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Departamento de Bioquímica, Instituto de Química, Universidade Federal do Rio de Janeiro, Brazil;
Department of Nutritional Sciences, University of California, Berkeley, CA; and
*
U.S. Department of Agriculture/ARS Western Human Nutrition Research Center, Davis, CA
3To whom correspondence and reprint requests should be addressed. E-mail: jking{at}whnrc.usda.gov.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • zinc • iron • absorption • supplementation • humans
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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,2
) and that excess zinc inhibits iron uptake (3
). Much less is known about the postabsorptive interactions between these nutrients (4
). Understanding these interactions is important for assessing the effects of iron or zinc supplementation on the nutritional status of the other nutrient.
Because iron and zinc commonly coexist in foods, marginal iron and zinc status are usually associated, particularly in developing countries (4
,5
) in which diets usually provide limited amounts of meat, a source of highly available iron and zinc. Iron supplementation is commonly practiced worldwide for prevention and treatment of iron deficiency (6
). Zinc supplementation is much less common, but it is recognized as a short-term strategy to combat zinc deficiency in infants, young children and pregnant women (5
). Because zinc and iron interact during absorption and, possibly also during metabolism (7
,8
), supplementation of only one of the two may affect the status of the other nutrient. This is particularly relevant in populations with poor iron and zinc nutriture. Therefore, the purpose of our study was to evaluate the effect of zinc or iron supplementation taken at bedtime without food on zinc and iron metabolism and absorption in young women with low iron reserves.
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SUBJECTS AND METHODS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Twenty-three women, 20–28 y of age, participated in the study. The women were nonsmokers, apparently healthy, without recent use of mineral/vitamin supplements, of acceptable weight for height, not engaged in heavy exercise, were current users of oral contraceptives, and had blood hemoglobin concentrations > 110 g/L and plasma ferritin concentrations < 20 µg/L at screening. Before participation in the study, subjects kept a 4-d record of all food and beverage intakes. Customary nutrient intake was estimated using The Food Processor (ESHA Research, Salem, OR). The subjects were instructed not to change their dietary and other lifestyle habits during the study.
The study was approved by the Committee for Protection of Human Subjects of the University of California, Berkeley, and by Radiation Safety of the University of California, Berkeley. Written informed consent was obtained from each subject.
Study design.
Each subject participated in a 70-d study period. A blood sample from fasting subjects and a spot, morning urine sample were collected on d 1 and 56 for measurements of zinc and iron indices. Absorption of iron and zinc from a test meal (described below) was also measured on d 1 and 56. A nonfasting blood sample was obtained on d 14 and 70 for determination of iron absorption. Spot urine samples were obtained on d 3–5 and d 58–60 for determination of zinc absorption. Subjects were randomly divided into two groups, i.e., a zinc-supplemented and an iron-supplemented group. Women in the zinc group (n = 11) ingested daily zinc supplements (22 mg Zn/d as zinc gluconate) from d 14 to 70, whereas those in the iron group (n = 12) ingested daily iron supplements (100 mg Fe/d as ferrous sulfate) during the same period. The women were instructed to take the supplement in the evening at least 2 h after dinner.
Test meal for measurement of iron and zinc absorption.
The test meal consisted of 40 g (dry weight) cooked kidney beans. The same batch of beans was used on the two test days (d 1 and 56) in each group of women but different bean batches were used for the two groups. Only water was allowed to be consumed with the bean meal, and for 3 h after. Before the absorption test, individual portions of the bean meal were equilibrated overnight at 5°C with an extrinsic label of iron (59Fe, 3.7 x 10-4 Bq, as 59FeCl3, Amersham, Buckinghamshire, UK) and an extrinsic label of zinc (68Zn, 3.0 mg as 68ZnO, 99.42% enriched, in the zinc-supplemented group; 67Zn, 1.0 mg, as 67ZnO, 94.6% enriched, in the iron-supplemented group; Oak Ridge National Laboratory, Oak Ridge, TN).
Preparation of Zn isotope for intravenous infusion.
67ZnO, 94.60% enriched, or 70ZnO, 85.03% enriched (Oak Ridge National Laboratory), was dissolved in concentrated HCl (Optima brand, Fisher Scientific, Pittsburgh, PA) (3 µL HCl/mg ZnO). The solution was diluted with triple deionized water to a final concentration of 1.0 mg 67Zn/mL or 0.3 mg 70Zn/mL. The solution was sterilized by filtration and pyrogen tested by the School of Pharmacy, University of California, San Francisco, CA. Doses (1.0 mL) containing 1.0 mg 67Zn or 0.3 mg 70Zn were stored in individually sealed, sterile vials until use in the zinc-supplemented and iron-supplemented groups, respectively.
Sample collection.
On d 1 and 56, subjects arrived at the metabolic unit at 0700 h after an overnight fast. A spot urine sample (
40 mL) was collected into Zn-free plastic containers and height and weight measured. A blood sample (30 mL) was drawn from the antecubital vein into Zn-free polypropylene syringes. Blood samples were kept on ice for no more than 1 h before processing.
The test meal was fed at 0715 h and consumed in < 15 min. At 0730 h, 1.0 mL solution of the intravenous (IV)4 zinc isotope was infused for 1 min into the antecubital vein of one arm, using a "butterfly" infusion set (Becton Dickinson and Company, Sandy, UT). The butterfly tubing was flushed with 5 mL sterile saline solution (9 g/L NaCl, Elkins-Sinn, Cherry Hill, NJ) to ensure that all isotope had been infused. The exact amount of the isotope solution infused was determined by weighing the syringe before and after the infusion. Sequential blood samples (total = 88 mL of blood) were drawn during 3 h after isotope infusion for studying the effect of supplementation on zinc kinetics. Results of this study will be reported separately.
Aliquots of blood samples from fasting subjects were used for determination of packed cell volume, erythrocyte zinc protoporphyrin (EZP) and hemoglobin, and for preparation of saline-washed erythrocytes. Packed erythrocytes were obtained by centrifugation of 2 mL blood, separation of plasma and removal of the buffy coat. The packed erythrocytes were washed twice with cold isotonic saline and diluted 1:1 with saline. Aliquots were stored at -70°C until analysis. Plasma was obtained by centrifugation (10 min at 1500 g) of the blood samples, transferred into polyethylene tubes and stored at -70°C until analysis.
On days 3, 4 and 5, and 58, 59 and 60, i.e., after each clinical test, subjects were instructed to collect at home the first morning urine voids (40–100 mL) into Zn-free plastic containers. All urine samples were acidified with HCl (Fisher Scientific, TM grade; 8 µL/mL of urine) and stored at -20°C until analyzed for total zinc and zinc isotopes. Creatinine was measured on nonacidified samples.
On d 14 and 70, subjects returned to the metabolic unit during the morning (fasting not required) for a blood draw to determine iron absorption. A blood sample (30 mL) was obtained by antecubital venipuncture using sodium heparin Vacutainer tubes (Becton Dickinson, Franklin Lakes, NJ). Whole-blood samples were kept at 5°C until measurement of 59Fe.
Laboratory analysis.
Zinc and iron contents in plasma, erythrocytes and urine were determined by atomic absorption spectroscopy (Thermo-Jarrell Ash 22, Franklin, MA). Appropriate aliquots of samples were diluted with 0.125 mol/L HNO3 (Fisher Scientific; TM grade) before measurement. A bovine liver standard (National Bureau of Standards, Gaithersburg, MD) was used as an analytical control. The CV for measurements of the bovine liver standard were 1.6% for Zn, and 2.1% for Fe.
Blood hemoglobin was determined with HemoCue Systems (Helsingborg, Sweden) and EZP by hematofluorometry (Helena ProtoFluor Reagent System, Beaumont, TX). Protein in erythrocytes was measured by the Lowry method using a kit (BioRad, Hercules, CA). Total iron-binding-capacity (TIBC) in plasma was measured using bathophenanthroline sulfonate and magnesium carbonate (9
). Plasma ferritin and plasma transferrin receptors were determined by ELISA using kits (Spectro Ferritin, S-22 and TfR, TF-94, Ramco Laboratories, Houston, TX). Creatinine in centrifuged urine samples was measured by an automated procedure (Cobas Fara Autoanalyzer, F. Hoffmann-La Roche, Basel, Switzerland).
Measurement of iron absorption.
Iron absorption was estimated on the basis of incorporation of the ingested radiolabel (59Fe) into RBC. 59Fe content in blood samples and test meal samples was determined after acid digestion, ion exchange chromatography and liquid scintillation as described by Viteri and Kohaut (10
). Recovery of known amounts of 59Fe added to samples was 99% and the CV was < 2%.
The content of 59Fe in total blood of the individual was calculated from the measurement in the blood sample and estimates of total blood volume by the method of Frenkel et al. (11
). These estimates take into consideration sex, weight and height of the individual. Incorporation of the radiolabel into total red cell mass was calculated assuming 85 and 90% incorporation for subjects with plasma ferritin values > or < 15 µg/L, respectively (10
). Iron absorption was calculated as the ratio of 59Fe in total red cell mass and the ingested dose of the isotope, as a percentage (10
).
Measurement of zinc absorption.
Urine zinc was purified by ion exchange chromatography as previously described (12
). Measurement of zinc isotopes in the purified samples was done by inductively coupled plasma-mass spectrometry (ICP-MS) using Sciex ELAN 5000 ICP-MS (Perkin Elmer, Norwalk, CT). Results from the three urine samples after each clinical test were averaged. Zinc absorption was estimated by the dual isotope tracer ratio method used by Lowe et al. (13
). Fractional zinc absorption (FZA) was calculated according to the following equation: FZA = (oral tracer:tracee ratio in urine/IV tracer:tracee ratio in urine) x (IV tracer dose in mg/oral tracer dose in mg).
Statistical analyses.
Data were tested for normality and log-transformed for plasma ferritin, plasma transferrin saturation, EZP and iron absorption before statistical analyses. The effect of zinc or iron supplementation was investigated by paired t test within the corresponding group. Differences were considered significant at P < 0.05.
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RESULTS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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). Fortified cereals contributed about half of the dietary intakes of iron and zinc. Red meat consumption was very low.
Plasma zinc at baseline was, on average, in the lower range of normality (15
) in each group of women (Table 1
), suggesting a marginal status. Erythrocyte zinc and urinary zinc at baseline were within the range previously observed in healthy adult women (16
). In the zinc-supplemented group, plasma and urinary zinc responded to supplementation, i.e., plasma zinc increased 17% and urinary zinc increased 48%. In the iron-supplemented group, zinc biochemical indices did not change after the 6-wk iron supplementation period.
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). More than half of the women in each group had plasma ferritin concentration <12 µg/L, indicative of depleted iron stores (17
). Other iron indices were, on average, within the normal range. In the zinc-supplemented women, plasma ferritin decreased 35% (P < 0.05) compared with baseline values. Blood hemoglobin did not change but EZP increased (P < 0.05). Plasma iron tended to decrease (P = 0.12), and TIBC increased (P < 0.01) with zinc supplementation, thus causing a decrease in the plasma percentage of transferrin saturation (P < 0.01). Soluble transferrin receptors increased (P < 0.05) after the zinc supplementation period. Although significant, the changes in iron indices with zinc supplementation were small (7–12%). In the iron-supplemented women, blood hemoglobin, plasma iron, plasma transferrin saturation and plasma ferritin increased after the supplementation period (P < 0.01). Plasma ferritin increased 66% compared with baseline values.
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) as previously observed from legumes due to the presence of several inhibitory factors, such as phytate (18
,19
). In the zinc-supplemented women, zinc absorption decreased (P < 0.001) after supplementation to about half the value at baseline, whereas iron absorption almost doubled (P < 0.01). In the iron-supplemented women, zinc absorption did not change, whereas iron absorption decreased to less than half of the initial value (P < 0.01).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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The initial low plasma zinc concentrations of the women may be due to the poor bioavailability of zinc in their diets. Also, the use of oral contraceptive agents, which reduce plasma zinc, may have contributed to the lower plasma zinc concentrations (20
). With zinc supplementation, erythrocyte zinc concentrations did not change, but plasma zinc concentrations increased; urinary zinc excretion also increased and the efficiency of zinc absorption from the test meal decreased. Taken together, these changes suggest that the zinc status of these women improved with zinc supplementation (21
). The use of oral contraceptive agents did not appear to interfere with the use of supplemental zinc for improving markers of zinc status.
Iron supplementation did not alter markers of zinc status or the percentage of zinc absorption from a test meal. Although there is evidence that supplemental iron interferes with zinc utilization (1
,2
), the use of supplemental iron for 2 mo at a level commonly used for prevention of iron deficiency (6
) did not affect the zinc status of these women. Ruz and co-workers (8
) did not find an effect of a 3-mo iron supplementation period (30–60 mg/d as ferrous sulfate) on fractional zinc absorption when the supplement was taken between meals. Moderate doses of supplemental iron (<60 mg/d) may not reduce zinc utilization when the iron is not taken with food.
Although the iron intakes of the women in our study were not low, they had low levels of iron storage, possibly due to the poor bioavailability of iron in their diets. Red meat consumption was very low. Most of the dietary iron came from fortified cereals; iron fortificants tend to be poorly absorbed because elemental iron is usually added (22
).
Supplementation with iron improved the measures of iron status as expected (17
). Plasma ferritin, an index of iron reserves, was 1.5 times the baseline value after 6 wk of supplementation. The reduction in the percentage of iron absorption from the test meal after iron supplementation was also consistent with an improved iron status. Zinc supplementation, however, caused a 35% decline in plasma ferritin concentrations, which were already very low at baseline (10.5 µg/L). Yadrick et al. (7
) also observed a significant decrease in serum ferritin concentrations when women with adequate iron reserves were supplemented with 50 mg of zinc for 10 wk; serum ferritin concentrations declined by 23%, from 36.6 to 28.2 µg/L. Our data suggest that only a modest amount of supplemental zinc, about three times the dietary reference intake (14
), taken for a relatively short time may reduce the iron stores of women who are already in a marginal state.
Zinc supplementation also altered other indices of iron status in a manner consistent with a reduction in iron stores. Plasma transferrin saturation decreased to <15%, indicating an inadequate tissue supply of iron. Iron absorption increased, and plasma soluble transferrin receptors, although still within the normal range, increased, suggesting an increase in cellular iron needs (23
). EZP decreased, suggesting reduced availability of cell iron for heme synthesis during erythropoiesis (17
). However, blood hemoglobin concentrations did not change, probably because of the short period of supplementation.
Although the data suggest that supplemental zinc reduced the iron status of our subjects, several other explanations may be considered. The decline in iron status could reflect the blood sampling during the study. At the beginning of the study, 63 mg of iron was removed in the blood drawn. This is equivalent to a daily loss of 1 mg iron over the course of the study. However, the women could replace this loss by increasing the efficiency of iron absorption from 10 to 17%. [This range of iron absorption is common in individuals with a marginal iron status (22
,24
).] In fact, the percentage of iron absorption from the test meal diet, taken as a proxy for whole-diet iron absorption, doubled in the zinc-supplemented women, indicating an increased efficiency of iron absorption during the study period that could compensate for the blood iron loss. Thus, it seems unlikely that the effect of blood sampling 2 mo earlier would still be reflected in the iron status measurements made on d 56.
It is also possible that the decline in iron status among the zinc-supplemented women reflects changes in cell metabolism induced by an increase in zinc status. Zinc is required for gene expression, protein synthesis and immune function (25
,26
). Supplementation with zinc may have suppressed a subclinical infection or inflammation in the women, which caused a fall in acute-phase proteins, including plasma ferritin. Unfortunately, other acute-phase proteins, such as C-reactive protein, were not measured. The increase in circulating transferrin and transferrin receptors may reflect an increase in protein synthesis due to zinc supplementation in a manner similar to the effects of zinc status on retinol-binding protein levels (27
). Also, an increase in cellular zinc may have mediated an increase in the synthesis of the gastrointestinal iron-responsive elements and their binding proteins (28
), which in turn increased the efficiency of iron absorption. Furthermore, the supplemental zinc may have increased the synthesis of intestinal protein carriers, such as DMT1 (29
), which respond to iron status (30
).
In conclusion, the results of our study suggest a postabsorptive systemic interaction between zinc and iron when 22 mg of supplemental zinc was given for 6 wk to women who had low iron stores. Additional studies are required to define the response to various doses of supplemental zinc in iron-deplete and iron-replete women and to identify the underlying mechanisms of the cellular iron/zinc interaction. These data suggest, however, that supplemental zinc further impairs the iron status of women with low iron stores.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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2 Supported in part by USDA/ARS Western Human Nutrition Research Center and a gift from Bristol Meyers/Squibb; CNPq and FAPERJ (Brazil) for C.M.D.
4 Abbreviations used: EZP, erythrocyte zinc protoprophyrin; FZA, fractional zinc absorption; ICP-MS, inductively coupled plasma-mass spectrometry; IV, intravenous; TIBC, total iron-binding capacity.
Manuscript received 8 January 2002. Initial review completed 30 January 2002. Revision accepted 13 March 2002.
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LITERATURE CITED |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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1. Whittaker, P. (1998) Iron and zinc interactions in humans. Am. J. Clin. Nutr. 68:442S-446S.[Abstract]
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3. Aggett, P. J., Crofton, R.W., Khin, C., Gvozdanovic, S. & Gvozdanovic, D. (1983) The mutual inhibitory effects on their bioavailability of inorganic zinc and iron. Prasad, A. S. Cadvar, A. Brewer, G. J. Agget, P. J. eds. Zinc Deficiency in Human Subjects 1983:117-124 Alan R. Liss New York, NY. .
4. Solomons, N. W. & Ruz, M. (1997) Zinc and iron interaction: concepts and perspectives in the developing world. Nutr. Res. 17:177-185.
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12. Lowe, N. M., Shames, D. M., Woodhouse, L. R., Matel, J. S., Roehl, R., Saccomani, M. P., Toffolo, G., Cobelli, C. & King, J. C. (1997) A compartmental model of zinc metabolism in healthy women using oral and intravenous stable isotope tracers. Am. J. Clin. Nutr. 65:1810-1819.
13. Lowe, N. M., Woodhouse, L. R., Matel, J. S. & King, J. C. (2000) Comparison of estimates of zinc absorption in humans by using 4 stable isotope tracer methods and compartment analysis. Am. J. Clin. Nutr. 71:523-529.
14. Institute of Medicine (2001) Dietary Reference Intakes: Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc 2001 National Academy Press Washington, DC. .
15. Alcock, N.W. (1999) Laboratory tests for assessing nutritional status. Shils, M. E. Olson, J. A. Shike, M. Ross, A.C. eds. Modern Nutrition in Health and Disease 1999:923-935 Lippincott Williams & Wilkins Baltimore, MD. .
16. Wallock, L. M., King, J. C., Hambidge, K. M., English-Westcott, J. E. & Pritts, J. (1993) Meal-induced changes in plasma, erythrocyte, and urinary zinc concentrations in adult women. Am. J. Clin. Nutr. 58:695-701.
17. Beard, J. L., Dawson, H. & Piñero, D. J. (1996) Iron metabolism: a comprehensive review. Nutr. Rev. 54:295-317.[Medline]
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19. Petterson, D. S., Sandström, B. & Cederblad, Å. (1994) Absorption of zinc from lupin (Lupinus angustifolius)–based foods. Br. J. Nutr. 72:865-871.[Medline]
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21. King, J. C. & Keen, C. L. (1999) Zinc. Shils, M. E. Olson, J. A. Shike, M. Ross, A.C. eds. Modern Nutrition in Health and Disease 1999:223-249 Lippincott Williams & Wilkins Baltimore, MD. .
22. Fairbanks, V.F. (1999) Iron in medicine and nutrition. Shils, M. E. Olson, J. A. Shike, M. Ross, A.C. eds. Modern Nutrition in Health and Disease 1999:193-221 Lippincott Williams & Wilkins Baltimore, MD. .
23. Cook, J. D., Skikne, B. S. & Baynes, R. D. (1993) Serum transferrin receptor. Annu. Rev. Med. 44:63-74.[Medline]
24. Hallberg, L., Hulten, L. & Gramatkovski, E. (1997) Iron absorption from the whole diet in men: how effective is the regulation of iron absorption. Am. J. Clin. Nutr. 66:347-356.
25. MacDonald, R. S. (2000) The role of zinc in growth and cell proliferation. J. Nutr. 130:1500S-1508S.
26. Franker, P. J., King, L. E., Laako, T. & Vollmer, T. L. (2000) The dynamic link between the integrity of the immune system and zinc status. J. Nutr. 130:1399S-1406S.
27. Christian, P. & West, K. P. (1998) Interactions between zinc and vitamin A: an update. Am. J. Clin. Nutr. 68(Suppl.):435S-441S.[Abstract]
28. Eisenstein, R. S. & Blemings, K. P. (1998) Iron regulatory proteins, iron responsive elements and iron homeostasis. J. Nutr. 128:2295-2298.
29. Yamaji, S., Tennant, J., Tandy, S., Williams, M., Srai, S.K.S. & Sharp, P. (2001) Zinc regulates the function and expression of the iron transporters DMT1 and IREG1 in human intestinal Caco-2 cells. FEBS Lett 507:137-141.[Medline]
30. Wood, R. J. & Han, O. (1998) Recently identified molecular aspects of intestinal iron absorption. J. Nutr. 128:1841-1844.
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