Dietary zinc depletion and repletion affects plasma proteins: an analysis of the plasma proteome.
ABSTRACT Zinc (Zn) deficiency is a problem world-wide. Current methods for assessing Zn status are limited to measuring plasma or serum Zn within populations suspected of deficiency. Despite the high prevalence of Zn deficiency in the human population there are no methods currently available for sensitively assessing Zn status among individuals. The purpose of this research was to utilize a proteomic approach using two-dimensional gel electrophoresis (2DE) and mass spectrometry to identify protein biomarkers that were sensitive to changes in dietary Zn levels in humans. Proteomic analysis was performed in human plasma samples (n = 6) obtained from healthy adult male subjects that completed a dietary Zn depletion/repletion protocol, current dietary zinc intake has a greater effect on fractional zinc absorption than does longer term zinc consumption in healthy adult men. Chung et al. (Am J Clin Nutr 87 (5):1224-1229, 2008). After a 13 day Zn acclimatization period where subjects consumed a Zn-adequate diet, the male subjects consumed a marginal Zn-depleted diet for 42 days followed by consumption of a Zn-repleted diet for 28 days. The samples at baseline, end of depletion and end of repletion were pre-fractionated through immuno-affinity columns to remove 14 highly abundant proteins, and each fraction separated by 2DE. Following staining by colloidal Coomassie blue and densitometric analysis, three proteins were identified by mass spectrometry as affected by changes in dietary Zn. Fibrin β and chain E, fragment double D were observed in the plasma protein fraction that remained bound to the immunoaffinity column. An unnamed protein that was related to immunoglobulins was observed in the immunodepleted plasma fraction. Fibrin β increased two-fold following the Zn depletion period and decreased to baseline values following the Zn repletion period; this protein may serve as a viable biomarker for Zn status in the future.
SourceAvailable from: Carla G Taylor[Show abstract] [Hide abstract]
ABSTRACT: The effects of hyperoxia and the response of oxygen free radical defense enzymes in the lung and extracellular environment of the lung were measured in Zn-deficient rats. Although lung was the target organ as indicated by the increased lung:body weight ratio in all hyperoxia-exposed rats regardless of dietary regimen, 85% oxygen exposure seemed to impose a stress on the whole animal as indicated by decreased feed intake and body weight in ad libitum-fed rats. Hyperoxia exposure superimposed on Zn deficiency did not further reduce the feed intake or body weight of Zn-deficient rats. After 7 d of hyperoxia exposure, the Zn-repleted and ad libitum-fed groups consistently had increased activity of lung CuZn-superoxide dismutase (CuZnSOD), glutathione peroxidase and catalase; but changes in CuZnSOD activity were not related to lung Cu or Zn concentrations. Although Zn-deficient and pair-fed rats were unable to increase CuZnSOD activity, they had an increased lung Zn concentration compared with their air-exposed counterparts. Hyperoxia exposure also caused an increase in ceruloplasmin activity of pair-fed and ad libitum-fed control rats. We concluded that dietary Zn repletion started at the beginning of 85% oxygen exposure was effective for increasing the activity of the lung oxygen free radical defense enzymes, thus preventing hyperoxia-induced lung damage in Zn-deficient rats.Journal of Nutrition 05/1991; 121(4):460-6. · 4.23 Impact Factor
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ABSTRACT: Zinc is essential for normal erythroid cell functions and therefore intracellular zinc homeostasis during erythroid differentiation is tightly regulated. However, a characterization of zinc transporters in erythrocytes has not been conducted. The membrane fraction of mature mouse RBC was screened for zinc transporter expression using western analysis as a first step in the characterization process. ZnT1, Zip8, and Zip10 were detected among the 12 transporter proteins tested. We examined expression of these zinc transporters during erythropoietin (EPO)-induced differentiation of splenic erythroid progenitor cells into reticulocytes. Both Zip8 and Zip10 mRNA increased by 2-6 h after addition of EPO to the cells. In contrast, maximal RNA levels for the zinc transporter ZnT1 and erythroid delta-aminolevulinic acid synthase were only produced by 24 h after EPO. We confirmed these changes in transcript abundance by western analysis. Dietary zinc status influences zinc-dependent functions of RBC. To determine whether the identified zinc transporters respond to dietary zinc status, mice were fed a zinc-deficient or control diet. Incorporation of (65)Zn into erythrocytes in vitro was significantly increased in cells from the zinc-deficient mice. Western analysis and densitometry revealed that erythrocyte Zip10 was upregulated and ZnT1 was downregulated in the zinc-depleted mice. Zip8 was not affected by restricted zinc intake. Collectively, these data suggest that the zinc transporters ZnT1, Zip8, and Zip10 are important for zinc homeostasis in erythrocytes and that ZnT1 and Zip10 respond to the dietary zinc supply.Journal of Nutrition 12/2008; 138(11):2076-83. DOI:10.3945/jn.108.093575 · 4.23 Impact Factor
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ABSTRACT: Zinc is a multi-functional element that is found in almost 300 enzymes where it performs catalytic, co-catalytic, and/or structural functions. In 1982, Gordon et al. (Am J Clin Ntr 35:849-857, 1982) found that a low zinc diet caused poor platelet aggregation and increased bleeding tendency in adult males. This fact drew interest to the role of zinc in blood clotting. It has been shown that hyperzincemia predisposes to increased coagulability, and hypozincemia to poor platelet aggregation and increased bleeding time. The blood clotting disturbances can be regressed by appropriate zinc intake management. Considering the importance of zinc as an essential element, its participation in regulation of the equilibrium between pro- and anti-thrombotic factors originating in platelets and endothelium prompted further investigations.Biological Trace Element Research 02/2008; 121(1):1-8. DOI:10.1007/s12011-007-8038-y · 1.61 Impact Factor