioli M, Cornia GL, Ursitti MA, Tolomelli M, Piazzi S, Barbara L. 1987. Urinary zinc excretion in Crohn’s disease. Dig Dis Sci 32:358–362. Prasad AS. 1976. Deficiency of zinc in man and its toxicity. In: Prasad AS, Oberleas D, eds. Trace Elements in Human Health and Disease, Volume 1. Zinc and Copper. New York: Academic Press. Pp. 1–20. Prasad AS. 1991. Discovery of human zinc deficiency and studies in an experimental human model. Am J Clin Nutr 53:403–412.

OCR for page 442
Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Prasad AS, Brewer GJ, Schoomaker EB, Rabbani P. 1978. Hypocupremia induced by zinc therapy in adults. J Am Med Assoc 240:2166–2168. Prasad AS, Fitzgerald JT, Hess JW, Kaplan J, Pelen F, Dardenne M. 1993. Zinc deficiency in elderly patients. Nutrition 9:218–224. Prasad AS, Mantzoros CS, Beck FW, Hess JW, Brewer GJ. 1996. Zinc status and serum testosterone levels of healthy adults. Nutrition 12:344–348. Roesijadi G, Bogumil R, Vasak M, Kagi JH. 1998. Modulation of DNA binding of a tramtrack zinc finger peptide by the metallothionein-thionein conjugate pair. J Biol Chem 273:17425–17432. Rossander-Hulten L, Brune M, Sandstrom B, Lonnerdal B, Hallberg L. 1991. Competitive inhibition of iron absorption by manganese and zinc in humans. Am J Clin Nutr 54:152–156. Roth HP, Kirchgessner M. 1985. Utilization of zinc from picolinic or citric acid complexes in relation to dietary protein source in rats. J Nutr 115:1641–1649. Ruz M, Cavan KR, Bettger WJ, Gibson RS. 1992. Erythrocytes, erythrocyte membranes, neutrophils and platelets as biopsy materials for the assessment of zinc status in humans. Br J Nutr 68:515–527. Samman S, Roberts DCK. 1987. The effect of zinc supplements on plasma zinc and copper levels and the reported symptoms in healthy volunteers. Med J Aust 146:246–249. Samman S, Roberts DCK. 1988. The effect of zinc supplements on lipoproteins and copper status. Atherosclerosis 70:247–252. Samman S, Soto S, Cooke L, Ahmad Z, Farmakalidis E. 1996. Is erythrocyte alkaline phosphatase activity a marker of zinc status in humans? Biol Trace Elem Res 51:285–291. Sandstead HH, Penland JG, Alcock NW, Dayal HH, Chen XC, Li JS, Zhao F, Yang JJ. 1998. Effects of repletion with zinc and other micronutrients on neuropsychologic performance and growth of Chinese children. Am J Clin Nutr 68:470S–475S. Sandstrom B, Lonnerdal B. 1989. Promoters and antagonists of zinc absorption. In: Mills CF, ed. Zinc in Human Biology. New York: Springer-Verlag. Pp. 57–78. Sandstrom B, Cederblad A, Lonnerdal B. 1983. Zinc absorption from human milk, cow’s milk, and infant formulas. Am J Dis Child 137:726–729. Scholl TO, Hediger ML, Schall JI, Fischer RL, Khoo CS. 1993. Low zinc intake during pregnancy: Its association with preterm and very preterm delivery. Am J Epidemiol 137:1115–1124. Seal CJ, Heaton FW. 1985. Effect of dietary picolinic acid on the metabolism of exogenous and endogenous zinc in the rat. J Nutr 115:986–993. Shankar AH, Prasad AS. 1998. Zinc and immune function: The biological basis of altered resistance to infection. Am J Clin Nutr 68:447S–463S. Sian L, Mingyan X, Miller LV, Tong L, Krebs NF, Hambidge KM. 1996. Zinc absorption and intestinal losses of endogenous zinc in young Chinese women with marginal zinc intakes. Am J Clin Nutr 63:348–353. Sievers E, Oldigs HD, Dorner K, Schaub J. 1992. Longitudinal zinc balances in breast-fed and formula-fed infants. Acta Paediatr 81:1–6. Singh H, Flynn A, Fox PF. 1989. Zinc binding in bovine milk. J Dairy Res 56:249–263. Smit-Vanderkooy PD, Gibson RS. 1987. Food consumption patterns of Canadian preschool children in relation to zinc and growth status. Am J Clin Nutr 45:609–616.

OCR for page 442
Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Snedeker SM, Smith SA, Greger JL. 1982. Effect of dietary calcium and phosphorus levels on the utilization of iron, copper, and zinc by adult males. J Nutr 112:136–143. Solomons NW, Jacob RA. 1981. Studies on the bioavailability of zinc in humans: Effects of heme and nonheme iron on the absorption of zinc. Am J Clin Nutr 34:475–482. Spencer H, Asmussen CR, Holtzman RB, Kramer L. 1979. Metabolic balances of cadmium, copper, manganese, and zinc in man. Am J Clin Nutr 32:1867–1875. Spencer H, Kramer L, Norris C, Osis D. 1984. Effect of calcium and phosphorus on zinc metabolism in man. Am J Clin Nutr 40:1213–1218. Srikumar TS, Johansson GK, Ockerman PA, Gustafsson JA, Akesson B. 1992. Trace element status in healthy subjects switching from a mixed to a lactovegetarian diet for 12 months. Am J Clin Nutr 55:885–890. Sullivan VK, Burnett FR, Cousins RJ. 1998. Metallothionein expression is increased in monocytes and erythrocytes of young men during zinc supplementation. J Nutr 128:707–713. Swanson CA, King JC. 1982. Zinc utilization in pregnant and nonpregnant women fed controlled diets providing the zinc RDA. J Nutr 112:697–707. Swanson CA, King JC. 1987. Zinc and pregnancy outcome. Am J Clin Nutr 46:763–771. Swanson CA, Mansourian R, Dirren H, Rapin CH. 1988. Zinc status of healthy elderly adults: Response to supplementation. Am J Clin Nutr 48:343–349. Taper LJ, Hinners ML, Ritchey SJ. 1980. Effects of zinc intake on copper balance in adult females. Am J Clin Nutr 33:1077–1082. Taylor CM, Bacon JR, Aggett PJ, Bremner I. 1991. Homeostatic regulation of zinc absorption and endogenous losses in zinc-deprived men. Am J Clin Nutr 53:755–763. Telford WG, Fraker PJ. 1995. Preferential induction of apoptosis in mouse CD4+CD8+αβTCRIoCD3εIo thymocytes by zinc. J Cell Physiol 164:259–270. Thomas AJ, Bunker VW, Hinks LJ, Sodha N, Mullee MA, Clayton BE. 1988. Energy, protein, zinc and copper status of twenty-one elderly inpatients: Analysed dietary intake and biochemical indices. Br J Nutr 59:181–191. Thomas EA, Bailey LB, Kauwell GA, Lee D-Y, Cousins RJ. 1992. Erythrocyte metallothionein response to dietary zinc in humans. J Nutr 122:2408–2414. Turnlund JR, Michel MC, Keyes WR, King JC, Margen S. 1982. Use of enriched stable isotopes to determine zinc and iron absorption in elderly men. Am J Clin Nutr 35:1033–1040. Turnlund JR, King JC, Keyes WR, Gong B, Michel MC. 1984. A stable isotope study of zinc absorption in young men: Effects of phytate and alpha-cellulose. Am J Clin Nutr 40:1071–1077. Turnlund JR, Durkin N, Costa F, Margen S. 1986. Stable isotope studies of zinc absorption and retention in young and elderly men. J Nutr 116:1239–1247. Turnlund JR, Keyes WR, Hudson CA, Betschart AA, Kretsch MJ, Sauberlich HE. 1991. A stable-isotope study of zinc, copper, and iron absorption and retention by young women fed vitamin B-6-deficient diets. Am J Clin Nutr 54:1059–1064. Udomkesmalee E, Dhanamitta S, Yhoung-Aree J, Rojroongwasinkul N, Smith JC Jr. 1990. Biochemical evidence suggestive of suboptimal zinc and vitamin A status in schoolchildren in northeast Thailand. Am J Clin Nutr 52:564–567.

OCR for page 442
Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Umeta M, West CE, Haidar J, Deurenberg P, Hautvast JGAJ. 2000. Zinc supplementation and stunted infants in Ethiopia: A randomised controlled trial. Lancet 355:2021–2026. Valberg LS, Flanagan PR, Chamberlain MJ. 1984. Effects of iron, tin, and copper on zinc absorption in humans. Am J Clin Nutr 40:536–541. Valberg LS, Flanagan PR, Kertesz A, Bondy DC. 1986. Zinc absorption in inflammatory bowel disease. Dig Dis Sci 31:724–731. Vallee BL, Galdes A. 1984. The metallobiochemistry of zinc enzymes. Adv Enzymol 56:283–429. Vuori E, Makinen SM, Kara R, Kuitunen P. 1980. The effects of the dietary intakes of copper, iron, manganese, and zinc on the trace element content of human milk. Am J Clin Nutr 33:227–231. Wada L, King JC. 1986. Effect of low zinc intakes on basal metabolic rate, thyroid hormones and protein utilization in adult men. J Nutr 116:1045–1053. Wada L, Turnlund JR, King JC. 1985. Zinc utilization in young men fed adequate and low zinc intakes. J Nutr 115:1345–1354. Walling A, Householder M, Walling A. 1989. Acrodermatitis enteropathica. Am Fam Physician 39:151–154. Walravens PA, Hambidge KM. 1976. Growth of infants fed a zinc supplemented formula. Am J Clin Nutr 29:1114–1121. Walravens PA, Krebs NF, Hambidge KM. 1983. Linear growth of low income preschool children receiving a zinc supplement. Am J Clin Nutr 38:195–201. Walravens PA, Hambidge KM, Koepfer DM. 1989. Zinc supplementation in infants with a nutritional pattern of failure to thrive: A double-blind, controlled study. Pediatrics 83:532–538. Walravens PA, Chakar A, Mokni R, Denise J, Lemonnier D. 1992. Zinc supplements in breastfed infants. Lancet 340:683–685. Wastney ME, Aamodt RL, Rumble WF, Henkin RI. 1986. Kinetic analysis of zinc metabolism and its regulation in normal humans. Am J Physiol 251:R398–R408. Whittaker P. 1998. Iron and zinc interactions in humans. Am J Clin Nutr 68:442S–446S. WHO (World Health Organization). 1996. Trace Elements in Human Nutrition and Health. Geneva: WHO. Pp. 72–104. Widdowson EM, Dickerson JWT. 1964. Chemical composition of the body. In: Comar CL, Bronner F, eds. Mineral Metabolism. An Advanced Treatise, Vol. II. The Elements, Part A. New York: Academic Press. Pp. 1–247. Williams AW, Erdman JW Jr. 1999. Food processing: Nutrition, safety, and quality balances. In: Shils ME, Olson JA, Shike M, Ross AC, eds. Modern Nutrition in Health and Disease, 9th ed. Baltimore: Williams & Wilkins. Pp. 1813–1821. Wisker E, Nagel R, Tanudjaja TK, Feldheim W. 1991. Calcium, magnesium, zinc, and iron balances in young women: Effects of a low-phytate barley-fiber concentrate. Am J Clin Nutr 54:553–559. Wood RJ, Zheng JJ. 1997. High dietary calcium intakes reduce zinc absorption and balance in humans. Am J Clin Nutr 65:1803–1809. Yadrick MK, Kenney MA, Winterfeldt EA. 1989. Iron, copper, and zinc status: Response to supplementation with zinc or zinc and iron in adult females. Am J Clin Nutr 49:145–150. Yokoi K, Alcock NW, Sandstead HH. 1994. Iron and zinc nutriture of premenopausal women: Associations of diet with serum ferritin and plasma zinc disappearance and of serum ferritin with plasma zinc and plasma zinc disappearance. J Lab Clin Med 124:852–861.

OCR for page 442
Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Yuzbasiyan-Gurkan V, Grider A, Nostrant T, Cousins RJ, Brewer GJ. 1992. Treatment of Wilson’s disease with zinc: X. Intestinal metallothionein induction. J Lab Clin Med 120:380–386. Zalewski PD, Forbes IJ, Seamark RF, Borlinghaus R, Betts WH, Lincoln SF, Ward AD. 1994. Flux of intracellular labile zinc during apoptosis (gene-directed cell death) revealed by a specific chemical probe, Zinquin. Chem Biol 1:153–161. Ziegler EE, Edwards BB, Jensen RL, Filer LJ, Fomon SJ. 1978. Zinc balance studies in normal infants. In: Kirchgessner M, ed. Trace Element Metabolism in Man and Animals—3. Freising-Weihenstephan: Arbeitskreis fier Tierernahrungsforschung. Pp. 292–295. Zlotkin SH, Cherian MG. 1988. Hepatic metallothionein as a source of zinc and cysteine during the first year of life. Pediatr Res 24:326–329.