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PubMed1982

The assessment of zinc status by the zinc tolerance test in various groups of patients.

The zinc status of young and aged subjects, hypertensives, geriatric patients with leg ulcers and cancer patients has been determined by various means. Serum, saliva, urine and hair zinc were measured by atomic absorption spectrometry and no correlation was observed between the zinc levels in any of these differing matrices. The mean hair and salivary zinc level showed little variation between the differing groups of patients and provided little or no indication of zinc status. The results of the present experiment indicate that the zinc tolerance test, that is, an unequivocal rise in serum zinc following per oral administration of this metal, provides the best indication of zinc status.

Administration, Oral↗

PubMed2003

Zinc is incorporated into cuticular "tools" after ecdysis: the time course of the zinc distribution in "tools" and whole bodies of an ant and a scorpion.

An understanding of the developmental course of specialized accumulations in the cuticular "tools" of arthropods will give clues to the chemical form, function and biology of these accumulations as well as to their evolutionary history. Specimens from individuals representing a range of developmental stages were examined using MeV - Ion microscopy. We found that zinc, manganese, calcium and chlorine began to accumulate in the mandibular teeth of the ant Tapinoma sessile after pre-ecdysial tanning, and the zinc mostly after eclosion; peak measured zinc concentrations reached 16% of dry mass. Accumulations in the pedipalp teeth, tarsal claws, cheliceral teeth and sting (aculeus) of the scorpion Vaejovis spinigeris also began after pre-ecdysial tanning and more than 48 h after ecdysis of the second instars. Zinc may be deposited in the fully formed cuticle through a network of nanometer scale canals that we observed only in the metal bearing cuticle of both the ants and scorpions. In addition to the elemental analyses of cuticular "tools", quantitative distribution maps for whole ants were obtained. The zinc content of the mandibular teeth was a small fraction of, and independent of, the total body content of zinc. We did not find specialized storage sites that were depleted when zinc was incorporated into the mandibular teeth. The similarities in the time course of zinc, manganese and calcium deposition in the cuticular "tools" of the ant (a hexapod arthropod) and those of the scorpion (a chelicerate arthropod) contribute to the evidence suggesting that heavy metal-halogen fortification evolved before these groups diverged.

Animals↗

PubMed1988

Zinc balance in premature infants given the minimal dietary zinc requirement.

A zinc balance study was conducted on low birth weight infants (670 to 2420 g) fed unsupplemented human milk (the mother's or pooled) (group 1, n = 17) or human milk with zinc supplementation (group 2, n = 17). The mean zinc concentrations of the diets in groups 1 and 2 were 2.2 +/- 1.1 mg/L and 8.4 +/- 0.8 mg/L, respectively, and the mean copper concentration of the diets in both groups was 0.45 +/- 0.12 mg/L. The studies were performed 7 to 128 days after birth, which corresponded to 29 to 43 weeks postconceptional age. The turning point of zinc balance from negative to positive appeared to be greatly influenced by the postconceptional age, being approximately 36 weeks in both group 1 and group 2, rather than other factors such as the zinc intake and the postnatal age. The calculated minimal requirement of dietary zinc during the period from 36 to 40 weeks postconceptional age, for an adequate amount of zinc retention in infants (250 micrograms/kg/d), was 0.8 mg/kg/d. Zinc supplementation did not appear to interfere with copper retention.

Absorption↗

PubMed2002

Crystal structure of a zinc-activated variant of human carbonic anhydrase I, CA I Michigan 1: evidence for a second zinc binding site involving arginine coordination.

The human genetic variant carbonic anhydrase I (CA I) Michigan 1 results from a single point mutation that changes His 67 to Arg in a critical region of the active site. This variant of the zinc metalloenzyme appears to be unique in that it possesses an esterase activity that is specifically enhanced by added free zinc ions. We have determined the three-dimensional structure of human CA I Michigan 1 by X-ray crystallography to a resolution of 2.6 A. In the absence of added zinc ions, the mutated residue, Arg 67, points out of the active site, hydrogen bonding with the carboxylate of Asn 69. This contrasts with the orientation of His 67, in the native isozyme, which points into the active site. The orientations of His 94, His 96, and His 119, that coordinate the catalytic zinc ion, and of the catalytically critical Thr 199-Glu 106 hydrogen bonding system, are largely unchanged in the mutant. The structure of an enzyme adduct with a second zinc bound was determined to a resolution of 2.0 A. The second zinc ion is coordinated to His 64, His 200, and Arg 67. This arginine residue reverses its orientation on zinc binding and turns into the active site. The residues at these three positions have been implicated in determining the specific kinetic properties of native CA I. This is, to our knowledge, the first example of a zinc ion coordinating with an arginine residue in a Zn(II) enzyme.

Arginine↗

PubMed1999

Induction of an immediate early gene egr-1 by zinc through extracellular signal-regulated kinase activation in cortical culture: its role in zinc-induced neuronal death.

Egr-1 is one of the immediate early transcription factors that are induced after brain insults. However, the mechanism and the role of Egr-1 induction are not yet determined. In the present study, using mouse cortical cultures, we examined the ionic mechanism of Egr-1 induction and its role in neuronal death. Although zinc, NMDA, or ionomycin induced comparable neuronal death in cortical culture, only zinc increased Egr-1 expression, which was attenuated by blocking zinc influx. It is intriguing that brief exposure to zinc induced sustained extracellular signal-regulated kinase (Erk) activation. PD098059, an inhibitor of the Erk 1/2 upstream kinase mitogen-activated protein kinase kinase 1 (MEK1), blocked Erk 1/2 activation, Egr-1 induction, and neuronal death by zinc. The present study has demonstrated that zinc, rather than calcium, induces lasting Egr-1 expression in cortical culture by activating Erk 1/2, which is part of a cascade that may play an active role in zinc neurotoxicity. We propose that translocation of endogenous zinc may be the key mechanism of Egr-1 induction and neuronal death in brain ischemia.

Animals↗

PubMed2001

Oral zinc therapy in patients with supposed mild zinc deficiency--a critical review.

The importance of zinc in many processes of diseases remains unclear up today. Nevertheless many biochemical or clinical studies let support a high clinical relevance of trace elements especially zinc in the therapeutic concepts of diseases. Unfortunately the border between severe (or real) and mild (or subclinical) zinc deficiency is not clear defined. In addition methodical problems in determination of trace elements and misinterpretations of study results lead to unjustified assignment from several diseases in the group of zinc deficiency disorders. Another current problem is the consideration of bioavailability of oral commercial trace element products. Especially the regulation of zinc uptake in human under normal conditions and in case of zinc deficiency is not clear at this time. These problems let become tangled the actual literature for the clinical active physician at the field of zinc. In this mini review there is given an overview about published clinical studies with oral zinc supplementation in the past years.

Administration, Oral↗

PubMed2006

Zinc supplementation of young men alters metallothionein, zinc transporter, and cytokine gene expression in leukocyte populations.

An effective measure to assess zinc status of humans has remained elusive, in contrast to iron, where a number of indicators of metabolism/function are available. Using monocytes, T lymphocytes, and granulocytes isolated by magnetic sorting and dried blood spots (DBS) derived from 50 mul of peripheral blood, we evaluated the response of metallothionein (MT), zinc transporter, and cytokine genes to a modest (15 mg of Zn per day) dietary zinc supplement in human subjects. Transcript abundance was measured by quantitative real-time RT-PCR (QRT-PCR). Zinc supplementation increased MT mRNA abundance by up to 2-fold in RNA from leukocyte subsets, and 4-fold in RNA from DBS. Transcript levels for the zinc transporter genes ZnT1 and Zip3 were increased and decreased, respectively, by zinc supplementation. Expression of the ZnT and Zip genes among leukocyte subsets differ by up to 270-fold. Monocytes and granulocytes from supplemented subjects were activated by LPS, whereas T lymphocytes were activated by mimicking antigen presentation. With zinc consumption, TNF-alpha and IL-1beta expression was greater in activated monocytes and granulocytes, and IFN-gamma mRNA levels were higher in activated T lymphocytes. These studies show that QRT-PCR is a tool to reliably measure transcript abundance for nutritionally responsive genes in human subjects, and that a small sample of whole dried blood, when appropriately collected, can be used as the source of total RNA for QRT-PCR analysis. The results obtained also show that zinc supplementation of human subjects programs specific leukocytic subsets to show enhanced cytokine expression upon activation by stimulators of immunity.

Adult↗

PubMed1991

Cysteine-rich intestinal protein binds zinc during transmucosal zinc transport.

The mechanism of zinc absorption has not been delineated, but kinetic studies show that both passive and carrier-mediated processes are involved. We have identified a low molecular mass zinc-binding protein in the soluble fraction of rat intestinal mucosa that could function as an intracellular zinc carrier. The protein was not detected in liver or pancreas, suggesting a role specific to the intestine. The protein binds zinc during transmucosal zinc transport and shows signs of saturation at higher luminal zinc concentrations, characteristics consistent with a role in carrier-mediated zinc absorption. Microsequence analysis of the protein purified by gel-filtration HPLC and SDS/PAGE showed complete identity within the first 41 N-terminal amino acids with the deduced protein sequence of cysteine-rich intestinal protein [Birkenmeier, E. H. & Gordon, J. I. (1986) Proc. Natl. Acad. Sci. USA 83, 2516-2520]. These investigators showed that the gene for this protein is developmentally regulated in neonates during the suckling period, conserved in many vertebrate species, and predominantly expressed in the small intestine. Cysteine-rich intestinal protein contains a recently identified conserved sequence of histidine and cysteine residues, the LIM motif, which our results suggest confers metal-binding properties that are important for zinc transport and/or functions of this micronutrient.

Amino Acid Sequence↗

PubMed1998

Regulation of the zinc transporter ZnT-1 by dietary zinc.

The understanding of mechanisms controlling zinc absorption and metabolism at the molecular level has advanced recently. Kinetics of zinc transport have been investigated for many years, but only recently have genes coding for proteins thought to be involved in the transport process been cloned. Four putative zinc transporters, known as ZnT-1 through ZnT-4, have now been described. Among these transporters, only ZnT-1 is ubiquitously expressed. In this report, we examine the pattern of ZnT-1 expression in the intestine and analyze the regulation of ZnT-1 by dietary zinc in both the intestine and liver. Immunofluorescence demonstrated that intestinal ZnT-1 was most abundant at the basolateral surface of enterocytes lining the villi of the duodenum and jejunum. By Western blot analysis, intestinal and liver ZnT-1 protein migrated as a 42- and 36-kDa protein, respectively. Dietary zinc supplementation elevated the level of intestinal ZnT-1 mRNA and protein approximately 50% and 10%, respectively, but had no effect in the liver. In response to an acute oral zinc dose, the level of intestinal ZnT-1 mRNA was up-regulated 8-fold, without a corresponding increase in ZnT-1 protein. Conversely, the acute oral dose did not affect liver ZnT-1 mRNA, but resulted in a 5-fold increase in liver ZnT-1 protein. These results represent studies on the expression of intestinal and hepatic ZnT-1 in an intact animal model. The data suggest that ZnT-1 is at least part of the mechanism by which dietary zinc is absorbed and that, despite the zinc responsiveness of the ZnT-1 gene, additional factors may be regulating the steady-state level of ZnT-1 transporter protein.

Animals↗

PubMed2003

A cytosolic domain of the yeast Zrt1 zinc transporter is required for its post-translational inactivation in response to zinc and cadmium.

Nutrient metals such as zinc are both essential to life and potentially toxic if overaccumulated by cells. Non-essential toxic metals like cadmium can enter cells through the uptake transporters responsible for nutrient metal acquisition. Therefore, in the face of ever changing extracellular metal levels, organisms tightly control their intracellular levels of nutrient metals and prevent accumulation of toxic metals. We show here that post-translational inactivation of the yeast Zrt1 zinc uptake transporter is important for zinc homeostasis. During the transition from zinc-limiting to zinc-replete growth conditions (i.e. zinc shock), the Zrt1 transporter is ubiquitinated, endocytosed, and subsequently degraded in the vacuole. To further understand this process at a molecular level, we mapped a region of Zrt1 required for ubiquitination and endocytosis in response to zinc to a domain located on the intracellular surface of the plasma membrane. This domain is a critical cis-acting component of the metal signaling pathway that controls Zrt1 protein trafficking. Using mutant alleles defective for metal-responsive inactivation, we also show that Zrt1 inactivation may be an important mechanism for preventing cadmium uptake and toxicity in zinc-limited cells.

Amino Acid Motifs↗

PubMed2003

Estrogen decreases zinc transporter 3 expression and synaptic vesicle zinc levels in mouse brain.

Previous studies suggest that female sex hormones modulate synaptic zinc levels, which may influence amyloid plaque formation and Alzheimer's disease progression. We examined the effects of ovariectomy and estrogen supplement on the levels of synaptic zinc and zinc transporter protein Znt3 in the brain. Ovariectomy was performed on 5-month-old mice, and 2 weeks later, pellets containing vehicle, low (0.18 mg/pellet), or high dose (0.72 mg) 17beta-estradiol were implanted. After 4 weeks, animals were decapitated, and blood and brain were collected for analysis. Blood analysis indicated that estrogen implants altered plasma estrogen levels in a dose-dependent manner. Analysis of brain tissue showed that ovariectomy raised hippocampal synaptic vesicle zinc levels, whereas estrogen replacement lowered these zinc levels. Western blots revealed that Znt3 levels in the brain were modulated in parallel with synaptic zinc levels, whereas no change was detected in the levels of Znt3 mRNA, as determined by Northern blot and reverse transcriptase-PCR analysis. However, mRNA levels of the delta subunit of adaptor protein complex (AP)-3, which modulates the level of Znt3 levels, were altered by estrogen depletion or replacement. These data demonstrate that estrogen alters the levels of Znt3 and synaptic vesicle zinc in female mice, probably through changing AP-3 delta expression. Since synaptic zinc may play a key role in neuronal death in acute brain injury as well as in plaque formation in Alzheimer's disease, and since estrogen may be beneficial in both conditions, our results may provide new insights into the effects of estrogen on the brain.

Adaptor Protein Complex 3↗

PubMed2001

Growth hormone-releasing factor affects macronutrient intake during the anabolic phase of zinc repletion: total hypothalamic growth hormone-releasing factor content and growth hormone-releasing factor immunoneutralization during zinc repletion.

Growth hormone-releasing factor (GRF) is thought to perform two distinct functions within the brain. GRF synthesized in the median eminence (ME) stimulates the release of growth hormone (GH) from the pituitary, while GRF in the suprachiasmatic nucleus and median preoptic area (SCN/MPOA) may stimulate selection of dietary protein. These two functions may be coupled to regulate and enhance growth. During zinc repletion, a period characterized by increased protein intake and accelerated growth, we examined this coupling by measuring GRF peptide content in hypothalamic sites and neutralizing GRF function by infusing anti-GRF antibody into the hypothalamus during zinc repletion. Total GRF content and GRF content in the ME and SCN/MPOA were decreased in zinc-deficient (Zn-) rats compared to zinc-adequate (Zn+) rats (P < 0.05). There were no differences in GRF content during zinc repletion in either nuclei. Subsequently, we investigated the macronutrient feeding patterns of rats chronically infused with anti-GRF IgG into the lateral ventricle of the brain during zinc repletion. All Zn- and Zn+ rats administered anti-GRF IgG exhibited a reduction in protein intake during zinc repletion. The Zn- rats receiving anti-GRF-IgG consumed equal amounts of total diet compared to those receiving vehicle during the repletion period however they consumed less carbohydrate (P < 0.05) and considerably more fat (P < 0.02). There were no significant differences in carbohydrate or fat intake in Zn+ rats receiving anti-GRF antibody. These results suggest that GRF likely directs protein intake during normal growth, but may interact with additional appetite-controlling neuropeptides during zinc repletion.

Animal Nutritional Physiological Phenomena↗

PubMed1999

Comparative analysis of KRAB zinc finger proteins in rodents and man: evidence for several evolutionarily distinct subfamilies of KRAB zinc finger genes.

Although the KRAB zinc finger proteins probably constitute the single largest class of transcription factors within the human genome, almost nothing is known about their biological function. To increase our knowledge about this interesting and relatively unexplored family of potent transcriptional repressors, we here present the cloning, structural analysis, and expression study of three novel mouse KRAB zinc finger proteins. In addition, we present an extensive comparative analysis of various members of this gene family based on the structure of the common KRAB A motif. At least three larger subfamilies of KRAB zinc finger proteins are identified: one carrying the classical KRAB A motif only, another holding both a classical KRAB A and a classical KRAB B motif, and a third holding a classical KRAB A and a highly divergent KRAB B domain, named b. A large variation both in size and in primary amino acid sequence was observed in the linker region between the KRAB domain and the C-terminally located zinc finger repeats. This variability indicates that this region is of minor importance for the biological function of KRAB-containing zinc finger proteins. The fact that in many zinc finger genes, the entire or almost the entire linker region is composed of degenerate finger motifs substantiates this conclusion. The absence of identifiable KRAB A and B motifs in the genome of yeast, Saccharomyces cerevisiae, indicates a relatively late appearance of the KRAB domain in evolution and may suggest that the biological functions are restricted to multicellular organisms. In addition, we show that the expression of individual members of one subfamily of KRAB zinc finger genes is restricted to specific hematopoietic cell lineages. This finding suggests that KRAB zinc finger proteins may play a role in lineage commitment, possibly silencing leakage transcription from nonlineage-expressed genes.

Amino Acid Sequence↗

PubMed1979

Zinc nutritional status of young middle-income children and effects of consuming zinc-fortified breakfast cereals.

The effects of consuming zinc-fortified ready-to-eat breakfast cereals were determined in a double-blind controlled study. The 96 healthy young children who participated (mean age 58 months) consumed either zinc-fortified cereal, providing 25% United States Recommended Dietary Allowance per 1 ounce serving (test children) or nonzinc-fortified cereals (controls) for a 9-month period. The test children were calculated on average to receive an additional 2.57 mg of zinc per day from this fortification program. This increment increased their mean daily zinc intake to a level that approached the Recommended Dietary Allowance (10 mg) of the National Academy of Sciences for children less than 10 years of age. By the end of the period, the test children (combined sexes) had a mean increment of plasma zinc that was 6.5 micrograms/dl greater than that of the control children (P less than 0.02). The test girls had a greater increment (28.5 micrograms/g) in hair zinc content than controls girls (P less than 0.05). There were no significant differences in other biochemical parameters including plasma copper and serum cholesterol. No significant differences in food intake or growth velocity were associated with the consumption of the zinc-fortified cereal. Multiple sex and time related differences occurred in plasma, hair, urine, and parotid saliva zinc concentrations that were unrelated to the type of cereal consumed.

Child↗

PubMed1983

Dietary cholesterol decreases the serum level of zinc: further evidence for the positive relationship between serum zinc and high-density lipoproteins.

The previous finding (Am J Clin Nutr 1981;34:2376-81) that the serum level of high-density lipoprotein (HDL) cholesterol is positively correlated with the serum concentration of zinc (r = +0.81; p less than 0.01) led us to evaluate further the zinc-HDL relationship as affected by dietary cholesterol. The two diets, one control diet containing no cholesterol and the other containing 1% cholesterol, were isocalorically formulated with an equal but adequate level of zinc. Cholesterol feeding produced a significant decrease in the serum level of HDL cholesterol at 8th wk of dietary treatment and a significant increase in very low density lipoprotein cholesterol at 4th and 8th wk. At the same intervals of dietary treatment, significant decreases in serum zinc levels were observed in cholesterol-fed rats; no changes were noted in the serum levels of other related elements such as copper, calcium, and magnesium. Linear regression analysis of the 44 pairs of serum HDL and zinc values revealed a significant positive correlation (r = +0.57; p less than 0.01) between the two parameters. The rather selective lowering of serum zinc due to cholesterol feeding and the observation of the positive serum zinc-HDL relationship observed in the present and previous studies warrant further investigation into the role of zinc in cholesterol and high-density lipoprotein metabolism.

Animals↗

PubMed1991

Homeostatic regulation of zinc absorption and endogenous losses in zinc-deprived men.

The mechanisms involved in the homeostatic regulation of zinc were studied in five male subjects by using stable 70Zn as a marker. When dietary zinc was reduced from 85 to 12 mumol/d, adaptation was achieved by a mean (+/- SEM) reduction in urine zinc of 48 +/- 7% and in fecal zinc of 46 +/- 12% over 25 d in four subjects. The latter was caused by an increase in the efficiency of zinc absorption from 38 +/- 3% to 93 +/- 1% after 15 d of zinic deprivation and by a reduction in intestinal endogenous losses of zinc. In a fifth subject, who had some evidence of a resolving alcohol-induced hepatitis, urine and fecal zinc were reduced by 64% and 41%, respectively, in 15 d and zinc absorption increased from 46% to 93%. More information on adaptive responses is needed to enable current dietary recommendations to be reconsidered.

Absorption↗

PubMed1992

Effects of dietary zinc depletion on seminal volume and zinc loss, serum testosterone concentrations, and sperm morphology in young men.

Identification of the andrological variables most sensitive to zinc depletion would expedite the diagnosis of male reproductive pathology induced by zinc deficiency. Eleven volunteers living on a metabolic ward were fed a diet composed of a mixture of a semisynthetic formula and conventional foods supplemented with ZnSO4 to supply a total of 1.4, 2.5, 3.4, 4.4, or 10.4 mg Zn/d. After an equilibration period of 28 d (10.4 mg Zn/d), all treatments were presented for 35 d each, the first four in random order and the fifth last. Compared with when they were consuming 10.4 mg Zn/d, volunteers consuming 1.4 mg Zn/d exhibited decreased semen volumes (3.30 vs 2.24 mL) and serum testosterone concentrations (26.9 vs 21.9 nmol/L), and no change in seminal zinc concentrations. Compared with 10.4 mg Zn/d, treatments of 1.4, 2.5, and 3.4 mg Zn/d decreased the total semen zinc loss per ejaculate (6.29 vs 3.81, 4.68, and 5.03 mumols/ejaculate). Seminal loss accounted for 9% of total body zinc loss when 1.4 mg Zn/d was consumed. Seminal phosphorus concentrations were elevated during all four phases of zinc depletion (28.4 vs 32.9, 31.0, 34.2, and 33.6 mmol/L). The findings suggest that serum testosterone concentrations, seminal volume, and total seminal zinc loss per ejaculate are sensitive to short-term zinc depletion in young men.

Adult↗

PubMed1988

The oral disposition of zinc following the use of an anticalculus toothpaste containing 0.5% zinc citrate.

Zinc is retained in the mouth after use of a toothpaste containing 0.5% zinc citrate. More than one third of the dose was found to be retained after normal brushing. Elevated zinc levels were also found in plaque. Saliva zinc levels were significantly above background for at least 2 h after brushing. In-vitro experiments demonstrated that zinc can bind to the pellicle-coated tooth surface and can subsequently adsorb into saliva. Plaque can calcify to form calculus containing appreciable levels of hydroxyapatite. Zinc adsorbs to hydroxyapatite inhibiting crystal growth. Levels of zinc in plaque were found to be considerably higher than those taken up by hydroxyapatite in an in-vitro test of crystal growth inhibition indicating the potential of zinc to inhibit calculus formation.

Adsorption↗