Science.gov

Sample records for zinc deficiency decreased

  1. Serum thymulin in human zinc deficiency.

    PubMed Central

    Prasad, A S; Meftah, S; Abdallah, J; Kaplan, J; Brewer, G J; Bach, J F; Dardenne, M

    1988-01-01

    The activity of thymulin (a thymic hormone) is dependent on the presence of zinc in the molecule. We assayed serum thymulin activity in three models of mildly zinc-deficient (ZD) human subjects before and after zinc supplementation: (a) two human volunteers in whom a specific and mild zinc deficiency was induced by dietary means; (b) six mildly ZD adult sickle cell anemia (SCA) subjects; and (c) six mildly ZD adult non-SCA subjects. Their plasma zinc levels were normal and they showed no overt clinical manifestations of zinc deficiency. The diagnosis of mild zinc deficiency was based on the assay of zinc in lymphocytes, granulocytes, and platelets. Serum thymulin activity was decreased as a result of mild zinc deficiency and was corrected by in vivo and in vitro zinc supplementation, suggesting that this parameter was a sensitive indicator of zinc deficiency in humans. An increase in T101-, sIg-cells, decrease in T4+/T8+ ratio, and decreased IL 2 activity were observed in the experimental human model during the zinc depletion phase, all of which were corrected after repletion with zinc. Similar changes in lymphocyte subpopulation, correctable with zinc supplementation, were also observed in mildly ZD SCA subjects. Inasmuch as thymulin is known to induce intra- and extrathymic T cell differentiation, our studies provide a possible mechanism for the role of zinc on T cell functions. Images PMID:3262625

  2. Tracing of Zinc Nanocrystals in the Anterior Pituitary of Zinc-Deficient Wistar Rats.

    PubMed

    Kuldeep, Anjana; Nair, Neena; Bedwal, Ranveer Singh

    2017-06-01

    The aim of this study was to trace zinc nanocrystals in the anterior pituitary of zinc-deficient Wistar rats by using autometallographic technique. Male Wistar rats (30-40 days of age, pre-pubertal period) of 40-50 g body weight were divided into the following: the ZC (zinc control) group-fed with 100 ppm zinc in diet, the ZD (zinc-deficient) group-fed with zinc-deficient (1.00 ppm) diet and the PF (pair-fed) group-received 100 ppm zinc in diet. The experiments were set for 2 and 4 weeks. Pituitary was removed and processed for the autometallographic technique. The control and pair-fed groups retained their normal morphological features. However, male Wistar rats fed on zinc-deficient diet for 2 and 4 weeks displayed a wide range of symptoms such as significant (P < 0.05) decrease in diet consumption, body weight and pituitary weight and decrease in gradation of intensity of zinc nanocrystals in the nuclei. The present findings suggest that the dietary zinc deficiency causes decreased intensity of zinc nanocrystals localization and their distribution in the pituitary thereby contributing to the dysfunction of the pituitary of the male Wistar rats. The severity of zinc deficiency symptoms progressed after the second week of the experiment. Decreased intensity of zinc nanocrystals attenuates the pituitary function which would exert its affect on other endocrine organs impairing their functions indicating that the metabolic regulation of pituitary is mediated to a certain extent by zinc and/or hypothalamus-hypophysial system which also reflects its essentiality during the period of growth.

  3. Decreased serum and mucosa immunoglobulin A levels in vitamin Aand zinc-deficient mice

    PubMed Central

    Kheirouri, Sorayya

    2014-01-01

    Simultaneous zinc and vitamin A deficiency are common health problems in developing countries. The objective of this study was to assess the effect of vitamin A- and zinc-deficient diet on immunoglobulin A (IgA) response. Six-week-old mice were assigned into two groups receiving a normal vitamin A and zinc or low vitamin A and zinc diet for five months. Serum and intestinal mucosa IgA levels were determined by the enzyme-linked immunosorbent assay method. The concentration of zinc in serum was determined using an inductively coupled plasma mass spectrometer. Vitamin A measurement in serum was carried out by high performance liquid chromatography. Mice maintained on a low vitamin A and zinc diet showed significantly greater food intake but lower production of IgA both in serum and mucosa. A mucosa IgA level was significantly higher in both control and deficient groups than the serum IgA level. Results indicated that zinc and vitamin A deficiency is associated with a lower production of IgA. Micronutrient intervention strategies addressing IgA-related gastrointestinal infections are needed. PMID:26155118

  4. Dietary calcium and zinc deficiency risks are decreasing but remain prevalent

    PubMed Central

    Kumssa, Diriba B.; Joy, Edward J. M.; Ander, E. Louise; Watts, Michael J.; Young, Scott D.; Walker, Sue; Broadley, Martin R.

    2015-01-01

    Globally, more than 800 million people are undernourished while >2 billion people have one or more chronic micronutrient deficiencies (MNDs). More than 6% of global mortality and morbidity burdens are associated with undernourishment and MNDs. Here we show that, in 2011, 3.5 and 1.1 billion people were at risk of calcium (Ca) and zinc (Zn) deficiency respectively due to inadequate dietary supply. The global mean dietary supply of Ca and Zn in 2011 was 684 ± 211 and 16 ± 3 mg capita−1 d−1 (±SD) respectively. Between 1992 and 2011, global risk of deficiency of Ca and Zn decreased from 76 to 51%, and 22 to 16%, respectively. Approximately 90% of those at risk of Ca and Zn deficiency in 2011 were in Africa and Asia. To our knowledge, these are the first global estimates of dietary Ca deficiency risks based on food supply. We conclude that continuing to reduce Ca and Zn deficiency risks through dietary diversification and food and agricultural interventions including fortification, crop breeding and use of micronutrient fertilisers will remain a significant challenge. PMID:26098577

  5. Dietary calcium and zinc deficiency risks are decreasing but remain prevalent

    NASA Astrophysics Data System (ADS)

    Kumssa, Diriba B.; Joy, Edward J. M.; Ander, E. Louise; Watts, Michael J.; Young, Scott D.; Walker, Sue; Broadley, Martin R.

    2015-06-01

    Globally, more than 800 million people are undernourished while >2 billion people have one or more chronic micronutrient deficiencies (MNDs). More than 6% of global mortality and morbidity burdens are associated with undernourishment and MNDs. Here we show that, in 2011, 3.5 and 1.1 billion people were at risk of calcium (Ca) and zinc (Zn) deficiency respectively due to inadequate dietary supply. The global mean dietary supply of Ca and Zn in 2011 was 684 ± 211 and 16 ± 3 mg capita-1 d-1 (±SD) respectively. Between 1992 and 2011, global risk of deficiency of Ca and Zn decreased from 76 to 51%, and 22 to 16%, respectively. Approximately 90% of those at risk of Ca and Zn deficiency in 2011 were in Africa and Asia. To our knowledge, these are the first global estimates of dietary Ca deficiency risks based on food supply. We conclude that continuing to reduce Ca and Zn deficiency risks through dietary diversification and food and agricultural interventions including fortification, crop breeding and use of micronutrient fertilisers will remain a significant challenge.

  6. Serum alkaline phosphatase activity during zinc deficiency and long-term inflammatory stress.

    PubMed

    Naber, T H; Baadenhuysen, H; Jansen, J B; van den Hamer, C J; van den Broek, W

    1996-05-30

    A decrease in serum zinc can be caused by a real zinc deficiency but can also be caused by an apparent zinc deficiency, e.g. in inflammatory stress. The aim of this study was to evaluate the diagnostic power of serum alkaline phosphatase (AP) activity in the discrimination between pathophysiologic states of "real" and "apparent" zinc deficiency. A decrease in serum zinc was induced in growing and adult rats, by providing a diet low in zinc and by causing inflammatory stress. AP activity was determined using reagents low or enriched in zinc. Serum AP was decreased in zinc-deficient adult rats (P < 0.01). In zinc-deficient growing rats AP activity was not different from normal rats but AP activity decreased rapidly. In the same growing rats a significant difference was found in AP activities determined using buffers low and enriched in zinc (P < 0.001) between both groups of rats. After inducing inflammatory stress a decrease in AP activity (P < 0.01) and serum zinc (P < 0.001) was seen during the first few days. After the initial phase of inflammation AP activity normalized, serum zinc showed a rise which after correction for the decrease in serum albumin reached the level of the control rats. A difference in AP activity in buffers low and enriched in zinc was observed only during the first few days after induction of inflammatory stress (P < 0.001). Probably the method of measurement of the difference in enzyme activity, using buffers low and enriched in zinc, can be used as an indication for zinc deficiency in situations with changing AP enzyme concentrations. AP activity is decreased during the initial phase of inflammatory stress due to a decrease in serum zinc.

  7. Dietary phytate, zinc and hidden zinc deficiency.

    PubMed

    Sandstead, Harold H; Freeland-Graves, Jeanne H

    2014-10-01

    Epidemiological data suggest at least one in five humans are at risk of zinc deficiency. This is in large part because the phytate in cereals and legumes has not been removed during food preparation. Phytate, a potent indigestible ligand for zinc prevents it's absorption. Without knowledge of the frequency of consumption of foods rich in phytate, and foods rich in bioavailable zinc, the recognition of zinc deficiency early in the illness may be difficult. Plasma zinc is insensitive to early zinc deficiency. Serum ferritin concentration≤20μg/L is a potential indirect biomarker. Early effects of zinc deficiency are chemical, functional and may be "hidden". The clinical problem is illustrated by 2 studies that involved US Mexican-American children, and US premenopausal women. The children were consuming home diets that included traditional foods high in phytate. The premenopausal women were not eating red meat on a regular basis, and their consumption of phytate was mainly from bran breakfast cereals. In both studies the presence of zinc deficiency was proven by functional responses to controlled zinc treatment. In the children lean-mass, reasoning, and immunity were significantly affected. In the women memory, reasoning, and eye-hand coordination were significantly affected. A screening self-administered food frequency questionnaire for office might help caregiver's identify patients at risk of zinc deficiency. Copyright © 2014 Elsevier GmbH. All rights reserved.

  8. Zinc deficiency during growth: influence on renal function and morphology.

    PubMed

    Tomat, Analía Lorena; Costa, María Angeles; Girgulsky, Luciana Carolina; Veiras, Luciana; Weisstaub, Adriana Ruth; Inserra, Felipe; Balaszczuk, Ana María; Arranz, Cristina Teresa

    2007-03-13

    This study was designed to investigate the effects of moderate zinc deficiency during growth on renal morphology and function in adult life. Weaned male Wistar rats were divided into two groups and fed either a moderately zinc-deficient diet (zinc: 8 mg/kg, n=12) or a control diet (zinc: 30 mg/kg, n=12) for 60 days. We evaluated: renal parameters, NADPH-diaphorase and nitric oxide synthase activity in kidney, renal morphology and apoptotic cells in renal cortex. Zinc-deficient rats showed a decrease in glomerular filtration rate and no changes in sodium and potassium urinary excretion. Zinc deficiency decreased NADPH diaphorase activity in glomeruli and tubular segment of nephrons, and reduced activity of nitric oxide synthase in the renal medulla and cortex, showing that zinc plays an important role in preservation of the renal nitric oxide system. A reduction in nephron number, glomerular capillary area and number of glomerular nuclei in cortical and juxtamedullary areas was observed in zinc deficient kidneys. Sirius red staining and immunostaining for alpha-smooth muscle-actin and collagen III showed no signs of fibrosis in the renal cortex and medulla. An increase in the number of apoptotic cells in distal tubules and cortical collecting ducts neighboring glomeruli and, to a lesser extent, in the glomeruli was observed in zinc deficient rats. The major finding of our study is the emergence of moderate zinc deficiency during growth as a potential nutritional factor related to abnormalities in renal morphology and function that facilitates the development of cardiovascular and renal diseases in adult life.

  9. Adverse effects of parental zinc deficiency on metal homeostasis and embryonic development in a zebrafish model.

    PubMed

    Beaver, Laura M; Nkrumah-Elie, Yasmeen M; Truong, Lisa; Barton, Carrie L; Knecht, Andrea L; Gonnerman, Greg D; Wong, Carmen P; Tanguay, Robert L; Ho, Emily

    2017-05-01

    The high prevalence of zinc deficiency is a global public health concern, and suboptimal maternal zinc consumption has been associated with adverse effects ranging from impaired glucose tolerance to low birthweights. The mechanisms that contribute to altered development and poor health in zinc deficient offspring are not completely understood. To address this gap, we utilized the Danio rerio model and investigated the impact of dietary zinc deficiency on adults and their developing progeny. Zinc deficient adult fish were significantly smaller in size, and had decreases in learning and fitness. We hypothesized that parental zinc deficiency would have an impact on their offspring's mineral homeostasis and embryonic development. Results from mineral analysis showed that parental zinc deficiency caused their progeny to be zinc deficient. Furthermore, parental dietary zinc deficiency had adverse consequences for their offspring including a significant increase in mortality and decreased physical activity. Zinc deficient embryos had altered expression of genes that regulate metal homeostasis including several zinc transporters (ZnT8, ZnT9) and the metal-regulatory transcription factor 1 (MTF-1). Zinc deficiency was also associated with decreased expression of genes related to diabetes and pancreatic development in the embryo (Insa, Pax4, Pdx1). Decreased expression of DNA methyltransferases (Dnmt4, Dnmt6) was also found in zinc deficient offspring, which suggests that zinc deficiency in parents may cause altered epigenetic profiles for their progeny. These data should inform future studies regarding zinc deficiency and pregnancy and suggest that supplementation of zinc deficient mothers prior to pregnancy may be beneficial. Published by Elsevier Inc.

  10. Adverse effects of parental zinc deficiency on metal homeostasis and embryonic development in a zebrafish model

    PubMed Central

    Beaver, Laura M.; Nkrumah-Elie, Yasmeen M.; Truong, Lisa; Barton, Carrie L.; Knecht, Andrea L.; Gonnerman, Greg D.; Wong, Carmen P.; Tanguay, Robert L.; Ho, Emily

    2017-01-01

    The high prevalence of zinc deficiency is a global public health concern, and suboptimal maternal zinc consumption has been associated with adverse effects ranging from impaired glucose tolerance to low birthweights. The mechanisms that contribute to altered development and poor health in zinc deficient offspring are not completely understood. To address this gap, we utilized the Danio rerio model and investigated the impact of dietary zinc deficiency on adults and their developing progeny. Zinc deficient adult fish were significantly smaller in size, and had decreases in learning and fitness. We hypothesized that parental zinc deficiency would have an impact on their offspring’s mineral homeostasis and embryonic development. Results from mineral analysis showed that parental zinc deficiency caused their progeny to be zinc deficient. Furthermore, parental dietary zinc deficiency had adverse consequences for their offspring including a significant increase in mortality and decreased physical activity. Zinc deficient embryos had altered expression of genes that regulate metal homeostasis including several zinc transporters (ZnT8, ZnT9) and the metal-regulatory transcription factor 1 (MTF-1). Zinc deficiency was also associated with decreased expression of genes related to diabetes and pancreatic development in the embryo (Insa, Pax4, Pdx1). Decreased expression of DNA methyltransferases (Dnmt4, Dnmt6) was also found in zinc deficient offspring, which suggests that zinc deficiency in parents may cause altered epigenetic profiles for their progeny. These data should inform future studies regarding zinc deficiency and pregnancy and suggest that supplementation of zinc deficient mothers prior to pregnancy may be beneficial. PMID:28268202

  11. Enhancement of hippocampal mossy fiber activity in zinc deficiency and its influence on behavior.

    PubMed

    Takeda, Atsushi; Itoh, Hiromasa; Yamada, Kohei; Tamano, Haruna; Oku, Naoto

    2008-10-01

    The extracellular concentration of glutamate in the hippocampus is increased by hippocampal perfusion with CaEDTA, a membrane-impermeable zinc chelator, suggesting that the activity of glutamatergic neurons in the hippocampus are influenced by the extracellular concentrations of zinc. In the present study, the relationship between the extracellular concentrations of zinc and mossy fiber activity in the hippocampus was examined in mice and rats fed a zinc-deficient diet for 4 weeks. Timm's stain, by which histochemically reactive zinc in the presynaptic vesicles is detected, was attenuated in the hippocampus in zinc deficiency. The extracellular signal of ZnAF-2, a membrane-impermeable zinc indicator, was also lower in the hippocampal CA3, suggesting that the basal extracellular concentrations of zinc are lower maintained in zinc deficiency. To check mossy fiber activity after 4-week zinc deprivation, the decrease in the signal of FM4-64, an indicator of presynaptic activity (exocytosis), at mossy fiber synapses was measured under the condition of spontaneous depolarization. The decrease was significantly facilitated by zinc deficiency, suggesting that the basal exocytosis at mossy fiber synapses is enhanced by zinc deficiency. On the other hand, the increase in anxiety-like behavior was observed in the open-field test after 4-week zinc deprivation. The present study demonstrates that the decrease in the basal extracellular concentrations of zinc may be linked to the enhancement of the basal mossy fiber activity in zinc deficiency. This decrease seems to be also involved in neuropsychological behavior in zinc deficiency.

  12. Prevalence of zinc deficiency among rural women during childbearing age in Peshawar, Pakistan.

    PubMed

    Akhtar, Tasleem; Khan, Mir Hassan; Zahoorullah; Hussain, Hamid; Nazli, Rubina; Lutfullah, Ghosia

    2014-01-01

    Zinc deficiency is a commonly reported health problem throughout the world. This cross sectional survey was conducted in rural Peshawar with an aim to estimate the prevalence of zinc deficiency in women of child bearing age and find its association with age, marital, pregnancy status and parity. Data was collected from 353 women age 15-45 years. EPI INFO version 6.04 was used for data analysis. Overall 98 (27.8 %) women were zinc deficient (<80 μg/dL) while 31 (8.8%) had severe zinc deficiency (<50μg/dL.). Mean zinc level was found to increase gradually with the increase in the age up to 40 years and then starts decreasing significantly beyond this age. A significant decrease (p<0.03) in zinc concentration was found in married as compared to unmarried women. Out of 31 female with severe zinc deficiency, 23 (74.2%) were pregnant. Pregnant women in second (OR (CI) 3.36 (1.52-7.44) p<0.0008) and third ((OR (CI) 3.73 (1.91-7.30) p<0.00002) trimester were 3.4 & 3.7 times, respectively more zinc deficient as compared to control women. Mean zinc levels were significantly lower in women having no children versus women with 1-5 numbers of children. This study concludes that severe zinc deficiency especially prevalent in pregnant women needs urgent correction through food supplementation.

  13. Transient symptomatic zinc deficiency in a preterm exclusively breast-fed infant.

    PubMed

    Laureano, André; Brás, Susana; Carvalho, Rodrigo; Amaro, Cristina; Cardoso, Jorge

    2014-02-18

    A 5-month-old female infant, preterm, exclusively breast-fed, presented with a 2-month history of erythematous, erosive, and crusted patches and plaques in a peri-oral, scalp, genital, and peri-anal distribution. A clinical diagnosis of zinc deficiency was confirmed by a low serum zinc level in the infant and decreased maternal breast milk zinc. Complete resolution occurred within two weeks of oral zinc supplementation. Acquired zinc deficiency is a rare nutritional disorder of infants. Early diagnosis and adequate treatment will prevent associated morbidity and complications.

  14. Dietary zinc deficiency predisposes mice to the development of preneoplastic lesions in chemically-induced hepatocarcinogenesis.

    PubMed

    Romualdo, Guilherme Ribeiro; Goto, Renata Leme; Henrique Fernandes, Ana Angélica; Cogliati, Bruno; Barbisan, Luis Fernando

    2016-10-01

    Although there is a concomitance of zinc deficiency and high incidence/mortality for hepatocellular carcinoma in certain human populations, there are no experimental studies investigating the modifying effects of zinc on hepatocarcinogenesis. Thus, we evaluated whether dietary zinc deficiency or supplementation alter the development of hepatocellular preneoplastic lesions (PNL). Therefore, neonatal male Balb/C mice were submitted to a diethylnitrosamine/2-acetylaminefluorene-induced hepatocarcinogenesis model. Moreover, mice were fed adequate (35 mg/kg diet), deficient (3 mg/kg) or supplemented (180 mg/kg) zinc diets. Mice were euthanized at 12 (early time-point) or 24 weeks (late time-point) after introducing the diets. At the early time-point, zinc deficiency decreased Nrf2 protein expression and GSH levels while increased p65 and p53 protein expression and the number of PNL/area. At the late time-point, zinc deficiency also decreased GSH levels while increased liver genotoxicity, cell proliferation into PNL and PNL size. In contrast, zinc supplementation increased antioxidant defense at both time-points but not altered PNL development. Our findings are the first to suggest that zinc deficiency predisposes mice to the PNL development in chemically-induced hepatocarcinogenesis. The decrease of Nrf2/GSH pathway and increase of liver genotoxicity, as well as the increase of p65/cell proliferation, are potential mechanisms to this zinc deficiency-mediated effect. Copyright © 2016 Elsevier Ltd. All rights reserved.

  15. Alterations in protein kinase C activity and processing during zinc-deficiency-induced cell death.

    PubMed

    Chou, Susan S; Clegg, Michael S; Momma, Tony Y; Niles, Brad J; Duffy, Jodie Y; Daston, George P; Keen, Carl L

    2004-10-01

    Protein kinases C (PKCs) are a family of serine/threonine kinases that are critical for signal transduction pathways involved in growth, differentiation and cell death. All PKC isoforms have four conserved domains, C1-C4. The C1 domain contains cysteine-rich finger-like motifs, which bind two zinc atoms. The zinc-finger motifs modulate diacylglycerol binding; thus, intracellular zinc concentrations could influence the activity and localization of PKC family members. 3T3 cells were cultured in zinc-deficient or zinc-supplemented medium for up to 32 h. Cells cultured in zinc-deficient medium had decreased zinc content, lowered cytosolic classical PKC activity, increased caspase-3 processing and activity, and reduced cell number. Zinc-deficient cytosols had decreased activity and expression levels of PKC-alpha, whereas PKC-alpha phosphorylation was not altered. Inhibition of PKC-alpha with Gö6976 had no effect on cell number in the zinc-deficient group. Proteolysis of the novel PKC family member, PKC-delta, to its 40-kDa catalytic fragment occurred in cells cultured in the zinc-deficient medium. Occurrence of the PKC-delta fragment in mitochondria was co-incident with caspase-3 activation. Addition of the PKC-delta inhibitor, rottlerin, or zinc to deficient medium reduced or eliminated proteolysis of PKC-delta, activated caspase-3 and restored cell number. Inhibition of caspase-3 processing by Z-DQMD-FMK (Z-Asp-Gln-Met-Asp-fluoromethylketone) did not restore cell number in the zinc-deficient group, but resulted in processing of full-length PKC-delta to a 56-kDa fragment. These results support the concept that intracellular zinc concentrations influence PKC activity and processing, and that zinc-deficiency-induced apoptosis occurs in part through PKC-dependent pathways.

  16. Behavioral impairments in animal models for zinc deficiency

    PubMed Central

    Hagmeyer, Simone; Haderspeck, Jasmin Carmen; Grabrucker, Andreas Martin

    2015-01-01

    Apart from teratogenic and pathological effects of zinc deficiency such as the occurrence of skin lesions, anorexia, growth retardation, depressed wound healing, altered immune function, impaired night vision, and alterations in taste and smell acuity, characteristic behavioral changes in animal models and human patients suffering from zinc deficiency have been observed. Given that it is estimated that about 17% of the worldwide population are at risk for zinc deficiency and that zinc deficiency is associated with a variety of brain disorders and disease states in humans, it is of major interest to investigate, how these behavioral changes will affect the individual and a putative course of a disease. Thus, here, we provide a state of the art overview about the behavioral phenotypes observed in various models of zinc deficiency, among them environmentally produced zinc deficient animals as well as animal models based on a genetic alteration of a particular zinc homeostasis gene. Finally, we compare the behavioral phenotypes to the human condition of mild to severe zinc deficiency and provide a model, how zinc deficiency that is associated with many neurodegenerative and neuropsychological disorders might modify the disease pathologies. PMID:25610379

  17. Effects of zinc-deficient diets on the cardiovascular system in rabbits

    SciTech Connect

    Carter, J.W.; Koo, S.I.

    1986-03-05

    The authors used male New Zealand white rabbits to study the effects of zinc-deficient diets on the cardiovascular system. These 10 week-old rabbits were fed semi-purified diets containing either 50 ppm or less than 1 ppm zinc for 12 weeks. Serum samples were analyzed at 3,6,9 and 12 weeks. Body weight and food consumption were measured weekly. At necropsy the liver and heart were removed and weighed. Then the heart was perfused at 100 mm Hg with 10% buffered formalin via the ascending aorta. Coronary arteries were block-dissected and processed for light microscopy. Food consumption and body weights were notmore » significantly altered throughout the study. Relative heart weights were not different; however, the relative liver weight of the zinc-deficient group was elevated by 11%. Neither total serum cholesterol or HDL-cholesterol were changed at any time. After 6 weeks treatment, serum zinc levels were depressed by 29% in the zinc-deficient group; no changes were observed for serum copper or calcium. Morphometric analysis of coronary arteries revealed a decreased combined thickness of the tunica intima and tunica media and a decreased area per unit length in the left coronary circumflex arteries of zinc-deficient rabbits. Significant changes reported here are probably related to possible alterations in lipoproteins metabolism and will be investigated in future studies.« less

  18. A dynamic model for predicting growth in zinc-deficient stunted infants given supplemental zinc.

    PubMed

    Wastney, Meryl E; McDonald, Christine M; King, Janet C

    2018-05-01

    Zinc deficiency limits infant growth and increases susceptibility to infections, which further compromises growth. Zinc supplementation improves the growth of zinc-deficient stunted infants, but the amount, frequency, and duration of zinc supplementation required to restore growth in an individual child is unknown. A dynamic model of zinc metabolism that predicts changes in weight and length of zinc-deficient, stunted infants with dietary zinc would be useful to define effective zinc supplementation regimens. The aims of this study were to develop a dynamic model for zinc metabolism in stunted, zinc-deficient infants and to use that model to predict the growth response when those infants are given zinc supplements. A model of zinc metabolism was developed using data on zinc kinetics, tissue zinc, and growth requirements for healthy 9-mo-old infants. The kinetic model was converted to a dynamic model by replacing the rate constants for zinc absorption and excretion with functions for these processes that change with zinc intake. Predictions of the dynamic model, parameterized for zinc-deficient, stunted infants, were compared with the results of 5 published zinc intervention trials. The model was then used to predict the results for zinc supplementation regimes that varied in the amount, frequency, and duration of zinc dosing. Model predictions agreed with published changes in plasma zinc after zinc supplementation. Predictions of weight and length agreed with 2 studies, but overpredicted values from a third study in which other nutrient deficiencies may have been growth limiting; the model predicted that zinc absorption was impaired in that study. The model suggests that frequent, smaller doses (5-10 mg Zn/d) are more effective for increasing growth in stunted, zinc-deficient 9-mo-old infants than are larger, less-frequent doses. The dose amount affects the duration of dosing necessary to restore and maintain plasma zinc concentration and growth.

  19. Effects of zinc deficiency on the vallate papillae and taste buds in rats.

    PubMed

    Chou, H C; Chien, C L; Huang, H L; Lu, K S

    2001-05-01

    Zinc deficiency is associated with multiple clinical complications, including taste disturbance, anorexia, growth retardation, skin changes, and hypogonadism. We investigated the zinc-deficiency-induced morphologic changes in the vallate taste buds of weanling and young adult male Wistar rats. A total of 24 weanling and 30 young adult rats were used. Each age group was further divided into a control group fed a zinc-adequate (50 ppm) diet, a zinc-deficient (< 1 ppm) diet group, and a zinc-adequate pair-fed group who were fed the same amount of food as that taken by the zinc-deficient group. Weanling rats were fed for 4 weeks and young adult rats were fed for 6 weeks. The morphometry and morphologic changes of vallate taste buds were analyzed using light and transmission electron microscopy. Light microscopy revealed no significant difference in papilla size and morphology among the various groups. In both weanling and young adult rats in the zinc-deficient diet and pair-fed groups, the number of taste buds per papilla (per animal) and the average profile area of the taste bud were significantly smaller than those of the corresponding controls (p < 0.05). Ultrastructural changes were seen only in the taste buds of weanling rats fed the zinc-deficient diet, with derangement of the architecture of the taste bud and widening of the intercellular space between taste bud cells. The proportion of type I taste bud cells in the taste buds of weanling rats fed the zinc-deficient diet decreased from 59% to 39%, and that of type II taste bud cells decreased from 25% to 12%. No obvious changes in the ultrastructure of type III taste bud cells were observed. The main effects of zinc deficiency in weanling and young adult rats and in adequate diet pair-fed rats were changes in the number and size of taste buds, and fine structure changes in the taste bud cells, especially during the accelerated growth stage after weaning.

  20. Zinc deficiency in field-grown pecan trees: changes in leaf nutrient concentrations and structure.

    PubMed

    Ojeda-Barrios, Dámaris; Abadía, Javier; Lombardini, Leonardo; Abadía, Anunciación; Vázquez, Saúl

    2012-06-01

    Zinc (Zn) deficiency is a typical nutritional disorder in pecan trees [Carya illinoinensis (Wangenh.) C. Koch] grown under field conditions in calcareous soils in North America, including northern Mexico and south-western United States. The aim of this study was to assess the morphological and nutritional changes in pecan leaves affected by Zn deficiency as well as the Zn distribution within leaves. Zinc deficiency led to decreases in leaf chlorophyll concentrations, leaf area and trunk cross-sectional area. Zinc deficiency increased significantly the leaf concentrations of K and Ca, and decreased the leaf concentrations of Zn, Fe, Mn and Cu. All nutrient values found in Zn-deficient leaves were within the sufficiency ranges, with the only exception of Zn, which was approximately 44, 11 and 9 µg g(-1) dry weight in Zn-sufficient, moderately and markedly Zn-deficient leaves, respectively. Zinc deficiency led to decreases in leaf thickness, mainly due to a reduction in the thickness of the palisade parenchyma, as well as to increases in stomatal density and size. The localisation of Zn was determined using the fluorophore Zinpyr-1 and ratio-imaging technique. Zinc was mainly localised in the palisade mesophyll area in Zn-sufficient leaves, whereas no signal could be obtained in Zn-deficient leaves. The effects of Zn deficiency on the leaf characteristics of pecan trees include not only decreases in leaf chlorophyll and Zn concentrations, but also a reduction in the thickness of the palisade parenchyma, an increase in stomatal density and pore size and the practical disappearance of Zn leaf pools. These characteristics must be taken into account to design strategies to correct Zn deficiency in pecan tree in the field. Copyright © 2012 Society of Chemical Industry.

  1. Genetic causes and gene–nutrient interactions in mammalian zinc deficiencies: acrodermatitis enteropathica and transient neonatal zinc deficiency as examples.

    PubMed

    Kasana, Shakhenabat; Din, Jamila; Maret, Wolfgang

    2015-01-01

    Discovering genetic causes of zinc deficiency has been a remarkable scientific journey. It started with the description of a rare skin disease, its treatment with various agents, the successful therapy with zinc, and the identification of mutations in a zinc transporter causing the disease. The journey continues with defining the molecular and cellular pathways that lead to the symptoms caused by zinc deficiency. Remarkably, at least two zinc transporters from separate protein families are now known to be involved in the genetics of zinc deficiency. One is ZIP4, which is involved in intestinal zinc uptake. Its mutations can cause acrodermatitis enteropathica (AE) with autosomal recessive inheritance. The other one is ZnT2, the transporter responsible for supplying human milk with zinc. Mutations in this transporter cause transient neonatal zinc deficiency (TNZD) with symptoms similar to AE but with autosomal dominant inheritance. The two diseases can be distinguished in affected infants. AE is fatal if zinc is not supplied to the infant after weaning, whereas TNZD is a genetic defect of the mother limiting the supply of zinc in the milk, and therefore the infant usually will obtain enough zinc once weaned. Although these diseases are relatively rare, the full functional consequences of the numerous mutations in ZIP4 and ZnT2 and their interactions with dietary zinc are not known. In particular, it remains unexplored whether some mutations cause milder disease phenotypes or increase the risk for other diseases if dietary zinc requirements are not met or exceeded. Thus, it is not known whether widespread zinc deficiency in human populations is based primarily on a nutritional deficiency or determined by genetic factors as well. This consideration becomes even more significant with regard to mutations in the other 22 human zinc transporters, where associations with a range of diseases, including diabetes, heart disease, and mental illnesses have been observed

  2. Dietary zinc deficiency effects dorso-lateral and ventral prostate of Wistar rats: histological, biochemical and trace element study.

    PubMed

    Joshi, Sangeeta; Nair, Neena; Bedwal, R S

    2014-10-01

    Zinc deficiency has become a global problem affecting the developed and developing countries due to inhibitors in the diet which prevents its absorption or due to a very low concentration of bioavailable zinc in the diet. Being present in high concentration in the prostate and having diverse biological function, we investigated the effects of dietary zinc deficiency for 2 and 4 weeks on dorso-lateral and ventral prostate. Sixty prepubertal rats were divided into three groups: zinc control (ZC), pair fed (PF) and zinc deficient (ZD) and fed on 100 μg/g (zinc control and pair fed groups) and 1 μg/g (zinc deficient) diet. Zinc deficiency was associated with degenerative changes in dorso-lateral and ventral prostate as made evident by karyolysis, karyorhexis, cytoplasmolysis, loss of cellularisation, decreased intraluminar secretion and degeneration of fibromuscular stroma. In response, protein carbonyl, nitric oxide, acid phosphatase, 3β-hydroxysteroid dehydrogenase and 17β-hydroxysteroid dehydrogenase increased, exhibiting variable level of significance. Total protein and total zinc concentration in dorso-lateral and ventral prostate as well as in serum decreased (P < 0.001). Decrease (P < 0.001) was recorded in serum FSH and testosterone after 2 and 4 weeks of zinc deficiency. The changes were more prominent after 4 weeks of synthetic zinc deficient diet. The results indicate that zinc deficiency during prepubertal period affects the prostate structure, total protein concentration, enhanced protein carbonyl concentration, nitric oxide as well as acid phosphatase activities and impaired hydroxysteroid dehydrogenase activities. Evidently these changes could be attributed to dysfunction of dorso-lateral and ventral prostate after dietary zinc deficiency as well as impairment of metabolic and secretory activity, reduced gonadotropin levels by hypothalamus -hypophysial system which is indicative of a critical role of zinc in maintaining the prostate integrity.

  3. [Effects of zinc deficiency in pregnancy on the mother and the newborn infant].

    PubMed

    Favier, A; Favier, M

    1990-01-01

    There seems to be a zinc deficiency during pregnancy in view of the low serum zinc levels, but especially low zinc levels in hair and leucocytes. The need for zinc supplements is still ill-defined but represents at least 5 mg per day which are not covered by the diet and taken from the maternal reserves. Therefore the risk of deficiency is real and its manifestations are numerous. There is a risk of spontaneous abortion, gravidic toxemia, treatment-resistant anemia, abnormally prolonged gestation and difficult delivery for the mother. As for the fetus, with zinc deficiency there is a risk of hypotrophism and malformations with potentialization of the teratogenic effect of alcohol and many medications. Besides, in animals, zinc deficiency during pregnancy results in late effects several months after birth: decrease immunity, learning or memory disorders. In view of all these consequences, administration of supplements is imperative and must be evaluated providing that it does not exceed 50 mg of zinc per day. Besides, it seems preferable to provide balanced multisupplements in minerals and vitamins, since supplement in iron alone results in zinc deficiency.

  4. Chronic zinc deficiency alters chick gut microbiota composition and function

    USDA-ARS?s Scientific Manuscript database

    Zinc (Zn) deficiency is a prevalent micronutrient insufficiency. Although the gut is a vital organ for Zn utilization, and Zn deficiency is associated with impaired intestinal permeability and a global decrease in gastrointestinal health, alterations in the gut microbial ecology of the host under co...

  5. Acute dietary zinc deficiency before conception compromises oocyte epigenetic programming and disrupts embryonic development.

    PubMed

    Tian, X; Diaz, F J

    2013-04-01

    Recent findings show that zinc is an important factor necessary for regulating the meiotic cell cycle and ovulation. However, the role of zinc in promoting oocyte quality and developmental potential is not known. Using an in vivo model of acute dietary zinc deficiency, we show that feeding a zinc deficient diet (ZDD) for 3-5 days before ovulation (preconception) dramatically disrupts oocyte chromatin methylation and preimplantation development. There was a dramatic decrease in histone H3K4 trimethylation and global DNA methylation in zinc deficient oocytes. Moreover, there was a 3-20 fold increase in transcript abundance of repetitive elements (Iap, Line1, Sineb1, Sineb2), but a decrease in Gdf9, Zp3 and Figla mRNA. Only 53% and 8% of mature eggs reached the 2-cell stage after IVF in animals receiving a 3 and 5 days ZDD, respectively, while a 5 day ZDD in vivo reduced the proportion of 2-cells to 49%. In vivo fertilized 2-cell embryos cultured in vitro formed fewer (38%) blastocysts compared to control embryos (74%). Likewise, fewer blastocyst and expanded blastocyst were collected from the reproductive tract of zinc deficient animals on day 3.5 of pregnancy. This could be due to a decrease in Igf2 and H19 mRNA in ZDD blastocyst. Supplementation with a methyl donor (SAM) during IVM restored histone H3K4me3 and doubled the IVF success rate from 17% to 43% in oocytes from zinc deficient animals. Thus, the terminal period of oocyte development is extremely sensitive to perturbation in dietary zinc availability. Copyright © 2013 Elsevier Inc. All rights reserved.

  6. Impaired Calcium Entry into Cells Is Associated with Pathological Signs of Zinc Deficiency12

    PubMed Central

    O’Dell, Boyd L.; Browning, Jimmy D.

    2013-01-01

    Zinc is an essential trace element whose deficiency gives rise to specific pathological signs. These signs occur because an essential metabolic function is impaired as the result of failure to form or maintain a specific metal-ion protein complex. Although zinc is a component of many essential metalloenzymes and transcription factors, few of these have been identified with a specific sign of incipient zinc deficiency. Zinc also functions as a structural component of other essential proteins. Recent research with Swiss murine fibroblasts, 3T3 cells, has shown that zinc deficiency impairs calcium entry into cells, a process essential for many cell functions, including proliferation, maturation, contraction, and immunity. Impairment of calcium entry and the subsequent failure of cell proliferation could explain the growth failure associated with zinc deficiency. Defective calcium uptake is associated with impaired nerve transmission and pathology of the peripheral nervous system, as well as the failure of platelet aggregation and the bleeding tendency of zinc deficiency. There is a strong analogy between the pathology of genetic diseases that result in impaired calcium entry and other signs of zinc deficiency, such as decreased and cyclic food intake, taste abnormalities, abnormal water balance, skin lesions, impaired reproduction, depressed immunity, and teratogenesis. This analogy suggests that failure of calcium entry is involved in these signs of zinc deficiency as well. PMID:23674794

  7. Discovery of Human Zinc Deficiency: Its Impact on Human Health and Disease123

    PubMed Central

    Prasad, Ananda S.

    2013-01-01

    The essentiality of zinc in humans was established in 1963. During the past 50 y, tremendous advances in both clinical and basic sciences of zinc metabolism in humans have been observed. The major factor contributing to zinc deficiency is high phytate-containing cereal protein intake in the developing world, and nearly 2 billion subjects may be zinc deficient. Conditioned deficiency of zinc has been observed in patients with malabsorption syndrome, liver disease, chronic renal disease, sickle cell disease, and other chronic illnesses. Major clinical problems resulting from zinc deficiency in humans include growth retardation; cell-mediated immune dysfunction, and cognitive impairment. In the Middle East, zinc-deficient dwarfs did not live beyond the age of 25 y, and they died because of intercurrent infections. In 1963, we knew of only 3 enzymes that required zinc for their activities, but now we know of >300 enzymes and >1000 transcription factors that are known to require zinc for their activities. Zinc is a second messenger of immune cells, and intracellular free zinc in these cells participate in signaling events. Zinc has been very successfully used as a therapeutic modality for the management of acute diarrhea in children, Wilson’s disease, the common cold and for the prevention of blindness in patients with age-related dry type of macular degeneration and is very effective in decreasing the incidence of infection in the elderly. Zinc not only modulates cell-mediated immunity but is also an antioxidant and anti-inflammatory agent. PMID:23493534

  8. Properties of Zip4 accumulation during zinc deficiency and its usefulness to evaluate zinc status: a study of the effects of zinc deficiency during lactation.

    PubMed

    Hashimoto, Ayako; Nakagawa, Miki; Tsujimura, Natsuki; Miyazaki, Shiho; Kizu, Kumiko; Goto, Tomoko; Komatsu, Yusuke; Matsunaga, Ayu; Shirakawa, Hitoshi; Narita, Hiroshi; Kambe, Taiho; Komai, Michio

    2016-03-01

    Systemic and cellular zinc homeostasis is elaborately controlled by ZIP and ZnT zinc transporters. Therefore, detailed characterization of their expression properties is of importance. Of these transporter proteins, Zip4 functions as the primarily important transporter to control systemic zinc homeostasis because of its indispensable function of zinc absorption in the small intestine. In this study, we closely investigated Zip4 protein accumulation in the rat small intestine in response to zinc status using an anti-Zip4 monoclonal antibody that we generated and contrasted this with the zinc-responsive activity of the membrane-bound alkaline phosphatase (ALP). We found that Zip4 accumulation is more rapid in response to zinc deficiency than previously thought. Accumulation increased in the jejunum as early as 1 day following a zinc-deficient diet. In the small intestine, Zip4 protein expression was higher in the jejunum than in the duodenum and was accompanied by reduction of ALP activity, suggesting that the jejunum can become zinc deficient more easily. Furthermore, by monitoring Zip4 accumulation levels and ALP activity in the duodenum and jejunum, we reasserted that zinc deficiency during lactation may transiently alter plasma glucose levels in the offspring in a sex-specific manner, without affecting homeostatic control of zinc metabolism. This confirms that zinc nutrition during lactation is extremely important for the health of the offspring. These results reveal that rapid Zip4 accumulation provides a significant conceptual advance in understanding the molecular basis of systemic zinc homeostatic control, and that properties of Zip4 protein accumulation are useful to evaluate zinc status closely. Copyright © 2016 the American Physiological Society.

  9. Zinc or copper deficiency-induced impaired inflammatory response to brain trauma may be caused by the concomitant metallothionein changes.

    PubMed

    Penkowa, M; Giralt, M; Thomsen, P S; Carrasco, J; Hidalgo, J

    2001-04-01

    The role of zinc- and copper-deficient diets on the inflammatory response to traumatic brain injury (TBI) has been evaluated in adult rats. As expected, zinc deficiency decreased food intake and body weight gain, and the latter effect was higher than that observed in pair-fed rats. In noninjured brains, zinc deficiency only affected significantly lectin (increasing) and glial fibrillary acidic protein (GFAP) and Cu,Zn-superoxide dismutase (Cu,Zn-SOD) (decreasing) immunoreactivities (irs). In injured brains, a profound gliosis was observed in the area surrounding the lesion, along with severe damage to neurons as indicated by neuron specific enolase (NSE) ir, and the number of cells undergoing apoptosis (measured by TUNEL) was dramatically increased. Zinc deficiency significantly altered brain response to TBI, potentiating the microgliosis and reducing the astrogliosis, while increasing the number of apoptotic cells. Metallothioneins (MTs) are important zinc- and copper-binding proteins in the CNS, which could influence significantly the brain response to TBI because of their putative roles in metal homeostasis and antioxidant defenses. MT-I+II expression was dramatically increased by TBI, and this response was significantly blunted by zinc deficiency. The MT-III isoform was moderately increased by both TBI and zinc deficiency. TBI strongly increased oxidative stress levels, as demonstrated by malondialdehyde (MDA), protein tyrosine nitration (NITT), and nuclear factor kappaB (NF-kappaB) levels irs, all of which were potentiated by zinc deficiency. Further analysis revealed unbalanced expression of prooxidant and antioxidant proteins besides MT, since the levels of inducible nitric oxide synthase (iNOS) and Cu,Zn-SOD were increased and decreased, respectively, by zinc deficiency. All these effects were attributable to zinc deficiency, since pair-fed rats did not differ from normally fed rats. In general, copper deficiency caused a similar pattern of responses

  10. Zinc deficiency-induced iron accumulation, a consequence of alterations in iron regulatory protein-binding activity, iron transporters, and iron storage proteins.

    PubMed

    Niles, Brad J; Clegg, Michael S; Hanna, Lynn A; Chou, Susan S; Momma, Tony Y; Hong, Heeok; Keen, Carl L

    2008-02-22

    One consequence of zinc deficiency is an elevation in cell and tissue iron concentrations. To examine the mechanism(s) underlying this phenomenon, Swiss 3T3 cells were cultured in zinc-deficient (D, 0.5 microM zinc), zinc-supplemented (S, 50 microM zinc), or control (C, 4 microM zinc) media. After 24 h of culture, cells in the D group were characterized by a 50% decrease in intracellular zinc and a 35% increase in intracellular iron relative to cells in the S and C groups. The increase in cellular iron was associated with increased transferrin receptor 1 protein and mRNA levels and increased ferritin light chain expression. The divalent metal transporter 1(+)iron-responsive element isoform mRNA was decreased during zinc deficiency-induced iron accumulation. Examination of zinc-deficient cells revealed increased binding of iron regulatory protein 2 (IRP2) and decreased binding of IRP1 to a consensus iron-responsive element. The increased IRP2-binding activity in zinc-deficient cells coincided with an increased level of IRP2 protein. The accumulation of IRP2 protein was independent of zinc deficiency-induced intracellular nitric oxide production but was attenuated by the addition of the antioxidant N-acetylcysteine or ascorbate to the D medium. These data support the concept that zinc deficiency can result in alterations in iron transporter, storage, and regulatory proteins, which facilitate iron accumulation.

  11. Zinc deficiency enhanced inflammatory response by increasing immune cell activation and inducing IL6 promoter demethylation

    PubMed Central

    Wong, Carmen P.; Rinaldi, Nicole A.; Ho, Emily

    2015-01-01

    Scope Zinc deficiency results in immune dysfunction and promotes systemic inflammation. The objective of this study was to examine the effects of zinc deficiency on cellular immune activation and epigenetic mechanisms that promote inflammation. This work is potentially relevant to the aging population given that age-related immune defects, including chronic inflammation, coincide with declining zinc status. Methods and results An in vitro cell culture system and the aged mouse model were used to characterize immune activation and DNA methylation profiles that may contribute to the enhanced proinflammatory response mediated by zinc deficiency. Zinc deficiency up-regulated cell activation markers ICAM1, MHC class II, and CD86 in THP1 cells, that coincided with increased IL1β and IL6 responses following LPS stimulation. A decreased zinc status in aged mice was similarly associated with increased ICAM1 and IL6 gene expression. Reduced IL6 promoter methylation was observed in zinc deficient THP1 cells, as well as in aged mice and human lymphoblastoid cell lines derived from aged individuals. Conclusion Zinc deficiency induced inflammatory response in part by eliciting aberrant immune cell activation and altered promoter methylation. Our results suggested potential interactions between zinc status, epigenetics, and immune function, and how their dysregulation could contribute to chronic inflammation. PMID:25656040

  12. Zinc in human health: effect of zinc on immune cells.

    PubMed

    Prasad, Ananda S

    2008-01-01

    Although the essentiality of zinc for plants and animals has been known for many decades, the essentiality of zinc for humans was recognized only 40 years ago in the Middle East. The zinc-deficient patients had severe immune dysfunctions, inasmuch as they died of intercurrent infections by the time they were 25 years of age. In our studies in an experimental human model of zinc deficiency, we documented decreased serum testosterone level, oligospermia, severe immune dysfunctions mainly affecting T helper cells, hyperammonemia, neurosensory disorders, and decreased lean body mass. It appears that zinc deficiency is prevalent in the developing world and as many as two billion subjects may be growth retarded due to zinc deficiency. Besides growth retardation and immune dysfunctions, cognitive impairment due to zinc deficiency also has been reported recently. Our studies in the cell culture models showed that the activation of many zinc-dependent enzymes and transcription factors were adversely affected due to zinc deficiency. In HUT-78 (T helper 0 [Th(0)] cell line), we showed that a decrease in gene expression of interleukin-2 (IL-2) and IL-2 receptor alpha(IL-2Ralpha) were due to decreased activation of nuclear factor-kappaB (NF-kappaB) in zinc deficient cells. Decreased NF-kappaB activation in HUT-78 due to zinc deficiency was due to decreased binding of NF-kappaB to DNA, decreased level of NF-kappaB p105 (the precursor of NF-kappaB p50) mRNA, decreased kappaB inhibitory protein (IkappaB) phosphorylation, and decreased Ikappa kappa. These effects of zinc were cell specific. Zinc also is an antioxidant and has anti-inflammatory actions. The therapeutic roles of zinc in acute infantile diarrhea, acrodermatitis enteropathica, prevention of blindness in patients with age-related macular degeneration, and treatment of common cold with zinc have been reported. In HL-60 cells (promyelocytic leukemia cell line), zinc enhances the up-regulation of A20 mRNA, which, via TRAF

  13. Zinc deficiency in the pediatric age group is common but underevaluated.

    PubMed

    Vuralli, Dogus; Tumer, Leyla; Hasanoglu, Alev

    2017-08-01

    Subclinical micronutrient deficiencies have been gradually becoming more important as a public health problem and drawing attention of the health authorities. Today it has been known that detecting and treating people having deficiency symptoms alone is no longer sufficient. It is important to detect and prevent any deficiency before it displays clinical manifestations. Zinc deficiency is one of the most widespread micronutrient deficiencies. In this study, we aimed to evaluate the zinc status and the associated factors in healthy school-age children. The study was carried out in schools in Altindag, the district of Ankara. A total of 1063 healthy children, 585 girls and 478 boys, aged 5-16 years were included in the study. Serum zinc, high-sensitivity C-reactive protein levels and white blood cell count were measured. A serum zinc level <65 μg/dL was considered as subclinical zinc deficiency for children <10 years of age. For children ≥10 years of age the cutoffs for serum zinc concentration were set at 66 μg/dL for females and 70 μg/dL for males. A questionnaire was developed to collect socioeconomic and demographic information of the participants. The prevalence of subclinical zinc deficiency in children attending the study was detected to be 27.8%. This high ratio showed zinc deficiency was an important health problem in the Altindag district of Ankara, Turkey. Evaluating the indicators of zinc deficiency such as serum zinc concentration, dietary zinc intake and stunting prevalence, this study is the most comprehensive epidemiological study performed in children in Turkey. This study reveals the high prevalence of subclinical zinc deficiency and indicates that zinc deficiency is a public health concern for the study population.

  14. Infantile zinc deficiency: Association with autism spectrum disorders

    PubMed Central

    Yasuda, Hiroshi; Yoshida, Kazuya; Yasuda, Yuichi; Tsutsui, Toyoharu

    2011-01-01

    Elucidation of the pathogenesis and effective treatment of autism spectrum disorders is one of the challenges today. In this study, we examine hair zinc concentrations for 1,967 children with autistic disorders (1,553 males and 414 females), and show considerable association with zinc deficiency. Histogram of hair zinc concentration was non-symmetric with tailing in lower range, and 584 subjects were found to have lower zinc concentrations than −2 standard deviation level of its reference range (86.3–193ppm). The incidence rate of zinc deficiency in infant group aged 0–3 year-old was estimated 43.5 % in male and 52.5 % in female. The lowest zinc concentration of 10.7 ppm was detected in a 2-year-old boy, corresponding to about 1/12 of the control mean level. These findings suggest that infantile zinc deficiency may epigenetically contribute to the pathogenesis of autism and nutritional approach may yield a novel hope for its treatment and prevention. PMID:22355646

  15. Expression and localization of taste receptor genes in the vallate papillae of rats: effect of zinc deficiency.

    PubMed

    Ikeda, Atsuo; Sekine, Hiroki; Takao, Kyoichi; Ikeda, Minoru

    2013-09-01

    We found a difference in expression sites between TAS2Rs and ENaC (epithelial sodium channels). The number of TAS2R-positive cells and ENaC-positive cells were decreased in zinc-deficient diet rats. These findings suggest that decreased expression of taste receptor genes may play an important role in the onset of zinc deficiency-associated taste disorder. The present study was aimed at histologically investigating the expression and localization of TAS2Rs and ENaC in the vallate taste buds of rats. Changes in expression of the taste receptor genes in zinc-deficient rats were also investigated. The vallate papillae of five rats fed a normal diet and five rats fed a zinc-deficient diet were used. In situ hybridization was performed to investigate the expression and localization of TAS2Rs and ENaC. TAS2R-positive cells per taste bud were counted, and differences in number between the normal and zinc-deficient diet rats were investigated. In the normal rats, expression of TAS2Rs was observed specifically in the taste bud cells. In contrast, ENaC-positive cells were observed in a part of the taste bud cells and a large number of epithelial cells. Fewer cells were positive for TAS2Rs and ENaC in the zinc-deficient diet rats.

  16. Clinically distinct presentations of copper deficiency myeloneuropathy and cytopenias in a patient using excessive zinc-containing denture adhesive.

    PubMed

    Cathcart, Sahara J; Sofronescu, Alina G

    2017-08-01

    While copper deficiency has long been known to cause cytopenias, copper deficiency myeloneuropathy is a more recently described entity. Here, we present the case of two clinically distinct presentations of acquired copper deficiency syndromes secondary to excessive use of zinc-containing denture adhesive over five years: myeloneuropathy and severe macrocytic anemia and neutropenia. Extensive laboratory testing and histologic evaluation of the liver and bone marrow, were necessary to rule out other disease processes and establish the diagnosis of copper deficiency. The initial presentation consisted of a myelopathy involving the posterior columns. Serum and urine copper were significantly decreased, and serum zinc was elevated. On second presentation (five years later), multiple hematological abnormalities were detected. Serum copper was again decreased, while serum zinc was elevated. Zinc overload is a preventable cause of copper deficiency syndromes. This rare entity presented herein highlights the importance of patient, as well as provider, education. Copyright © 2017 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.

  17. Supplemental levels of iron and calcium interfere with repletion of zinc status in zinc-deficient animals.

    PubMed

    Jayalakshmi, S; Platel, Kalpana

    2016-05-18

    Negative interactions between minerals interfering with each other's absorption are of concern when iron and calcium supplements are given to pregnant women and children. We have previously reported that supplemental levels of iron and calcium inhibit the bioaccessibility of zinc, and compromise zinc status in rats fed diets with high levels of these two minerals. The present study examined the effect of supplemental levels of iron and calcium on the recovery of zinc status during a zinc repletion period in rats rendered zinc-deficient. Iron and calcium, both individually and in combination, significantly interfered with the recovery of zinc status in zinc deficient rats during repletion with normal levels of zinc in the diet. Rats maintained on diets containing supplemental levels of these two minerals had significantly lower body weight, and the concentration of zinc in serum and organs was significantly lower than in zinc-deficient rats not receiving the supplements. Iron and calcium supplementation also significantly inhibited the activity of zinc-containing enzymes in the serum as well as liver. Both iron and calcium independently exerted this negative effect on zinc status, while their combination seemed to have a more prominent effect, especially on the activities of zinc containing enzymes. This investigation is probably the first systematic study on the effect of these two minerals on the zinc status of zinc deficient animals and their recovery during repletion with normal amounts of zinc.

  18. Zinc Deficiency Impacts CO2 Assimilation and Disrupts Copper Homeostasis in Chlamydomonas reinhardtii*

    PubMed Central

    Malasarn, Davin; Kropat, Janette; Hsieh, Scott I.; Finazzi, Giovanni; Casero, David; Loo, Joseph A.; Pellegrini, Matteo; Wollman, Francis-André; Merchant, Sabeeha S.

    2013-01-01

    Zinc is an essential nutrient because of its role in catalysis and in protein stabilization, but excess zinc is deleterious. We distinguished four nutritional zinc states in the alga Chlamydomonas reinhardtii: toxic, replete, deficient, and limited. Growth is inhibited in zinc-limited and zinc-toxic cells relative to zinc-replete cells, whereas zinc deficiency is visually asymptomatic but distinguished by the accumulation of transcripts encoding ZIP family transporters. To identify targets of zinc deficiency and mechanisms of zinc acclimation, we used RNA-seq to probe zinc nutrition-responsive changes in gene expression. We identified genes encoding zinc-handling components, including ZIP family transporters and candidate chaperones. Additionally, we noted an impact on two other regulatory pathways, the carbon-concentrating mechanism (CCM) and the nutritional copper regulon. Targets of transcription factor Ccm1 and various CAH genes are up-regulated in zinc deficiency, probably due to reduced carbonic anhydrase activity, validated by quantitative proteomics and immunoblot analysis of Cah1, Cah3, and Cah4. Chlamydomonas is therefore not able to grow photoautotrophically in zinc-limiting conditions, but supplementation with 1% CO2 restores growth to wild-type rates, suggesting that the inability to maintain CCM is a major consequence of zinc limitation. The Crr1 regulon responds to copper limitation and is turned on in zinc deficiency, and Crr1 is required for growth in zinc-limiting conditions. Zinc-deficient cells are functionally copper-deficient, although they hyperaccumulate copper up to 50-fold over normal levels. We suggest that zinc-deficient cells sequester copper in a biounavailable form, perhaps to prevent mismetallation of critical zinc sites. PMID:23439652

  19. Combinatorial effects of zinc deficiency and arsenic exposure on zebrafish (Danio rerio) development

    PubMed Central

    Truong, Lisa; Barton, Carrie L.; Chase, Tyler T.; Gonnerman, Greg D.; Wong, Carmen P.; Tanguay, Robert L.; Ho, Emily

    2017-01-01

    Zinc deficiency and chronic low level exposures to inorganic arsenic in drinking water are both significant public health concerns that affect millions of people including pregnant women. These two conditions can co-exist in the human population but little is known about their interaction, and in particular, whether zinc deficiency sensitizes individuals to arsenic exposure and toxicity, especially during critical windows of development. To address this, we utilized the Danio rerio (zebrafish) model to test the hypothesis that parental zinc deficiency sensitizes the developing embryo to low-concentration arsenic toxicity, leading to altered developmental outcomes. Adult zebrafish were fed defined zinc deficient and zinc adequate diets and were spawned resulting in zinc adequate and zinc deficient embryos. The embryos were treated with environmentally relevant concentrations of 0, 50, and 500 ppb arsenic. Arsenic exposure significantly reduced the amount of zinc in the developing embryo by ~7%. The combination of zinc deficiency and low-level arsenic exposures did not sensitize the developing embryo to increased developmental malformations or mortality. The combination did cause a 40% decline in physical activity of the embryos, and this decline was significantly greater than what was observed with zinc deficiency or arsenic exposure alone. Significant changes in RNA expression of genes that regulate zinc homeostasis, response to oxidative stress and insulin production (including zip1, znt7, nrf2, ogg1, pax4, and insa) were found in zinc deficient, or zinc deficiency and arsenic exposed embryos. Overall, the data suggests that the combination of zinc deficiency and arsenic exposure has harmful effects on the developing embryo and may increase the risk for developing chronic diseases like diabetes. PMID:28837703

  20. Mild zinc deficiency in male and female rats: early postnatal alterations in renal nitric oxide system and morphology.

    PubMed

    Tomat, Analia Lorena; Veiras, Luciana Cecilia; Aguirre, Sofía; Fasoli, Héctor; Elesgaray, Rosana; Caniffi, Carolina; Costa, María Ángeles; Arranz, Cristina Teresa

    2013-03-01

    Fetal and postnatal zinc deficiencies induce an increase in arterial blood pressure and impair renal function in male adult rats. We therefore hypothesized that these renal alterations are present in early stages of life and that there are sexual differences in the adaptations to this nutritional injury. The aim was to study the effects of moderate zinc deficiency during fetal life and lactation on renal morphology, oxidative stress, apoptosis, and the nitric oxide system in male and female rats at 21 d of life. Female Wistar rats received low (8 ppm) or control (30 ppm) zinc diets from the beginning of pregnancy to weaning. Glomerulus number, morphology, oxidative stress, apoptotic cells, nitric oxide synthase activity, and protein expression were evaluated in the kidneys of offspring at 21 d. Zinc deficiency decreased the nephron number, induced glomerular hypertrophy, increased oxidative damage, and decreased nitric oxide synthase activity in the male and female rat kidneys. Nitric oxide synthase activity was not affected by inhibitors of the neuronal or inducible isoforms, so nitric oxide was mainly generated by the endothelial isoenzyme. Gender differences were observed in glomerular areas and antioxidant enzyme activities. Zinc deficiency during fetal life and lactation induces an early decrease in renal functional units, associated with a decrease in nitric oxide activity and an increase in oxidative stress, which would contribute to increased arterial blood pressure and renal dysfunction in adulthood. The sexual differences observed in this model may explain the dissimilar development of hypertension and renal diseases in adult life. Copyright © 2013 Elsevier Inc. All rights reserved.

  1. Effect of zinc gluconate, sage oil on inflammatory patterns and hyperglycemia in zinc deficient diabetic rats.

    PubMed

    Elseweidy, Mohamed M; Ali, Abdel-Moniem A; Elabidine, Nabila Zein; Mursey, Nada M

    2017-11-01

    The relationship between zinc homeostasis and pancreatic function had been established. In this study we aimed firstly to configure the inflammatory pattern and hyperglycemia in zinc deficient diabetic rats. Secondly to illustrate the effect of two selected agents namely Zinc gluconate and sage oil (Salvia Officinalis, family Lamiaceae). Rats were fed on Zinc deficient diet, deionized water for 28days along with Zinc level check up at intervals to achieve zinc deficient state then rats were rendered diabetic through receiving one dose of alloxan monohydrate (120mg/kg) body weight, classified later into 5 subgroups. Treatment with sage oil (0.042mg/kg IP) and Zinc gluconate orally (150mg/kg) body weight daily for 8 weeks significantly reduced serum glucose, C-reactive protein (CRP), Tumor necrosis factor alpha (TNF- α), interleukins-6 1 β, inflammatory8 (IFN ȣ), pancreatic 1L1-β along with an increase in serum Zinc and pancreatic Zinc transporter 8 (ZNT8). Histopathological results of pancreatic tissues showed a good correlation with the biochemical findings. Both sage oil and zinc gluconate induced an improvement in the glycemic and inflammatory states. This may be of value like the therapeutic agent for diabetes. Copyright © 2017 Elsevier Masson SAS. All rights reserved.

  2. Gender Dependent Evaluation of Autism like Behavior in Mice Exposed to Prenatal Zinc Deficiency

    PubMed Central

    Grabrucker, Stefanie; Boeckers, Tobias M.; Grabrucker, Andreas M.

    2016-01-01

    Zinc deficiency has recently been linked to the etiology of autism spectrum disorders (ASD) as environmental risk factor. With an estimated 17% of the world population being at risk of zinc deficiency, especially zinc deficiency during pregnancy might be a common occurrence, also in industrialized nations. On molecular level, zinc deficiency has been shown to affect a signaling pathway at glutamatergic synapses that has previously been identified through genetic mutations in ASD patients, the Neurexin-Neuroligin-Shank pathway, via altering zinc binding Shank family members. In particular, prenatal zinc deficient but not acute zinc deficient animals have been reported to display autism like behavior in some behavioral tests. However, a full behavioral analysis of a possible autism like behavior has been lacking so far. Here, we performed an extensive behavioral phenotyping of mice born from mothers with mild zinc deficiency during all trimesters of pregnancy. Prenatal zinc deficient animals were investigated as adults and gender differences were assessed. Our results show that prenatal zinc deficient mice display increased anxiety, deficits in nest building and various social interaction paradigm, as well as mild alterations in ultrasonic vocalizations. A gender specific analysis revealed only few sex specific differences. Taken together, given that similar behavioral abnormalities as reported here are frequently observed in ASD mouse models, we conclude that prenatal zinc deficient animals even without specific genetic susceptibility for ASD, already show some features of ASD like behavior. PMID:26973485

  3. Influence of zinc deficiency on cell-membrane fluidity in Jurkat, 3T3 and IMR-32 cells.

    PubMed Central

    Verstraeten, Sandra V; Zago, M Paola; MacKenzie, Gerardo G; Keen, Carl L; Oteiza, Patricia I

    2004-01-01

    We investigated whether zinc deficiency can affect plasma membrane rheology. Three cell lines, human leukaemia T-cells (Jurkat), rat fibroblasts (3T3) and human neuroblastoma cells (IMR-32), were cultured for 48 h in control medium, in zinc-deficient medium (1.5 microM zinc; 1.5 Zn), or in the zinc-deficient medium supplemented with 15 microM zinc (15 Zn). The number of viable cells was lower in the 1.5 Zn group than in the control and 15 Zn groups. The frequency of apoptosis was higher in the 1.5 Zn group than in the control and 15 Zn groups. Membrane fluidity was evaluated using the 6-(9-anthroyloxy)stearic acid and 16-(9-anthroyloxy)palmitic acid probes. Membrane fluidity was higher in 1.5 Zn cells than in the control cells; no differences were observed between control cells and 15 Zn cells. The effect of zinc deficiency on membrane fluidity at the water/lipid interface was associated with a higher phosphatidylserine externalization. The higher membrane fluidity in the hydrophobic region of the bilayer was correlated with a lower content of arachidonic acid. We suggest that the increased fluidity of the membrane secondary to zinc deficiency is in part due to a decrease in arachidonic acid content and the apoptosis-related changes in phosphatidylserine distribution. PMID:14629198

  4. Developmental programming of vascular dysfunction by prenatal and postnatal zinc deficiency in male and female rats.

    PubMed

    Mendes Garrido Abregú, Facundo; Gobetto, María Natalia; Juriol, Lorena Vanesa; Caniffi, Carolina; Elesgaray, Rosana; Tomat, Analía Lorena; Arranz, Cristina

    2018-06-01

    Micronutrient malnutrition during intrauterine and postnatal growth may program cardiovascular diseases in adulthood. We examined whether moderate zinc restriction in male and female rats throughout fetal life, lactation and/or postweaning growth induces alterations that can predispose to the onset of vascular dysfunction in adulthood. Female Wistar rats were fed low- or control zinc diets from pregnancy to offspring weaning. After weaning, offspring were fed either a low- or a control zinc diet until 81 days. We evaluated systolic blood pressure (SBP), thoracic aorta morphology, nitric oxide (NO) system and vascular reactivity in 6- and/or 81-day-old offspring. At day 6, zinc-deficient male and female offspring showed a decrease in aortic NO synthase (NOS) activity accompanied by an increase in oxidative stress. Zinc-deficient 81-day-old male rats exhibited an increase in collagen deposition in tunica media, as well as lower activity of endothelial NOS (eNOS) that could not be reversed with an adequate zinc diet during postweaning life. Zinc deficiency programmed a reduction in eNOS protein expression and higher SBP only in males. Adult zinc-deficient rats of both sexes showed reduced vasodilator response dependent on eNOS activity and impaired aortic vasoconstrictor response to angiotensin-II associated with alterations in intracellular calcium mobilization. Female rats were less sensitive to the effects of zinc deficiency and exhibited higher eNOS activity and/or expression than males, without alterations in SBP or aortic histology. This work strengthens the importance of a balanced intake of micronutrients during perinatal growth to ensure adequate vascular function in adult life. Copyright © 2018 Elsevier Inc. All rights reserved.

  5. Reversing Sports-Related Iron and Zinc Deficiencies.

    ERIC Educational Resources Information Center

    Loosli, Alvin R.

    1993-01-01

    Many active athletes do not consume enough zinc or iron, which are important for oxygen activation, electron transport, and injury healing. Subclinical deficiencies may impair performance and impair healing times. People who exercise regularly need counseling about the importance of adequate dietary intake of iron and zinc. (SM)

  6. [Advances in the research of zinc deficiency and zinc supplementation treatment in patients with severe burns].

    PubMed

    Wang, X X; Zhang, M J; Li, X B

    2018-01-20

    Zinc is one of the essential trace elements in human body, which plays an important role in regulating acute inflammatory response, glucose metabolism, anti-oxidation, immune and gastrointestinal function of patients with severe burns. Patients with severe burns may suffer from zinc deficiency because of insufficient amount of zinc intake from the diet and a large amount of zinc lose through wounds and urine. Zinc deficiency may affect their wound healing process and prognosis. This article reviews the characteristics of zinc metabolism in patients with severe burns through dynamic monitoring the plasma and urinary concentration of zinc. An adequate dosage of zinc supplemented to patients with severe burns by an appropriate method can increase the level of zinc in plasma and skin tissue and improve wound healing, as well as reduce the infection rates and mortality. At the same time, it is important to observe the symptoms and signs of nausea, dizziness, leukopenia and arrhythmia in patients with severe burns after supplementing excessive zinc.

  7. Dietary Zinc Deficiency Exaggerates Ethanol-Induced Liver Injury in Mice: Involvement of Intrahepatic and Extrahepatic Factors

    PubMed Central

    Sun, Xinguo; Song, Zhenyuan; McClain, Craig J.; Zhou, Zhanxiang

    2013-01-01

    Clinical studies have demonstrated that alcoholics have a lower dietary zinc intake compared to health controls. The present study was undertaken to determine the interaction between dietary zinc deficiency and ethanol consumption in the pathogenesis of alcoholic liver disease. C57BL/6N mice were subjected to 8-week feeding of 4 experimental liquid diets: (1) zinc adequate diet, (2) zinc adequate diet plus ethanol, (3) zinc deficient diet, and (4) zinc deficient diet plus ethanol. Ethanol exposure with adequate dietary zinc resulted in liver damage as indicated by elevated plasma alanine aminotransferase level and increased hepatic lipid accumulation and inflammatory cell infiltration. Dietary zinc deficiency alone increased hepatic lipid contents, but did not induce hepatic inflammation. Dietary zinc deficiency showed synergistic effects on ethanol-induced liver damage. Dietary zinc deficiency exaggerated ethanol effects on hepatic genes related to lipid metabolism and inflammatory response. Dietary zinc deficiency worsened ethanol-induced imbalance between hepatic pro-oxidant and antioxidant enzymes and hepatic expression of cell death receptors. Dietary zinc deficiency exaggerated ethanol-induced reduction of plasma leptin, although it did not affect ethanol-induced reduction of white adipose tissue mass. Dietary zinc deficiency also deteriorated ethanol-induced gut permeability increase and plasma endotoxin elevation. These results demonstrate, for the first time, that dietary zinc deficiency is a risk factor in alcoholic liver disease, and multiple intrahepatic and extrahepatic factors may mediate the detrimental effects of zinc deficiency. PMID:24155903

  8. Effect of iron and zinc deficiency on short term memory in children.

    PubMed

    Umamaheswari, K; Bhaskaran, Mythily; Krishnamurthy, Gautham; Vasudevan, Hemamalini; Vasudevan, Kavita

    2011-04-01

    To evaluate the effect of iron and zinc deficiency on short term memory of children in the age group of 6-11 years and to assess the response to supplementation therapy. Interventional study. 100 children in the age group of 6-11 years (subdivided into 6-8 yr and 9-11 yr groups) from an urban corporation school. After collection of demographic data, the study children underwent hematological assessment which included serum iron, serum zinc, and hemoglobin estimation. Based on the results, they were divided into Iron deficient, Zinc deficient, and Combined deficiency groups. Verbal and nonverbal memory assessment was done in all the children. Iron (2mg/kg bodyweight in two divided doses) and zinc (5mg once-a-day) supplementation for a period of 3 months for children in the deficient group. All children with iron and zinc deficiency in both the age groups had memory deficits. Combined deficiency in 9-11 years group showed severe degree of affectation in verbal (P<0.01) and non-verbal memory (P<0.01), and improved after supplementation (P = 0.05 and P< 0.01, respectively). In 6-8 years group, only non-verbal form of memory (P =0.02) was affected, which improved after supplementation. Iron and zinc deficiency is associated with memory deficits in children. There is a marked improvement in memory after supplementation. Post supplementation IQ scores do not show significant improvement in deficient groups in 6-8 year olds.

  9. Zinc deficiency induces vascular pro-inflammatory parameters associated with NF-kappaB and PPAR signaling.

    PubMed

    Shen, Huiyun; Oesterling, Elizabeth; Stromberg, Arnold; Toborek, Michal; MacDonald, Ruth; Hennig, Bernhard

    2008-10-01

    Marginal intake of dietary zinc can be associated with increased risk of cardiovascular diseases. In the current study we hypothesized that vascular dysfunction and associated inflammatory events are activated during a zinc deficient state. We tested this hypothesis using both vascular endothelial cells and mice lacking the functional LDL-receptor gene. Zinc deficiency increased oxidative stress and NF-kappaB DNA binding activity, and induced COX-2 and E-selectin gene expression, as well as monocyte adhesion in cultured endothelial cells. The NF-kappaB inhibitor CAPE significantly reduced the zinc deficiency-induced COX-2 expression, suggesting regulation through NF-kappaB signaling. PPAR can inhibit NF-kappaB signaling, and our previous data have shown that PPAR transactivation activity requires adequate zinc. Zinc deficiency down-regulated PPARalpha expression in cultured endothelial cells. Furthermore, the PPARgamma agonist rosiglitazone was unable to inhibit the adhesion of monocytes to endothelial cells during zinc deficiency, an event which could be reversed by zinc supplementation. Our in vivo data support the importance of PPAR dysregulation during zinc deficiency. For example, rosiglitazone induced inflammatory genes (e.g., MCP-1) only during zinc deficiency, and adequate zinc was required for rosiglitazone to down-regulate pro-inflammatory markers such as iNOS. In addition, rosiglitazone increased IkappaBalpha protein expression only in zinc adequate mice. Finally, plasma data from LDL-R-deficient mice suggest an overall pro-inflammatory environment during zinc deficiency and support the concept that zinc is required for proper anti-inflammatory or protective functions of PPAR. These studies suggest that zinc nutrition can markedly modulate mechanisms of the pathology of inflammatory diseases such as atherosclerosis.

  10. Nutrition intervention strategies to combat zinc deficiency in developing countries.

    PubMed

    Gibson, R S; Ferguson, E L

    1998-06-01

    Widespread zinc deficiency is likely to exist in developing countries where staple diets are predominantly plant based and intakes of animal tissues are low. The severe negative consequences of zinc deficiency on human health in developing countries, however, have only recently been recognized. An integrated approach employing targeted supplementation, fortification and dietary strategies must be used to maximize the likelihood of eliminating zinc deficiency at a national level in developing countries. Supplementation is appropriate only for populations whose zinc status must be improved over a relatively short time period, and when requirements cannot be met from habitual dietary sources. As well, the health system must be capable of providing consistent supply, distribution, delivery and consumption of the zinc supplement to the targeted groups. Uncertainties still exist about the type, frequency, and level of supplemental zinc required for prevention and treatment of zinc deficiency. Salts that are readily absorbed and at levels that will not induce antagonistic nutrient interactions must be used. At a national level, fortification with multiple micronutrients could be a cost effective method for improving micronutrient status, including zinc, provided that a suitable food vehicle which is centrally processed is available. Alternatively, fortification could be targeted for certain high risk groups (e.g. complementary foods for infants). Efforts should be made to develop protected fortificants for zinc, so that potent inhibitors of zinc absorption (e.g. phytate) present either in the food vehicle and/or indigenous meals do not compromise zinc absorption. Fortification does not require any changes in the existing food beliefs and practices for the consumer and, unlike supplementation, does not impose a burden on the health sector. A quality assurance programme is required, however, to ensure the quality of the fortified food product from production to consumption

  11. A question mark on zinc deficiency in 185 million people in Pakistan--possible way out.

    PubMed

    Khalid, Nauman; Ahmed, Anwaar; Bhatti, Muhammad Shahbaz; Randhawa, Muhammad Atif; Ahmad, Asif; Rafaqat, Rabab

    2014-01-01

    This paper reviews research published in recent years concerning the effects of zinc deficiency, its consequences, and possible solutions. Zinc is an essential trace element necessary for over 300 zinc metalloenzymes and required for normal nucleic acid, protein, and membrane metabolism. Zinc deficiency is one of the ten biggest factors contributing to burden of disease in developing countries. Populations in South Asia, South East Asia, and sub-Saharan Africa are at greatest risk of zinc deficiency. Zinc intakes are inadequate for about a third of the population and stunting affects 40% of preschool children. In Pakistan, zinc deficiency is an emerging health problem as about 20.6% children are found in the levels of zinc, below 60 μg/dL. Signs and symptoms caused by zinc deficiency are poor appetite, weight loss, and poor growth in childhood, delayed healing of wounds, taste abnormalities, and mental lethargy. As body stores of zinc decline, these symptoms worsen and are accompanied by diarrhea, recurrent infection, and dermatitis. Daily zinc requirements for an adult are 12-16 mg/day. Iron, calcium and phytates inhibit the absorption of zinc therefore simultaneous administration should not be prescribed. Zinc deficiency and its effects are well known but the ways it can help in treatment of different diseases is yet to be discovered. Improving zinc intakes through dietary improvements is a complex task that requires considerable time and effort. The use of zinc supplements, dietary modification, and fortifying foods with zinc are the best techniques to combat its deficiency.

  12. Short-Term Subclinical Zinc Deficiency in Weaned Piglets Affects Cardiac Redox Metabolism and Zinc Concentration.

    PubMed

    Brugger, Daniel; Windisch, Wilhelm M

    2017-04-01

    Background: Subclinical zinc deficiency (SZD) represents the common zinc malnutrition phenotype. However, its association with oxidative stress is not well understood. The heart muscle may be a promising target for studying early changes in redox metabolism. Objective: We investigated the effects of short-term SZD on cardiac redox metabolism in weaned piglets. Methods: Forty-eight weaned German Large White × Landrace × Piétrain piglets (50% castrated males and 50% females; body weight of 8.5 kg) were fed diets with different zinc concentrations for 8 d. Measurements included cardiac parameters of antioxidative capacity, stress-associated gene expression, and tissue zinc status. Analyses comprised (linear, broken-line) regression models and Pearson correlation coefficients. Results: Glutathione and α-tocopherol concentrations as well as catalase, glutathione reductase, B-cell lymphoma 2-associated X protein, and caspase 9 gene expression plateaued in response to reduction in dietary zinc from 88.0 to 57.6, 36.0, 36.5, 41.3, 55.3, and 33.8 mg/kg, respectively ( P < 0.0001). Further reduction in dietary zinc promoted a linear decrease of glutathione and α-tocopherol (30 and 0.6 nmol/mg dietary Zn, respectively; P < 0.05) and a linear increase of gene expression [0.02, 0.01, 0.003, and 0.02 Log 10 (2 -ΔΔCt )/mg dietary Zn, respectively; P < 0.05)]. Tissue zinc declined linearly with reduction in dietary zinc (0.21 mg tissue Zn/mg dietary Zn; P = 0.004) from 88.0 to 42.7 mg/kg ( P < 0.0001), below which it linearly increased inversely to further reduction in dietary zinc (0.57 mg tissue Zn/mg dietary Zn; P = 0.006). H 2 O 2 -detoxification activity and metallothionein 1A gene expression decreased linearly with reduction in dietary zinc from 88.0 to 28.1 mg/kg [0.02 mU and 0.008 Log 10 (2 -ΔΔCt )/mg dietary Zn, respectively; P < 0.05]. Fas cell-surface death receptor, etoposide-induced 2.4 and cyclin-dependent kinase inhibitor 1A gene expression correlated

  13. Severe dermatitis with loss of epidermal Langerhans cells in human and mouse zinc deficiency

    PubMed Central

    Kawamura, Tatsuyoshi; Ogawa, Youichi; Nakamura, Yuumi; Nakamizo, Satoshi; Ohta, Yoshihiro; Nakano, Hajime; Kabashima, Kenji; Katayama, Ichiro; Koizumi, Schuichi; Kodama, Tatsuhiko; Nakao, Atsuhito; Shimada, Shinji

    2012-01-01

    Zinc deficiency can be an inherited disorder, in which case it is known as acrodermatitis enteropathica (AE), or an acquired disorder caused by low dietary intake of zinc. Even though zinc deficiency diminishes cellular and humoral immunity, patients develop immunostimulating skin inflammation. Here, we have demonstrated that despite diminished allergic contact dermatitis in mice fed a zinc-deficient (ZD) diet, irritant contact dermatitis (ICD) in these mice was more severe and prolonged than that in controls. Further, histological examination of ICD lesions in ZD mice revealed subcorneal vacuolization and epidermal pallor, histological features of AE. Consistent with the fact that ATP release from chemically injured keratinocytes serves as a causative mediator of ICD, we found that the severe ICD response in ZD mice was attenuated by local injection of soluble nucleoside triphosphate diphosphohydrolase. In addition, skin tissue from ZD mice with ICD showed increased levels of ATP, as did cultured wild-type keratinocytes treated with chemical irritants and the zinc-chelating reagent TPEN. Interestingly, numbers of epidermal Langerhans cells (LCs), which play a protective role against ATP-mediated inflammatory signals, were decreased in ZD mice as well as samples from ZD patients. These findings suggest that upon exposure to irritants, aberrant ATP release from keratinocytes and impaired LC-dependent hydrolysis of nucleotides may be important in the pathogenesis of AE. PMID:22214844

  14. The Prevalence and Implication of Zinc Deficiency in Patients With Chronic Liver Disease.

    PubMed

    Katayama, Kazuhiro; Kawaguchi, Takumi; Shiraishi, Koichi; Ito, Toshifumi; Suzuki, Kazutomo; Koreeda, Chizu; Ohtake, Takaaki; Iwasa, Motoh; Tokumoto, Yoshio; Endo, Ryujin; Kawamura, Naohiro; Shiraki, Makoto; Hanai, Tatsunori; Habu, Daiki; Tsuruta, Satoru; Sakai, Hironori; Miwa, Yoshiyuki; Kawada, Norifumi; Kato, Akinobu; Takei, Yoshiyuki; Mine, Tetsuya; Kohgo, Yutaka; Seki, Toshihito; Sata, Michio; Ito, Yuri; Fukui, Keisuke; Nishiguchi, Shuhei; Moriwaki, Hisataka; Suzuki, Kazuyuki

    2018-05-01

    Patients with liver cirrhosis often exhibit zinc deficiency. Although zinc is involved in many bioactivities, many aspects of clinical implications of zinc deficiency in liver cirrhosis remain unclear. We aimed to reveal the prevalence and implications of zinc deficiency in liver cirrhosis by assessing associations with parameters such as clinical symptoms and laboratory data. In 235 cirrhosis patients enrolled at multiple medical institutions in 2009, we assessed how blood zinc levels were associated with their clinical symptoms, patients characteristics, and liver function test results. Blood zinc levels were most strongly correlated with blood albumin levels among the study parameters (r = 0.587, P < 0.0001). When blood albumin levels were ≤ 3.5 g/dL, blood zinc levels were < 70 μg/dL in 88% of patients. Additionally, significant correlations were observed with age (r = -0.253, P = 0.0014), aspartate aminotransferase levels (r = -0.254, P = 0.0020), total bilirubin levels (r = -0.222, P = 0.0053), prothrombin time (r = -0.255, P = 0.0029), branched-chain amino acid to tyrosine ratio (r = 0.357, P < 0.0001), Child-Pugh score (r = 0.469, P < 0.0001), ammonia levels (r = -0.246, P = 0.0028), and total cholesterol levels (r = 0.314, P < 0.0001). Blood zinc levels were significantly lower in patients with edema/ascites (P < 0.0001), those with hepatic encephalopathy (P = 0.0215), those receiving oral diuretics (P = 0.0045), and those receiving oral branched-chain amino acids (P < 0.0001) than in those without these conditions. Zinc deficiency is prevalent in cirrhosis patients, whereas nitrogen metabolic disorders, particularly hypoalbuminemia, can be an indicator of zinc deficiency. Thus, cirrhosis patients exhibiting a nitrogen metabolic disorder should be examined for the presence of zinc deficiency.

  15. Zinc deficiency with reduced mastication impairs spatial memory in young adult mice.

    PubMed

    Kida, Kumiko; Tsuji, Tadataka; Tanaka, Susumu; Kogo, Mikihiko

    2015-12-01

    Sufficient oral microelements such as zinc and fully chewing of foods are required to maintain cognitive function despite aging. No knowledge exists about the combination of factors such as zinc deficiency and reduced mastication on learning and memory. Here we show that tooth extraction only in 8-week-old mice did not change the density of glial fibrillary acidic protein-labeled astrocytes in the hippocampus or spatial memory parameters. However, tooth extraction followed by zinc deprivation strongly impaired spatial memory and led to an increase in astrocytic density in the hippocampal CA1 region. The impaired spatial performance in the zinc-deficient only (ZD) mice also coincided well with the increase in the astrocytic density in the hippocampal CA1 region. After switching both zinc-deficient groups to a normal diet with sufficient zinc, spatial memory recovered, and more time was spent in the quadrant with the goal in the probe test in the mice with tooth extraction followed by zinc deprivation (EZD) compared to the ZD mice. Interestingly, we found no differences in astrocytic density in the CA1 region among all groups at 22 weeks of age. Furthermore, the escape latency in a visible probe test at all times was longer in zinc-deficient groups than the others and demonstrated a negative correlation with body weight. No significant differences in escape latency were observed in the visible probe test among the ZD, EZD, and normal-fed control at 4 weeks (CT4w) groups in which body weight was standardized to that of the EZD group, or in the daily reduction in latency between the normal-fed control and CT4w groups. Our data showed that zinc-deficient feeding during a young age impairs spatial memory performance and leads to an increase in astrocytic density in the hippocampal CA1 region and that zinc-sufficient feeding is followed by recovery of the impaired spatial memory along with changes in astrocytic density. The combination of the two factors, zinc deficiency

  16. Zinc Deficiency Is associated With Depressive Symptoms-Results From the Berlin Aging Study II.

    PubMed

    Jung, Alissa; Spira, Dominik; Steinhagen-Thiessen, Elisabeth; Demuth, Ilja; Norman, Kristina

    2017-08-01

    Zinc plays an important role for behavioral and mental function, maintaining the correct functions of intracellular signal transduction, cellular and trans-membrane transport, protein synthesis, and antioxidant system. We investigated both dietary zinc intake and plasma zinc levels and the correlation with depressive symptoms in a large sample of community-dwelling old. One thousand five hundred fourteen older people (aged 60-84 years, 772 women) from the Berlin Aging Study II were included. Zinc intake was assessed by the EPIC Food Frequency Questionnaire. Plasma zinc levels were assessed with atomic-absorption spectrophotometry. Depressive symptoms were assessed with the "Center for Epidemiological Studies Depression Scale" and the "Geriatric Depression Scale." Zinc deficiency in blood plasma was found in 18.7% of participants, and depressive symptoms in 15.7%. Participants with depressive symptoms had lower energy-adjusted zinc intake (median 11.1 vs 11.6 µmol/L; p = .048) and lower plasma zinc levels (median 12.2 vs12.3 mg/dL; p = .037). Even after adjustment for known predictors of depression, plasma zinc deficiency remained significantly associated with depressive symptoms (odds ratio: 1.490, 95% confidence interval: 1.027-2.164; p = .036). In the multiple logistic regression model stratified by sex, we found that plasma zinc deficiency was strongly associated with a higher risk for depressive symptoms in women (odds ratio: 1.739, 95% confidence interval: 1.068-2.833; p = .026). Plasma zinc deficiency was common in our old study population. An increase in dietary zinc and higher plasma zinc levels may reduce the risk of depressive symptoms. A screening for reduced dietary zinc intake or plasma zinc deficiency might be beneficial in older people at risk of depressive symptoms. © The Author 2016. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

  17. Zinc deficiency promotes cystitis-related bladder pain by enhancing function and expression of Cav3.2 in mice.

    PubMed

    Ozaki, Tomoka; Matsuoka, Junki; Tsubota, Maho; Tomita, Shiori; Sekiguchi, Fumiko; Minami, Takeshi; Kawabata, Atsufumi

    2018-01-15

    Ca v 3.2 T-type Ca 2+ channel activity is suppressed by zinc that binds to the extracellular histidine-191 of Ca v 3.2, and enhanced by H 2 S that interacts with zinc. Ca v 3.2 in nociceptors is upregulated in an activity-dependent manner. The enhanced Ca v 3.2 activity by H 2 S formed by the upregulated cystathionine-γ-lyase (CSE) is involved in the cyclophosphamide (CPA)-induced cystitis-related bladder pain in mice. We thus asked if zinc deficiency affects the cystitis-related bladder pain in mice by altering Ca v 3.2 function and/or expression. Dietary zinc deficiency for 2 weeks greatly decreased zinc concentrations in the plasma but not bladder tissue, and enhanced the bladder pain/referred hyperalgesia (BP/RH) following CPA at 200mg/kg, a subeffective dose, but not 400mg/kg, a maximal dose, an effect abolished by pharmacological blockade or gene silencing of Ca v 3.2. Acute zinc deficiency caused by systemic N,N,N',N'-tetrakis-(2-pyridylmethyl)-ethylendiamine (TPEN), a zinc chelator, mimicked the dietary zinc deficiency-induced Ca v 3.2-dependent promotion of BP/RH following CPA at 200mg/kg. CPA at 400mg/kg alone or TPEN plus CPA at 200mg/kg caused Ca v 3.2 overexpression accompanied by upregulation of Egr-1 and USP5, known to promote transcriptional expression and reduce proteasomal degradation of Ca v 3.2, respectively, in the dorsal root ganglia (DRG). The CSE inhibitor, β-cyano-l-alanine, prevented the BP/RH and upregulation of Ca v 3.2, Egr-1 and USP5 in DRG following TPEN plus CPA at 200mg/kg. Together, zinc deficiency promotes bladder pain accompanying CPA-induced cystitis by enhancing function and expression of Ca v 3.2 in nociceptors, suggesting a novel therapeutic avenue for treatment of bladder pain, such as zinc supplementation. Copyright © 2017 Elsevier B.V. All rights reserved.

  18. Deficient maternal zinc intake-but not folate-is associated with lower fetal heart rate variability.

    PubMed

    Spann, Marisa N; Smerling, Jennifer; Gustafsson, Hanna; Foss, Sophie; Altemus, Margaret; Monk, Catherine

    2015-03-01

    Few studies of maternal prenatal diet and child development examine micronutrient status in relation to fetal assessment. Twenty-four-hour dietary recall of zinc and folate and 20min of fetal heart rate were collected from 3rd trimester pregnant adolescents. Deficient zinc was associated with less fetal heart rate variability. Deficient folate had no associations with HRV. Neither deficient zinc nor deficient folate was related to fetal heart rate. These findings, from naturalistic observation, are consistent with emerging data on prenatal zinc supplementation using a randomized control design. Taken together, the findings suggest that maternal prenatal zinc intake is an important and novel factor for understanding child ANS development. Copyright © 2015. Published by Elsevier Ireland Ltd.

  19. Effects of Zinc Supplementation on DNA Damage in Rats with Experimental Kidney Deficiency.

    PubMed

    Yegin, Sevim Çiftçi; Dede, Semiha; Mis, Leyla; Yur, Fatmagül

    2017-04-01

    This study was carried out to determine the effect of zinc on oxidative DNA damage in rats with experimental acute and chronic kidney deficiency. Six groups of five Wistar-Albino rats each were assigned as controls (C), acute kidney deficiency (AKD), zinc-supplemented (+Zn), acute kidney deficiency, zinc-supplemented (AKD + Zn), chronic kidney deficiency (CKD) and zinc-supplemented chronic kidney deficiency (CKD + Zn). The levels of 8-Oxo-2'-deoxyguanosine (8-OHdG) were determined, being the lowest in the CKD group (p < 0.05), higher in the C group than those of rats with CKD but lower than that of all the other groups (p < 0.05). There were no significant differences between the controls and the CKD + Zn group, or between the AKD and the +Zn groups. Among all groups, the highest 8-OHdG level was found in the AKD + Zn group (p < 0.05). DNA damage was greater in acute renal failure than in rats with chronic renal failure. The DNA damage in the zinc group was significantly higher than in the controls.

  20. Zinc deficiency alters soybean susceptibility to pathogens and pests

    USDA-ARS?s Scientific Manuscript database

    Inadequate plant nutrition and biotic stress are key threats to current and future crop yields. Zinc deficiency and toxicity in major crop plants have been documented, but there is limited information on how pathogen and pest damage may be affected by differing plant zinc levels. In our study, we us...

  1. Leptin, NPY, Melatonin and Zinc Levels in Experimental Hypothyroidism and Hyperthyroidism: The Relation to Zinc.

    PubMed

    Baltaci, Abdulkerim Kasım; Mogulkoc, Rasim

    2017-06-01

    Since zinc mediates the effects of many hormones or is found in the structure of numerous hormone receptors, zinc deficiency leads to various functional impairments in the hormone balance. And also thyroid hormones have important activity on metabolism and feeding. NPY and leptin are affective on food intake and regulation of appetite. The present study is conducted to determine how zinc supplementation and deficiency affect thyroid hormones (free and total T3 and T4), melatonin, leptin, and NPY levels in thyroid dysfunction in rats. The experiment groups in the study were formed as follows: Control (C); Hypothyroidism (PTU); Hypothyroidism+Zinc (PTU+Zn); Hypothyroidism+Zinc deficient; Hyperthyroidism (H); Hyperthyroidism+Zinc (H+Zn); and Hyperthyroidism+Zinc deficient. Thyroid hormone parameters (FT 3 , FT 4 , TT 3 , and TT 4 ) were found to be reduced in hypothyroidism groups and elevated in the hyperthyroidism groups. Melatonin values increased in hyperthyroidism and decreased in hypothyroidism. Leptin and NPY levels both increased in hypo- and hyperthyroidism. Zinc levels, on the other hand, decreased in hypothyroidism and increased in hyperthyroidism. Zinc supplementation, particularly when thyroid function is impaired, has been demonstrated to markedly prevent these changes.

  2. Prevention of upper aerodigestive tract cancer in zinc-deficient rodents: Inefficacy of genetic or pharmacological disruption of COX-2

    PubMed Central

    Fong, Louise Y.Y.; Jiang, Yubao; Riley, Maurisa; Liu, Xianglan; Smalley, Karl J.; Guttridge, Denis C.; Farber, John L.

    2009-01-01

    Zinc deficiency in humans is associated with an increased risk of upper aerodigestive tract (UADT) cancer. In rodents, zinc deficiency predisposes to carcinogenesis by causing proliferation and alterations in gene expression. We examined whether in zinc-deficient rodents, targeted disruption of the cyclooxygenase (COX)-2 pathway by the COX-2 selective inhibitor celecoxib or by genetic deletion prevent UADT carcinogenesis. Tongue cancer prevention studies were conducted in zinc-deficient rats previously exposed to a tongue carcinogen by celecoxib treatment with or without zinc replenishment, or by zinc replenishment alone. The ability of genetic COX-2 deletion to protect against chemically-induced for-estomach tumorigenesis was examined in mice on zinc-deficient versus zinc-sufficient diet. The expression of 3 predictive bio-markers COX-2, nuclear factor (NF)-κ B p65 and leukotriene A4 hydrolase (LTA4H) was examined by immunohistochemistry. In zinc-deficient rats, celecoxib without zinc replenishment reduced lingual tumor multiplicity but not progression to malignancy. Celecoxib with zinc replenishment or zinc replenishment alone significantly lowered lingual squamous cell carcinoma incidence, as well as tumor multiplicity. Celecoxib alone reduced overexpression of the 3 biomarkers in tumors slightly, compared with intervention with zinc replenishment. Instead of being protected, zinc-deficient COX-2 null mice developed significantly greater tumor multiplicity and forestomach carcinoma incidence than wild-type controls. Additionally, zinc-deficient COX-2−/− forestomachs displayed strong LTA4H immunostaining, indicating activation of an alter-native pathway under zinc deficiency when the COX-2 pathway is blocked. Thus, targeting only the COX-2 pathway in zinc-deficient animals did not prevent UADT carcinogenesis. Our data suggest zinc supplementation should be more thoroughly explored in human prevention clinical trials for UADT cancer. PMID:17985342

  3. Arsenite binding-induced zinc loss from PARP-1 is equivalent to zinc deficiency in reducing PARP-1 activity, leading to inhibition of DNA repair

    SciTech Connect

    Sun, Xi; Zhou, Xixi; Du, Libo

    2014-01-15

    Inhibition of DNA repair is a recognized mechanism for arsenic enhancement of ultraviolet radiation-induced DNA damage and carcinogenesis. Poly(ADP-ribose) polymerase-1 (PARP-1), a zinc finger DNA repair protein, has been identified as a sensitive molecular target for arsenic. The zinc finger domains of PARP-1 protein function as a critical structure in DNA recognition and binding. Since cellular poly(ADP-ribosyl)ation capacity has been positively correlated with zinc status in cells, we hypothesize that arsenite binding-induced zinc loss from PARP-1 is equivalent to zinc deficiency in reducing PARP-1 activity, leading to inhibition of DNA repair. To test this hypothesis, we compared the effects ofmore » arsenite exposure with zinc deficiency, created by using the membrane-permeable zinc chelator TPEN, on 8-OHdG formation, PARP-1 activity and zinc binding to PARP-1 in HaCat cells. Our results show that arsenite exposure and zinc deficiency had similar effects on PARP-1 protein, whereas supplemental zinc reversed these effects. To investigate the molecular mechanism of zinc loss induced by arsenite, ICP-AES, near UV spectroscopy, fluorescence, and circular dichroism spectroscopy were utilized to examine arsenite binding and occupation of a peptide representing the first zinc finger of PARP-1. We found that arsenite binding as well as zinc loss altered the conformation of zinc finger structure which functionally leads to PARP-1 inhibition. These findings suggest that arsenite binding to PARP-1 protein created similar adverse biological effects as zinc deficiency, which establishes the molecular mechanism for zinc supplementation as a potentially effective treatment to reverse the detrimental outcomes of arsenic exposure. - Highlights: • Arsenite binding is equivalent to zinc deficiency in reducing PARP-1 function. • Zinc reverses arsenic inhibition of PARP-1 activity and enhancement of DNA damage. • Arsenite binding and zinc loss alter the conformation of

  4. Zinc: physiology, deficiency, and parenteral nutrition.

    PubMed

    Livingstone, Callum

    2015-06-01

    The essential trace element zinc (Zn) has a large number of physiologic roles, in particular being required for growth and functioning of the immune system. Adaptive mechanisms enable the body to maintain normal total body Zn status over a wide range of intakes, but deficiency can occur because of reduced absorption or increased gastrointestinal losses. Deficiency impairs physiologic processes, leading to clinical consequences that include failure to thrive, skin rash, and impaired wound healing. Mild deficiency that is not clinically overt may still cause nonspecific consequences, such as susceptibility to infection and poor growth. The plasma Zn concentration has poor sensitivity and specificity as a test of deficiency. Consequently, diagnosis of deficiency requires a combination of clinical assessment and biochemical tests. Patients receiving parenteral nutrition (PN) are susceptible to Zn deficiency and its consequences. Nutrition support teams should have a strategy for assessing Zn status and optimizing this by appropriate supplementation. Nutrition guidelines recommend generous Zn provision from the start of PN. This review covers the physiology of Zn, the consequences of its deficiency, and the assessment of its status, before discussing its role in PN. © 2015 American Society for Parenteral and Enteral Nutrition.

  5. The effect of zinc deficiency on salt taste acuity, preference, and dietary sodium intake in hemodialysis patients.

    PubMed

    Kim, So Mi; Kim, Miyeon; Lee, Eun Kyoung; Kim, Soon Bae; Chang, Jai Won; Kim, Hyun Woo

    2016-07-01

    Introduction High sodium intake is the main cause of fluid overload in hemodialysis (HD) patients, leading to increased cardiovascular mortality. High sodium intake is known to be associated with low salt taste acuity and/or high preference. As the zinc status could influence taste acuity, we analyzed the effect of zinc deficiency on salt taste acuity, preference, and dietary sodium intake in HD patients. Methods A total of 77 HD patients was enrolled in this cross-sectional study. Zinc deficiency was defined as serum zinc level with below 70 µg/mL. The patients were divided into two groups based on serum zinc level. Salt taste acuity and preference were determined by a sensory test using varying concentrations of NaCl solution, and dietary sodium intake was estimated using 3-day dietary recall surveys. Findings The mean salt recognition threshold and salt taste preference were significantly higher in the zinc deficient group than in the non-zinc deficient group. And there was significant positive correlation between salt taste preference and dietary sodium intake in zinc deficient group (r = 0.43, P = 0.002). Although, the dietary sodium intake showed a high tendency with no significance (P = 0.052), interdialytic weight gain was significantly higher in the zinc deficient group than in the non-zinc deficient group (2.68 ± 1.02 kg vs. 3.18 ± 1.02 kg; P = 0.047). Discussion Zinc deficiency may be related to low salt taste acuity and high salt preference, leading to high dietary sodium intake in HD patients. © 2016 International Society for Hemodialysis.

  6. Activation of the Yeast UBI4 Polyubiquitin Gene by Zap1 Transcription Factor via an Intragenic Promoter Is Critical for Zinc-deficient Growth*

    PubMed Central

    MacDiarmid, Colin W.; Taggart, Janet; Jeong, Jeeyon; Kerdsomboon, Kittikhun; Eide, David J.

    2016-01-01

    Stability of many proteins requires zinc. Zinc deficiency disrupts their folding, and the ubiquitin-proteasome system may help manage this stress. In Saccharomyces cerevisiae, UBI4 encodes five tandem ubiquitin monomers and is essential for growth in zinc-deficient conditions. Although UBI4 is only one of four ubiquitin-encoding genes in the genome, a dramatic decrease in ubiquitin was observed in zinc-deficient ubi4Δ cells. The three other ubiquitin genes were strongly repressed under these conditions, contributing to the decline in ubiquitin. In a screen for ubi4Δ suppressors, a hypomorphic allele of the RPT2 proteasome regulatory subunit gene (rpt2E301K) suppressed the ubi4Δ growth defect. The rpt2E301K mutation also increased ubiquitin accumulation in zinc-deficient cells, and by using a ubiquitin-independent proteasome substrate we found that proteasome activity was reduced. These results suggested that increased ubiquitin supply in suppressed ubi4Δ cells was a consequence of more efficient ubiquitin release and recycling during proteasome degradation. Degradation of a ubiquitin-dependent substrate was restored by the rpt2E301K mutation, indicating that ubiquitination is rate-limiting in this process. The UBI4 gene was induced ∼5-fold in low zinc and is regulated by the zinc-responsive Zap1 transcription factor. Surprisingly, Zap1 controls UBI4 by inducing transcription from an intragenic promoter, and the resulting truncated mRNA encodes only two of the five ubiquitin repeats. Expression of a short transcript alone complemented the ubi4Δ mutation, indicating that it is efficiently translated. Loss of Zap1-dependent UBI4 expression caused a growth defect in zinc-deficient conditions. Thus, the intragenic UBI4 promoter is critical to preventing ubiquitin deficiency in zinc-deficient cells. PMID:27432887

  7. History of Zinc in Agriculture12

    PubMed Central

    Nielsen, Forrest H.

    2012-01-01

    Zinc was established as essential for green plants in 1926 and for mammals in 1934. However, >20 y would pass before the first descriptions of zinc deficiencies in farm animals appeared. In 1955, it was reported that zinc supplementation would cure parakeratosis in swine. In 1958, it was reported that zinc deficiency induced poor growth, leg abnormalities, poor feathering, and parakeratosis in chicks. In the 1960s, zinc supplementation was found to alleviate parakeratosis in grazing cattle and sheep. Within 35 y, it was established that nearly one half of the soils in the world may be zinc deficient, causing decreased plant zinc content and production that can be prevented by zinc fertilization. In many of these areas, zinc deficiency is prevented in grazing livestock by zinc fertilization of pastures or by providing salt licks. For livestock under more defined conditions, such as poultry, swine, and dairy and finishing cattle, feeds are easily supplemented with zinc salts to prevent deficiency. Today, the causes and consequences of zinc deficiency and methods and effects of overcoming the deficiency are well established for agriculture. The history of zinc in agriculture is an outstanding demonstration of the translation of research into practical application. PMID:23153732

  8. Promoting effect of foliage sprayed zinc sulfate on accumulation of sugar and phenolics in berries of Vitis vinifera cv. Merlot growing on zinc deficient soil.

    PubMed

    Song, Chang-Zheng; Liu, Mei-Ying; Meng, Jiang-Fei; Chi, Ming; Xi, Zhu-Mei; Zhang, Zhen-Wen

    2015-02-02

    The effect of foliage sprayed zinc sulfate on berry development of Vitis vinifera cv. Merlot growing on arid zone Zn-deficient soils was investigated over two consecutive seasons, 2013 and 2014. Initial zinc concentration in soil and vines, photosynthesis at three berry developmental stages, berry weight, content of total soluble solids, titratable acidity, phenolics and expression of phenolics biosynthetic pathway genes throughout the stages were measured. Foliage sprayed zinc sulfate showed promoting effects on photosynthesis and berry development of vines and the promotion mainly occurred from veraison to maturation. Zn treatments enhanced the accumulation of total soluble solids, total phenols, flavonoids, flavanols, tannins and anthocyanins in berry skin, decreasing the concentration of titratable acidity. Furthermore, foliage sprayed zinc sulfate could significantly influence the expression of phenolics biosynthetic pathway genes throughout berry development, and the results of expression analysis supported the promotion of Zn treatments on phenolics accumulation. This research is the first comprehensive and detailed study about the effect of foliage sprayed Zn fertilizer on grape berry development, phenolics accumulation and gene expression in berry skin, providing a basis for improving the quality of grape and wine in Zn-deficient areas.

  9. Moderate zinc deficiency increases cell death after brain injury in the rat.

    PubMed

    Yeiser, E Carden; Vanlandingham, Jacob W; Levenson, Cathy W

    2002-10-01

    Zinc supplementation has been used clinically to reduce Zn losses and protein turnover in patients suffering from traumatic brain injury. Despite the known role of zinc in cell survival and integrity, the influence of zinc status on central nervous system wound healing in the weeks and months after brain injury has not been addressed. In this investigation, we examined cell death after unilateral cortical stab wounds in adult rats (n = 5 per group) that were provided diets containing adequate zinc (30 mg Zn/kg diet), supplemental zinc (180 mg/kg), or moderately deficient zinc (5 mg/kg). Four weeks following the brain injury there was a 1.82-2.65-fold increase in terminal deoxynucleotidyl transferase-mediated biotinylated dUTP nick-end labeling (TUNEL)-positive cells with DNA fragmentation at the site of injury in animals receiving a moderately zinc deficient diet compared to animals receiving a zinc-adequate or supplemented diet (p0.05). Examination of the nuclear morphology of these cells suggested the presence of both apoptosis and necrosis. Immunohistochemistry showed that the TUNEL-positive cells expressed both ED-1 and OX-42, identifying them as microglia/macrophages. Thus it appears that adequate zinc status may be necessary to minimize the amount of neuroimmune cell death after brain injury.

  10. Zinc decreases C-reactive protein, lipid peroxidation, and inflammatory cytokines in elderly subjects: a potential implication of zinc as an atheroprotective agent123

    PubMed Central

    Bao, Bin; Prasad, Ananda S; Beck, Frances WJ; Fitzgerald, James T; Snell, Diane; Bao, Ginny W; Singh, Tapinder; Cardozo, Lavoisier J

    2010-01-01

    Background: Chronic inflammation and oxidative stress are common risk factors for atherosclerosis. Zinc is an essential micronutrient that can function as an antiinflammatory and antioxidative agent, and as such, it may have atheroprotective properties. Objective: We hypothesized that zinc down-regulates the production of atherosclerosis-related cytokines/molecules in humans. Design: To examine these effects, we conducted a randomized, double-blinded, placebo trial of zinc supplementation in elderly subjects. We recruited 40 healthy elderly subjects (aged 56–83 y) and randomly assigned them to 2 groups. One group was given an oral dose of 45 mg zinc/d as a gluconate for 6 mo. The other group was given a placebo. Cell culture models were conducted to study the mechanism of zinc as an atheroprotective agent. Results: After 6 mo of supplementation, the intake of zinc, compared with intake of placebo, increased the concentrations of plasma zinc and decreased the concentrations of plasma high-sensitivity C-reactive protein (hsCRP), interleukin (IL)-6, macrophage chemoattractant protein 1 (MCP-1), vascular cell adhesion molecule 1 (VCAM-1), secretory phospholipase A2, and malondialdehyde and hydroxyalkenals (MDA+HAE) in elderly subjects. Regression analysis showed that changes in concentrations of plasma zinc were inversely associated with changes in concentrations of plasma hsCRP, MCP-1, VCAM-1, and MDA+HAE after 6 mo of supplementation. In cell culture studies, we showed that zinc decreased the generation of tumor necrosis factor-α, IL-1β, VCAM-1, and MDA+HAE and the activation of nuclear transcription factor κB and increased antiinflammatory proteins A20 and peroxisome proliferator–activated receptor-α in human monocytic leukemia THP-1 cells and human aortic endothelial cells compared with zinc-deficient cells. Conclusion: These findings suggest that zinc may have a protective effect in atherosclerosis because of its antiinflammatory and antioxidant functions

  11. Risk of zinc, iodine and other micronutrient deficiencies among school children in North East Thailand.

    PubMed

    Thurlow, R A; Winichagoon, P; Pongcharoen, T; Gowachirapant, S; Boonpraderm, A; Manger, M S; Bailey, K B; Wasantwisut, E; Gibson, R S

    2006-05-01

    Micronutrient deficiencies during childhood can contribute to impairments in growth, immune competence, and mental and physical development, and the coexistence of several such deficiencies can adversely affect the efficacy of single micronutrient interventions. To assess the prevalence of zinc and iodine deficiency and their interrelationships with vitamin A deficiency and anemia and associations with socio-economic status, hemoglobin type, and anthropometry in a cross-sectional study. A total of 10 primary schools in North East Thailand. Non-fasting venipuncture blood samples and casual urine samples were collected from 567 children aged 6-13 years. Anthropometric measures and serum zinc, albumin, C-reactive protein and urinary iodine, are reported here and integrated with published data on vitamin A, anemia, and socio-economic status. Of the children, 57% had low serum zinc and 83% had urinary iodine levels below the 100 microg/l cutoff. Suboptimal serum zinc and urinary iodine concentrations may result from low intakes of zinc and iodized salt. Significant risk factors for low serum zinc were serum retinol <1.05 micromol/l and being male. Those for urinary iodine <100 microg/l were height-for-age score>median and being female. For serum retinol <1.05 micromol/l, risk factors were low hemoglobin, low serum zinc, and <9 years, and for low hemoglobin indicative of anemia risk factors were <9 years, AE hemoglobinopathy, and serum retinol <1.05 micromol/l. Of the children, 60% were at risk of two or more coexisting micronutrient deficiencies, most commonly suboptimal urinary iodine and low serum zinc. The findings emphasize the need for multimicronutrient interventions in North East Thailand.

  12. Lipopolysaccharide-induced overproduction of nitric oxide and overexpression of iNOS and interleukin-1β proteins in zinc-deficient rats.

    PubMed

    Miyazaki, Takashi; Takenaka, Tsuneo; Inoue, Tsutomu; Sato, Makiko; Miyajima, Yuka; Nodera, Makoto; Hanyu, Mayuko; Ohno, Yoichi; Shibazaki, Satomi; Suzuki, Hiromichi

    2012-03-01

    Zinc deficiency leads to decreased cellular immune responses. The overproduction of nitrogen species derived from inducible nitric oxide synthase (iNOS), its enzyme, and interleukine-1 beta (IL-1β), and inflammatory cytokine have been implicated in immune responses. The goal of this study was to investigate the effects of lipopolysaccharide (LPS)-induced changes in NO metabolites, iNOS, and IL-1β protein expression in the lungs of zinc-deficient rats. Male Sprague-Dawley rats (body weight, 100 g) were divided into two groups and were fed either a zinc-deficient diet (ZnD) or a zinc-containing diet (Cont). After 4 weeks on these diets, rats received a 10-mg/kg dose of LPS injected via the tail vein and were then maintained for an additional 72 h. To determine total NO concentrations in the blood, serum zinc concentration, iNOS protein expression, IL-1β, and iNOS immunohistochemistry, blood and lung samples were obtained at pre-LPS injection, 5, 24, and 72 h after injection. Total NO levels were significantly increased at 5, at 24, and at 72 h after LPS injection compared with pre-LPS injection level in ZnD group; significant changes in total NO levels was elevated at 5 h from at pre-LPS level but not significant changes from basal level at 24 and 72 h in the control group. Based on western blot analyses and immunohistochemistry, clear bands indicating iNOS and IL-1β protein expression and iNOS antibody-stained inflammatory cells were detected at 5 and 24 h in the ZnD group and 5 h in the Cont group, not observed at 24 and 72 h in the control group. These results suggest that zinc deficiency induces overexpression of iNOS and IL-1β proteins from inflammatory cells around the alveolar blood vessels, resulting in overproduction of total NO and persisted inflammatory response in the zinc-deficient rat lung. Taken together, overexpression of LPS-induced iNOS, overproduction of iNOS-derived NO, and overexpression of IL-1β may induce nitrosative and oxidative

  13. The co-occurrence of zinc deficiency and social isolation has the opposite effects on mood compared with either condition alone due to changes in the central norepinephrine system.

    PubMed

    Mitsuya, Hironori; Omata, Naoto; Kiyono, Yasushi; Mizuno, Tomoyuki; Murata, Tetsuhito; Mita, Kayo; Okazawa, Hidehiko; Wada, Yuji

    2015-05-01

    Nutritional and social environmental problems during the early stages of life are closely associated with the pathophysiology of mood disorders such as depression. Disruption or dysfunction of the central norepinephrine (NE) system is also considered to play a role in mood disorders. Therefore, we evaluated the effects of zinc deficiency and/or social isolation on mood and changes in the central NE system using rats. Compared with the controls, the rats subjected to zinc deficiency or social isolation alone exhibited increased anxiety-related behavior in the elevated plus maze and greater depression-like behavior in the forced swim test. However, the co-occurrence of zinc deficiency and social isolation resulted in decreased anxiety-related behavior and control levels of depression-like behavior. Social isolation alone decreased the rats' cerebral NE concentrations. The expression of the NE transporter was not affected by social isolation alone, but its expression in the locus coeruleus was markedly decreased by the co-occurrence of social isolation and zinc deficiency, and this change was accompanied by an increase in the blood concentration of 3-methoxy-4-hydroxyphenylglycol, which is a marker of central NE system activity. These findings suggest that zinc deficiency or social isolation alone induce anxious or depressive symptoms, but the presence of both conditions has anxiolytic or antidepressive effects. Furthermore, these opposing effects of mood-related behaviors were found to be associated with changes in the central NE system. Copyright © 2015 The Authors. Published by Elsevier B.V. All rights reserved.

  14. Effect of Zinc-Deficient Diet on Oral Tissues and Periodontal Indices in Rats

    PubMed Central

    Seyedmajidi, Seyed Ali; Seyedmajidi, Maryam; Moghadamnia, Aliakbar; Khani, Zohreh; Zahedpasha, Samir; Jenabian, Niloofar; Jorsaraei, Gholamali; Halalkhor, Sohrab; Motallebnejad, Mina

    2014-01-01

    Zinc (Zn) as a nutritional factor affects the health of the oral tissues. This study was done for the evaluation of the effects of zinc deficiency on the oral tissues of rats. The study was carried out on 14 male Wistar rats, cessation of lactation on the 24th day after birth. The rats were randomly divided into two groups. Zinc deficient (ZD) diet was used for one group and another group was fed with a zinc-containing (ZC) diet. The alterations of the oral tissues in both groups were evaluated clinically after four weeks. Also the gingival index and periodontal pocket depth were recorded. The measurement of serum zinc level was done by atomic absorption spectrophotometry. The microscopic slides of oral tissue specimen were evaluated quantitatively. The serum zinc level of the ZD rats was lower than the ZC group (p< 0.001). According clinical findings, the gingival index was lower in ZC rat (p=0.001), but there was no significant difference regarding the periodontal pocket depth between two groups (p=0.07). Aphthous ulcer was observed in ZD rats on the floor of the mouth. There was no significant difference regarding the epithelial and keratin thickening between two groups. This study indicated that oral and periodontal health was better in ZC rats than in ZD rats. Aphthous lesions were more prominent in ZD rats. This study confirmed that zinc deficiency may endanger oral and periodo ntal structures. PMID:25035857

  15. Decrease of non-point zinc runoff using porous concrete.

    PubMed

    Harada, Shigeki; Komuro, Yoshinori

    2010-01-01

    The use of porous concrete columns to decrease the amount of zinc in stormwater runoff is examined. The concentration of zinc in a simulated stormwater fluid (zinc acetate solution), fed through concrete columns (slashed circle10x10cm) decreased by 50-81%, suggesting physical adsorption of zinc by the porous concrete. We propose the use of porous concrete columns (slashed circle50x10cm) as the base of sewage traps. Longer-term, high-zinc concentration monitoring revealed that porous concrete blocks adsorb 38.6mgcm(-3) of zinc. A period of no significant zinc runoff (with an acceptable concentration of zinc in runoff of 0.03mgL(-1), a zinc concentration equal to the Japanese Environmental Standard) is estimated for 41years using a 1-ha catchment area with 20 porous concrete sewage traps. Scanning electron microscopy of the porous concrete used in this study indicates that the needle-like particles formed by hydration action significantly increase zinc adsorption. Evidence suggests that the hydrant is ettringite and has an important role in zinc adsorption, the resulting immobilization of zinc and the subsequent effects on groundwater quality. Copyright 2009 Elsevier Ltd. All rights reserved.

  16. A syndrome of acute zinc deficiency during total parenteral alimentation in man.

    PubMed Central

    Kay, R G; Tasman-Jones, C; Pybus, J; Whiting, R; Black, H

    1976-01-01

    Changes in the plasma and urine levels of the trace metal zinc have been followed in a series of 37 adult patients totally supported by intravenous alimentation. Copper has also been determined in more recent cases. In such a seriously ill group, although urinary zinc loss may be very high at the height of catabolism, severe plasma depletion does not occur unless there is a subsequent phase of sustained anabolism and weight gain. In four patients plasma zinc fell to very low levels during this phase and three of this group developed a syndrome characterized by diarrhea, mental depression, para-nasal, oral and peri-oral dermatitis, and alopecia. The response to oral or intravenous zinc therapy is striking, except for hair regrowth which is delayed but eventually complete. The syndrome we have recognized in adult man has not been previously described. It resembles however the parakeratosis of zinc deficient swine and it is also very similar to Acrodermatitis enteropathica, a genetically determined disorder of infants very recently linked to zinc deficiency. Zinc is clearly essential to human metabolism and it should be included in all parenteral alimentation regimes particularly during the period of rapid, sustained, weight gain. Images Fig. 1. Fig. 2. Fig. 3. Fig. 6. Fig. 7. Fig. 9. Fig. 10. PMID:817677

  17. A micronutrient powder with low doses of highly absorbable iron and zinc reduces iron and zinc deficiency and improves weight-for-age Z-scores in South African children.

    PubMed

    Troesch, Barbara; van Stuijvenberg, Martha E; van Stujivenberg, Martha E; Smuts, Cornelius M; Kruger, H Salomè; Biebinger, Ralf; Hurrell, Richard F; Baumgartner, Jeannine; Zimmermann, Michael B

    2011-02-01

    Micronutrient powders (MNP) are often added to complementary foods high in inhibitors of iron and zinc absorption. Most MNP therefore include high amounts of iron and zinc, but it is no longer recommended in malarial areas to use untargeted MNP that contain the Reference Nutrient Intake for iron in a single serving. The aim was to test the efficacy of a low-iron and -zinc (each 2.5 mg) MNP containing iron as NaFeEDTA, ascorbic acid (AA), and an exogenous phytase active at gut pH. In a double-blind controlled trial, South African school children with low iron status (n = 200) were randomized to receive either the MNP or the unfortified carrier added just before consumption to a high-phytate maize porridge 5 d/wk for 23 wk; primary outcomes were iron and zinc status and a secondary outcome was somatic growth. Compared with the control, the MNP increased serum ferritin (P < 0.05), body iron stores (P < 0.01) and weight-for-age Z-scores (P < 0.05) and decreased transferrin receptor (P < 0.05). The prevalence of iron deficiency fell by 30.6% (P < 0.01) and the prevalence of zinc deficiency decreased by 11.8% (P < 0.05). Absorption of iron from the MNP was estimated to be 7-8%. Inclusion of an exogenous phytase combined with NaFeEDTA and AA may allow a substantial reduction in the iron dose from existing MNP while still delivering adequate iron and zinc. In addition, the MNP is likely to enhance absorption of the high native iron content of complementary foods based on cereals and/or legumes.

  18. A high prevalence of zinc- but not iron-deficiency among women in rural Malawi: a cross-sectional study.

    PubMed

    Siyame, Edwin W P; Hurst, Rachel; Wawer, Anna A; Young, Scott D; Broadley, Martin R; Chilimba, Allan D C; Ander, Louise E; Watts, Michael J; Chilima, Benson; Gondwe, Jellita; Kang'ombe, Dalitso; Kalimbira, Alexander; Fairweather-Tait, Susan J; Bailey, Karl B; Gibson, Rosalind S

    2013-01-01

    Zinc deficiency is often associated with nutritional iron deficiency (ID), and may be exacerbated by low selenium status. To investigate risk of iron and zinc deficiency in women with contrasting selenium status. In a cross-sectional study, 1-day diet composites and blood samples were collected from self-selected Malawian women aged 18-50 years from low- (Zombwe) (n=60) and high-plant-available soil selenium (Mikalango) (n=60) districts. Diets were analyzed for trace elements and blood for biomarkers. Zinc deficiency (>90 %) was greater than ID anemia (6 %), or ID (5 %), attributed to diets low in zinc (median 5.7 mg/day) with high phytate:zinc molar ratios (20.0), but high in iron (21.0 mg/day) from soil contaminant iron. Zombwe compared to Mikalango women had lower (p<0.05) intakes of selenium (6.5 vs. 55.3 µg/day), zinc (4.8 vs. 6.4 mg/day), iron (16.6 vs. 29.6 mg/day), lower plasma selenium (0.72 vs. 1.60 µmol/L), and higher body iron (5.3 vs. 3.8 mg/kg), although plasma zinc was similar (8.60 vs. 8.87 µmol/L). Body iron and plasma zinc were positive determinants of hemoglobin. Risk of zinc deficiency was higher than ID and was shown not to be associated with selenium status. Plasma zinc was almost as important as body iron as a hemoglobin determinant.

  19. Zinc transporter 7 deficiency affects lipid synthesis in adipocytes by inhibiting insulin-dependent Akt activity and glucose uptake

    USDA-ARS?s Scientific Manuscript database

    Mice deficient for zinc transporter 7 (Znt7) are mildly zinc deficient, accompanied with low body weight gain and body fat accumulation. To investigate the underlying mechanism of Znt7 deficiency in body adiposity, we investigated fatty acid composition and insulin sensitivity in visceral (epididyma...

  20. The downregulation of Wnt/β-catenin signaling pathway is associated with zinc deficiency-induced proliferative deficit of C17.2 neural stem cells.

    PubMed

    Zhao, Jianya; Han, Jingling; Jiang, Junkang; Shi, Shangshi; Ma, Xia; Liu, Xinhang; Wang, Cheng; Nie, Xiaoke; He, Yunhua; Jiang, Shengyang; Wan, Chunhua

    2015-07-30

    Zinc is an essential nutrient that is important for normal brain development. Zinc deficiency has been linked to aberrant neurological development and functioning. However, the molecular mechanisms underlying Zinc deficiency-induced neurological disorders remain largely elusive. In the present study, we showed that the proliferation of C17.2 neural stem cells (NSCs) was evidently impaired after exposed to low levels of Zinc chelator, N,N,N',N'-tetrakis-(2-pyridylmethy) ethylenediamine (TPEN). In addition, we found that TPEN-induced proliferative deficit of NSCs was related with significant downregulation of Wnt/β-catenin signaling. Zinc deficiency impaired the proliferation of neural stem cells in dose- and time-dependent manners. Western blot revealed that the levels of p-Ser9-glycogensynthase kinase-3β (p-GSK-3β) and β-catenin were remarkably downregulated during TPEN-induced C17.2 proliferative impairment. Moreover, immunofluorescent analysis indicated that the level of nuclear β-catenin was apparently decreased following TPEN exposure. Furthermore, application with GSK-3β inhibitor lithium chloride (LiCl) reversed TPEN-induced downregulation of β-catenin and impairment of cell proliferation. Flow cytometry analysis also showed that TPEN-induced impairment of NSC proliferation could be reversed by LiCl. Taken together, these findings suggested that the disturbance of canonical Wnt/β-catenin signaling pathway partially accounted for Zinc deficiency-induced proliferative impairment of NSCs. Copyright © 2015 Elsevier B.V. All rights reserved.

  1. The permissive effect of zinc deficiency on uroguanylin and inducible nitric oxide synthase gene upregulation in rat intestine induced by interleukin 1alpha is rapidly reversed by zinc repletion.

    PubMed

    Cui, Li; Blanchard, Raymond K; Cousins, Robert J

    2003-01-01

    Deficient intake of zinc from the diet upregulates both uroguanylin (UG) and inducible nitric oxide synthase (iNOS) expression in rats. Because these changes influence intestinal fluid secretion and intestinal cell pathophysiology, they relate to the incidence of diarrheal disease and its reversal by zinc as well as intestinal inflammation in general. A model of moderate zinc deficiency in rats, which changes molecular indices of zinc deficiency, was used to further explore the effects of the proinflammatory cytokine interleukin (IL)-1alpha and zinc repletion on these changes. IL-1alpha has been shown to have a role in the intestinal inflammation that occurs with bacterial infection. Our results showed a permissive effect of zinc deficiency on both UG and iNOS expression. Specifically, UG expression was responsive to zinc deficiency and IL-1alpha challenge, which were additive when combined, whereas iNOS expression was upregulated by IL-1alpha only during the deficiency. Immunohistochemistry showed that the increase in UG was limited to enterocytes of the upper villus but, in contrast, the increase in iNOS was principally in cells of the lamina propria of IL-1alpha-treated rats. Cells exhibiting UG upregulation did not co-express serotonin. Repletion with zinc reversed upregulation of the iNOS gene within 1 d, whereas UG upregulation required 3-4 d to return to normal. This differential response to repletion suggests that mechanisms of UG and iNOS dysregulation are different. Dysregulation of both genes may contribute to the severity of zinc-responsive diarrheal disease and intestinal inflammatory disease.

  2. [A neonate with anaemia of prematurity: zinc protoporphyrin identifies iron deficiency anaemia without iron deficiency].

    PubMed

    van der Feen, Diederik E; van Hillegersberg, Jacqueline L A M; Schippers, Johannes A

    2015-01-01

    Anaemia is a common problem in premature infants and is generally easy to treat with iron supplementation. If the anaemia persists despite appropriate correction of deficiencies, more extensive evaluation is required. We describe a case of a premature male infant with a production-deficient anaemia without metabolic deficiencies, eventually identified as anaemia of prematurity. This type of anaemia is commonly diagnosed but its highly variable and complex aetiology and phenotype are often poorly understood. A probable explanation for the anaemia of prematurity in this case was a transient iron incorporation defect, identifiable by high levels of zinc protoporphyrin.

  3. Effect of increased concentrations of atmospheric carbon dioxide on the global threat of zinc deficiency: a modelling study.

    PubMed

    Myers, Samuel S; Wessells, K Ryan; Kloog, Itai; Zanobetti, Antonella; Schwartz, Joel

    2015-10-01

    Increasing concentrations of atmospheric carbon dioxide (CO2) lower the content of zinc and other nutrients in important food crops. Zinc deficiency is currently responsible for large burdens of disease globally, and the populations who are at highest risk of zinc deficiency also receive most of their dietary zinc from crops. By modelling dietary intake of bioavailable zinc for the populations of 188 countries under both an ambient CO2 and elevated CO2 scenario, we sought to estimate the effect of anthropogenic CO2 emissions on the global risk of zinc deficiency. We estimated per capita per day bioavailable intake of zinc for the populations of 188 countries at ambient CO2 concentrations (375-384 ppm) using food balance sheet data for 2003-07 from the Food and Agriculture Organization. We then used previously published data from free air CO2 enrichment and open-top chamber experiments to model zinc intake at elevated CO2 concentrations (550 ppm, which is the concentration expected by 2050). Estimates developed by the International Zinc Nutrition Consultative Group were used for country-specific theoretical mean daily per-capita physiological requirements for zinc. Finally, we used these data on zinc bioavailability and population-weighted estimated average zinc requirements to estimate the risk of inadequate zinc intake among the populations of the different nations under the two scenarios (ambient and elevated CO2). The difference between the population at risk at elevated and ambient CO2 concentrations (ie, population at new risk of zinc deficiency) was our measure of impact. The total number of people estimated to be placed at new risk of zinc deficiency by 2050 was 138 million (95% CI 120-156). The people likely to be most affected live in Africa and South Asia, with nearly 48 million (32-63) residing in India alone. Global maps of increased risk show significant heterogeneity. Our results indicate that one heretofore unquantified human health effect associated

  4. Early-in-life dietary zinc deficiency and supplementation and mammary tumor development in adulthood female rats.

    PubMed

    da Silva, Flávia R M; Grassi, Tony F; Zapaterini, Joyce R; Bidinotto, Lucas T; Barbisan, Luis F

    2017-06-01

    Zinc deficiency during pregnancy and postnatal life can adversely increase risk of developing human diseases at adulthood. The present study was designed to evaluate whether dietary zinc deficiency or supplementation during the pregnancy, lactation and juvenile stages interferes in the development of mammary tumors induced by 7,12-dimethylbenzanthracene (DMBA) in female Sprague-Dawley (SD) rats. Pregnant female SD rats were allocated into three groups: zinc-adequate diet (ZnA - 35-mg/kg chow), zinc-deficient diet (ZnD - 3-mg/kg chow) or zinc-supplemented diet (ZnS - 180-mg/kg chow) during gestational day 10 (GD 10) until the litters' weaning. Female offspring received the same diets as their dams until postnatal day (PND) 51. At PND 51, the animals received a single dose of DMBA (50 mg/kg, ig) and zinc-adequate diets. At PND 180, female were euthanized, and tumor samples were processed for histological evaluation and gene expression microarray analysis. The ZnD induced a significant reduction in female offspring body weight evolution and in mammary gland development. At late in life, the ZnD or ZnS did not alter the latency, incidence, multiplicity, volume or histological types of mammary tumors in relation to the ZnA group. However, the total tumor number in ZnS group was higher than in ZnA group, accompanied by distinct expression of 4 genes up- and 15 genes down-regulated. The present findings indicate that early-in-life dietary zinc supplementation, differently to zinc deficiency, has a potential to modify the susceptibility to the development of mammary tumors induced by DMBA. Copyright © 2017 Elsevier Inc. All rights reserved.

  5. Maternal and fetal plasma zinc in pre-eclampsia.

    PubMed

    Bassiouni, B A; Foda, A I; Rafei, A A

    1979-04-01

    Zinc is important for fetal growth and is involved in several important enzyme systems. Maternal and umbilical plasma zinc concentrations were determined in 52 parturient women with mild and severe pre-eclampsia, and were compared with those obtained from 20 women in labor whose pregnancies had progressed normally. A decrease in maternal as well as umbilical plasma zinc concentrations was observed in pre-eclamptic women, and this decrease was statistically significant in severe pre-eclampsia. The causes of these changes in plasma zinc concentrations in pre-eclampsia were discussed, and the possible adverse effects of zinc deficiency on the mother and fetus were mentioned. Low plasma zinc concentrations in pre-eclampsia may be a sign of zinc deficiency, implying possible risks to the mother and her fetus. It is recommended that maintenance of adequate dietary zinc nutrition during pregnancy, and particularly in pre-eclampsia, is important.

  6. The prevalence of zinc deficiency in patients with thalassemia in South East of iran, sistan and baluchistan province.

    PubMed

    Mashhadi, Mohammad Ali; Sepehri, Zahra; Heidari, Zahra; Shirzaee, Eghbal; Kiani, Zohre

    2014-08-01

    There are different and controversial reports about zinc deficiency in patients with major thalassemia. The aim of this study was to evaluate zinc status in patients with major thalassemia in Sistan and Baluchistan province, southeastern Iran. The study was performed in Ali Asghar Hospital, a specialized governmental hospital located in Zahedan, Iran. In this cross-sectional study, 369 patients with a history of major thalassemia for more than 5 years entered the study using convenience sampling method. Thirty-six subjects were excluded from the study based on our exclusion criteria. Zinc level was measured in all patients after 12 hours fasting using atomic absorption spectrometry method in 2012. Of 369 cases, 333 patients were eligible and evaluated. The mean age was 15.63 ± 7.4 years. One hundred ninety two cases were male and others were female (141 cases). About 27% (90) of the cases were 5-10 years-old, 24% (80) were 10-15 years-old and 49% were older than 15 years old. Iron chelator in 65.46% was Desferrioxamine, in 28.2% was Deferasirox and in 19.5% was combination of Desferrioxamine and Deferiprone. All cases had zinc deficiency, and 98.5% had severe zinc deficiency. Others (1.5%) had mild deficiency. Our study on 333 patients with major thalassemia documented severe zinc deficiency in all cases. We had no cases with normal or increased zinc levels. It was different with other reports in the world.

  7. Induction of Nickel Accumulation in Response to Zinc Deficiency in Arabidopsis thaliana

    PubMed Central

    Nishida, Sho; Kato, Aki; Tsuzuki, Chisato; Yoshida, Junko; Mizuno, Takafumi

    2015-01-01

    Excessive accumulation of nickel (Ni) can be toxic to plants. In Arabidopsis thaliana, the Fe2+ transporter, iron (Fe)-regulated transporter1 (IRT1), mediates Fe uptake and also implicates in Ni2+ uptake at roots; however, the underlying mechanism of Ni2+ uptake and accumulation remains unelucidated. In the present study, we found that zinc (Zn) deficient conditions resulted in increased accumulation of Ni in plants, particularly in roots, in A. thaliana. In order to elucidate the underlying mechanisms of Ni uptake correlating zinc condition, we traced 63Ni isotope in response to Zn and found that (i) Zn deficiency induces short-term Ni2+ absorption and (ii) Zn2+ inhibits Ni2+ uptake, suggesting competitive uptake between Ni and Zn. Furthermore, the Zrt/Irt-like protein 3 (ZIP3)-defective mutant with an elevated Zn-deficient response exhibited higher Ni accumulation than the wild type, further supporting that the response to Zn deficiency induces Ni accumulation. Previously, expression profile study demonstrated that IRT1 expression is not inducible by Zn deficiency. In the present study, we found increased Ni accumulation in IRT1-null mutant under Zn deficiency in agar culture. These suggest that Zn deficiency induces Ni accumulation in an IRT1-independen manner. The present study revealed that Ni accumulation is inducible in response to Zn deficiency, which may be attributable to a Zn uptake transporter induced by Zn deficiency. PMID:25923075

  8. Evaluation of the serum zinc level in adult patients with melasma: Is there a relationship with serum zinc deficiency and melasma?

    PubMed

    Rostami Mogaddam, Majid; Safavi Ardabili, Nastaran; Iranparvar Alamdari, Manouchehr; Maleki, Nasrollah; Aghabalaei Danesh, Maryam

    2017-11-12

    Melasma is a common acquired hypermelanosis of sun-exposed skin, particularly on the face, which presents as symmetric, light- to gray-brown-colored macules and patches. There are several studies of serum zinc levels in cutaneous disorders. So far, no studies have been carried out to assess the serum zinc level in patients with melasma. The aim of this study is to determine the serum zinc level in patients with melasma compared to healthy subjects. A total of 118 patients with melasma and 118 healthy controls were enrolled in this prospective cross-sectional study. The two groups were matched for age and sex. Atomic absorption spectrophotometry was used to measure serum zinc levels. The statistical analysis was performed using SPSS software. The mean serum level of zinc in melasma patients and controls was 77.4±23.2 μg/dL and 82.2±23.9 μg/dL, respectively (P-value=.0001). Serum zinc deficiency was found in 45.8% and 23.7% of melasma patients and control subjects, respectively. A positive family history of melasma in first-degree relatives was present in 46 (39%) of the cases, and a history of taking oral contraceptive pill was found in 95 (81%) of women with melasma. The aggravating factors for melasma were stated as: sun exposure (11.1%), pregnancy (15.3%), nutrition (2.5%), oral contraceptive pills (18.6%), and emotional stress (5.9%). The malar and centrofacial patterns were seen in 3.4% and 72% of cases, respectively, whereas 24.6% of the patients had both centrofacial distribution and malar distribution, and there was no patient with mandibular pattern. Among patients with melasma, 20.3% had thyroid dysfunction, while in the control subjects, 8.4% had thyroid dysfunction (P=.001). There is a significant relationship between low levels of zinc and melasma. Zinc deficiency may be involved in the pathogenesis of melasma. Also, treatment with oral zinc supplements can be tried in these patients to see the outcome. However, to make recommendations on

  9. The Prevalence of Zinc Deficiency in Patients With Thalassemia in South East of Iran, Sistan and Baluchistan Province

    PubMed Central

    Mashhadi, Mohammad Ali; Sepehri, Zahra; Heidari, Zahra; Shirzaee, Eghbal; Kiani, Zohre

    2014-01-01

    Background: There are different and controversial reports about zinc deficiency in patients with major thalassemia. Objectives: The aim of this study was to evaluate zinc status in patients with major thalassemia in Sistan and Baluchistan province, southeastern Iran. Patients and Methods: The study was performed in Ali Asghar Hospital, a specialized governmental hospital located in Zahedan, Iran. In this cross-sectional study, 369 patients with a history of major thalassemia for more than 5 years entered the study using convenience sampling method. Thirty-six subjects were excluded from the study based on our exclusion criteria. Zinc level was measured in all patients after 12 hours fasting using atomic absorption spectrometry method in 2012. Results: Of 369 cases, 333 patients were eligible and evaluated. The mean age was 15.63 ± 7.4 years. One hundred ninety two cases were male and others were female (141 cases). About 27% (90) of the cases were 5-10 years-old, 24% (80) were 10-15 years-old and 49% were older than 15 years old. Iron chelator in 65.46% was Desferrioxamine, in 28.2% was Deferasirox and in 19.5% was combination of Desferrioxamine and Deferiprone. All cases had zinc deficiency, and 98.5% had severe zinc deficiency. Others (1.5%) had mild deficiency. Conclusions: Our study on 333 patients with major thalassemia documented severe zinc deficiency in all cases. We had no cases with normal or increased zinc levels. It was different with other reports in the world. PMID:25389495

  10. Zinc is an Antioxidant and Anti-Inflammatory Agent: Its Role in Human Health

    PubMed Central

    Prasad, Ananda S.

    2014-01-01

    Zinc supplementation trials in the elderly showed that the incidence of infections was decreased by approximately 66% in the zinc group. Zinc supplementation also decreased oxidative stress biomarkers and decreased inflammatory cytokines in the elderly. In our studies in the experimental model of zinc deficiency in humans, we showed that zinc deficiency per se increased the generation of IL-1β and its mRNA in human mononuclear cells following LPS stimulation. Zinc supplementation upregulated A20, a zinc transcription factor, which inhibited the activation of NF-κB, resulting in decreased generation of inflammatory cytokines. Oxidative stress and chronic inflammation are important contributing factors for several chronic diseases attributed to aging, such as atherosclerosis and related cardiac disorders, cancer, neurodegeneration, immunologic disorders and the aging process itself. Zinc is very effective in decreasing reactive oxygen species (ROS). In this review, the mechanism of zinc actions on oxidative stress and generation of inflammatory cytokines and its impact on health in humans will be presented. PMID:25988117

  11. Risk Factors for Vitamin D, Zinc, and Selenium Deficiencies in Korean Patients with Inflammatory Bowel Disease.

    PubMed

    Han, Yoo Min; Yoon, Hyuk; Lim, Soo; Sung, Mi-Kyung; Shin, Cheol Min; Park, Young Soo; Kim, Nayoung; Lee, Dong Ho; Kim, Joo Sung

    2017-05-15

    Studies on the micronutrient status of Asian patients with inflammatory bowel disease (IBD) are scarce. We evaluated the prevalence of micronutrient deficiency and verified the risk factors for micronutrient deficiency in Korean patients with IBD. We measured the serum levels of 25-hydroxyvitamin D3 [25-(OH)D], zinc, and selenium to analyze the clinical risk factors for micronutrient levels below the reference values. In addition, we compared the 25-(OH)D levels of patients with IBD to those of age- and sex-matched healthy controls. Among the 83 patients, 74 (89.2%) had suboptimal serum 25-(OH)D levels. The mean plasma 25-(OH)D level in patients with IBD was significantly reduced compared to that of the healthy controls (12.3±6.2 ng/mL vs 20.0±6.7 ng/mL; p<0.001). The proportions of patients with lower serum zinc and selenium levels were 39.0% and 30.9%, respectively. Female sex (p=0.012) and Crohn's disease (p=0.012) were associated with vitamin D deficiency. Patients younger than 40 years were at increased risk for zinc deficiency (p=0.045). Female sex (p=0.015) and low serum albumin level (<3.3 g/dL) (p=0.047) were risk factors for selenium deficiency. Many Korean patients with IBD have vitamin D, zinc, and selenium deficiencies, suggesting the necessity for monitoring levels of these micronutrients.

  12. Zinc deficiency in children with environmental enteropathy—development of new strategies: report from an expert workshop1234

    PubMed Central

    Young, Graeme P; Mortimer, Elissa K; Gopalsamy, Geetha L; Alpers, David H; Binder, Henry J; Manary, Mark J; Ramakrishna, Balakrishnan S; Brown, Ian L; Brewer, Thomas G

    2014-01-01

    Zinc deficiency is a major cause of childhood morbidity and mortality. The WHO/UNICEF strategy for zinc supplementation as adjunctive therapy for diarrhea is poorly implemented. A conference of experts in zinc nutrition and gastrointestinal disorders was convened to consider approaches that might complement the current recommendation and what research was needed to develop these approaches. Several key points were identified. The design of novel zinc interventions would be facilitated by a better understanding of how disturbed gut function, such as environmental (or tropical) enteropathy, affects zinc absorption, losses, and homeostasis. Because only 10% of zinc stores are able to be rapidly turned over, and appear to be rapidly depleted by acute intestinal illness, they are probably best maintained by complementary regular supplementation in a primary prevention strategy rather than secondary prevention triggered by acute diarrhea. The assessment of zinc status is challenging and complex without simple, validated measures to facilitate field testing of novel interventions. Zinc bioavailability may be a crucial factor in the success of primary prevention strategies, and a range of options, all still inadequately explored, might be valuable in improving zinc nutrition. Some therapeutic actions of zinc on diarrhea seem attributable to pharmacologic effects, whereas others are related to the reversal of deficiency (ie, nutritional). The distinction between these 2 mechanisms cannot be clarified given the insensitivity of serum zinc to identify subclinical deficiency states. Why zinc seems to be less effective than expected at all ages, and ineffective for secondary prevention of diarrhea in children <12 mo of age, remains unclear. It was concluded that a reframing of the current recommendation is warranted with consideration of how to better optimize and deliver zinc and whether to provide a complementary public health primary prevention zinc strategy. This requires

  13. Zinc deficiency in children with environmental enteropathy - development of new strategies: Report from an expert workshop

    USDA-ARS?s Scientific Manuscript database

    Zinc deficiency is a major cause of childhood morbidity and mortality. The WHO/UNICEF strategy for zinc supplementation as adjunctive therapy for diarrhea is poorly implemented. A conference of experts in zinc nutrition and gastrointestinal disorders was convened to consider approaches that might co...

  14. [Improvement in zinc nutrition due to zinc transporter-targeting strategy].

    PubMed

    Kambe, Taiho

    2016-07-01

    Adequate intake of zinc from the daily diet is indispensable to maintain health. However, the dietary zinc content often fails to fulfill the recommended daily intake, leading to zinc deficiency and also increases the risk of developing chronic diseases, particularly in elderly individuals. Therefore, increased attention is required to overcome zinc deficiency and it is important to improve zinc nutrition in daily life. In the small intestine, the zinc transporter, ZIP4, functions as a component that is essential for zinc absorption. In this manuscript, we present a brief overview regarding zinc deficiency. Moreover, we review a novel strategy, called "ZIP4-targeting", which has the potential to enable efficient zinc absorption from the diet. ZIP4-targeting strategy is possibly a major step in preventing zinc deficiency and improving human health.

  15. Loss of synaptic zinc transport in progranulin deficient mice may contribute to progranulin-associated psychopathology and chronic pain.

    PubMed

    Hardt, Stefanie; Heidler, Juliana; Albuquerque, Boris; Valek, Lucie; Altmann, Christine; Wilken-Schmitz, Annett; Schäfer, Michael K E; Wittig, Ilka; Tegeder, Irmgard

    2017-11-01

    Affective and cognitive processing of nociception contributes to the development of chronic pain and vice versa, pain may precipitate psychopathologic symptoms. We hypothesized a higher risk for the latter with immanent neurologic diseases and studied this potential interrelationship in progranulin-deficient mice, which are a model for frontotemporal dementia, a disease dominated by behavioral abnormalities in humans. Young naïve progranulin deficient mice behaved normal in tests of short-term memory, anxiety, depression and nociception, but after peripheral nerve injury, they showed attention-deficit and depression-like behavior, over-activity, loss of shelter-seeking, reduced impulse control and compulsive feeding behavior, which did not occur in equally injured controls. Hence, only the interaction of 'pain x progranulin deficiency' resulted in the complex phenotype at young age, but neither pain nor progranulin deficiency alone. A deep proteome analysis of the prefrontal cortex and olfactory bulb revealed progranulin-dependent alterations of proteins involved in synaptic transport, including neurotransmitter transporters of the solute carrier superfamily. In particular, progranulin deficiency was associated with a deficiency of nuclear and synaptic zinc transporters (ZnT9/Slc30a9; ZnT3/Slc30a3) with low plasma zinc. Dietary zinc supplementation partly normalized the attention deficit of progranulin-deficient mice, which was in part reminiscent of autism-like and compulsive behavior of synaptic zinc transporter Znt3-knockout mice. Hence, the molecular studies point to defective zinc transport possibly contributing to progranulin-deficiency-associated psychopathology. Translated to humans, our data suggest that neuropathic pain may precipitate cognitive and psychopathological symptoms of an inherent, still silent neurodegenerative disease. Copyright © 2017. Published by Elsevier B.V.

  16. Zinc Deficiency Induces Apoptosis via Mitochondrial p53- and Caspase-Dependent Pathways in Human Neuronal Precursor Cells

    ERIC Educational Resources Information Center

    Seth, Rohit; Corniola, Rikki S.; Gower-Winter, Shannon D.; Morgan, Thomas J., Jr.; Bishop, Brian; Levenson, Cathy W.

    2015-01-01

    Previous studies have shown that zinc deficiency leads to apoptosis of neuronal precursor cells in vivo and in vitro. In addition to the role of p53 as a nuclear transcription factor in zinc deficient cultured human neuronal precursors (NT-2), we have now identified the translocation of phosphorylated p53 to the mitochondria and p53-dependent…

  17. Iron and Vitamin C Co-Supplementation Increased Serum Vitamin C Without Adverse Effect on Zinc Level in Iron Deficient Female Youth

    PubMed Central

    Khoshfetrat, Mohammad Reza; Mortazavi, Sima; Neyestani, Tirang; Mahmoodi, Mohammad Reza; Zerafati-Shoae, Nahid; Mohammadi-Nasrabadi, Fatemeh

    2014-01-01

    Background: Iron supplementation can decrease the absorption of zinc and influence other antioxidants levels such as vitamin C. This study aimed to investigate the effect of iron supplements alone and in combination with vitamin C on zinc and vitamin C status in iron deficient female students. Methods: In a double-blind randomized clinical trail, 60 iron deficient students were selected from 289 volunteers residing in dormitory. After matching, subjects were randomly assigned into two groups: Group I (50 mg elemental iron supplements) and Group II (50 mg elemental iron + 500 mg ascorbic acid). Serum ferritin, iron, serum zinc, and plasma vitamin C concentrations were measured by using enzyme-linked immunosorbent assay, spectrophotometer, atomic absorption spectrometer, and colorimeter, respectively after 6 and 12 weeks supplementation. Student's t-test and repeated measures analysis of variance were applied to analyze the data using SPSS software. Results: Serum zinc levels had no significant differences between 2 groups at the baseline; however, its concentration decreased from 80.9 ± 4.2-68.9 ± 2.7 μg/dl to 81.2 ± 4.5-66.1 ± 2.9 μg/dl (P < 0.001) in Groups I and II, respectively after 6 weeks of supplementation. Continuous supplementation increased serum zinc concentration to baseline levels (79.0 ± 2.9 μg/dl; P < 0.01) in Group I and 70.5 ± 3.1 μg/dl in Group II following 12 weeks of supplementation. Plasma vitamin C increased from 3 ± 0/1-3.3 ± 0.2 mg/dl to 2.7 ± 0. 1-4.2 ± 0.2 mg/dl (P < 0.01) in Groups I and II, respectively. At the end of study, plasma vitamin C significantly increased from 3.3 ± 0.3-4.7 ± 0.3 (P < 0.01) to 4.2 ± 0.2-7.1 ± 0.2 (P < 0.001) in Groups I and II, respectively. Conclusions: Iron supplementation with and without vitamin C led to reduction in serum Zn in iron-deficient female students after 6 weeks. However, the decreasing trend stops after repletion of iron stores and Zn levels returned to the approximately

  18. Two iron-regulated transporter (IRT) genes showed differential expression in poplar trees under iron or zinc deficiency.

    PubMed

    Huang, Danqiong; Dai, Wenhao

    2015-08-15

    Two iron-regulated transporter (IRT) genes were cloned from the iron chlorosis resistant (PtG) and susceptible (PtY) Populus tremula 'Erecta' lines. Nucleotide sequence analysis showed no significant difference between PtG and PtY. The predicted proteins contain a conserved ZIP domain with 8 transmembrane (TM) regions. A ZIP signature sequence was found in the fourth TM domain. Phylogenetic analysis revealed that PtIRT1 was clustered with tomato and tobacco IRT genes that are highly responsible to iron deficiency. The PtIRT3 gene was clustered with the AtIRT3 gene that was related to zinc and iron transport in plants. Tissue specific expression indicated that PtIRT1 only expressed in the root, while PtIRT3 constitutively expressed in all tested tissues. Under iron deficiency, the expression of PtIRT1 was dramatically increased and a significantly higher transcript level was detected in PtG than in PtY. Iron deficiency also enhanced the expression of PtIRT3 in PtG. On the other hand, zinc deficiency down-regulated the expression of PtIRT1 and PtIRT3 in both PtG and PtY. Zinc accumulated significantly under iron-deficient conditions, whereas the zinc deficiency showed no significant effect on iron accumulation. A yeast complementation test revealed that the PtIRT1 and PtIRT3 genes could restore the iron uptake ability under the iron uptake-deficiency condition. The results will help understand the mechanisms of iron deficiency response in poplar trees and other woody species. Copyright © 2015 Elsevier GmbH. All rights reserved.

  19. Copper, iron and zinc absorption, retention and status of young women fed vitamin B-6 deficient diets

    SciTech Connect

    Turnlund, J.R.; Keyes, W.R.; Hudson, C.A.

    1991-03-11

    A study was conducted in young women to determine the effect of vitamin B-6 deficient diets on copper, iron and zinc metabolism. Young women were confined to a metabolic research unit for 84 and 98 days. They were fed a vitamin B-6 deficient formula diet initially, followed by food diet containing four increasing levels of vitamin B-6. Copper, iron and zinc absorption, retention and status were determined at intervals throughout the study. Absorption was determined using the stable isotopes {sup 65}Cu, {sup 54}Fe, and {sup 67}Zn. Status was based on serum copper and zinc, hemoglobin, hematocrit and mean corpuscular volume.more » Copper absorption averaged 18 {plus minus} 1% during vitamin B-6 depletion, significantly lower than 24 {plus minus} 1% during repletion, but serum copper was not affected and balance was positive. Iron absorption was not impaired significantly by vitamin B-6 deficient diets, but status declined during the depletion period. Zinc absorption averaged 40 {plus minus} 2% during depletion and 27 {plus minus} 2% during repletion. Zinc absorption and retention were significantly greater during vitamin B-6 depletion, but serum zinc declined suggesting the absorbed zinc was not available for utilization. The results suggest that vitamin B-6 depletion of young women may inhibit copper absorption, affect iron status and alter zinc metabolism. The effects of vitamin B-6 depletion differ markedly among these elements.« less

  20. Effects of serum zinc level on tinnitus.

    PubMed

    Berkiten, Güler; Kumral, Tolgar Lütfi; Yıldırım, Güven; Salturk, Ziya; Uyar, Yavuz; Atar, Yavuz

    2015-01-01

    The aim of this study was to assess zinc levels in tinnitus patients, and to evaluate the effects of zinc deficiency on tinnitus and hearing loss. One-hundred patients, who presented to an outpatient clinic with tinnitus between June 2009 and 2014, were included in the study. Patients were divided into three groups according to age: Group I (patients between 18 and 30years of age); Group II (patients between 31 and 60years of age); and Group III (patients between 61 and 78years of age). Following a complete ear, nose and throat examination, serum zinc levels were measured and the severity of tinnitus was quantified using the Tinnitus Severity Index Questionnaire (TSIQ). Patients were subsequently asked to provide a subjective judgment regarding the loudness of their tinnitus. The hearing status of patients was evaluated by audiometry and high-frequency audiometry. An average hearing sensitivity was calculated as the mean value of hearing thresholds between 250 and 20,000Hz. Serum zinc levels between 70 and 120μg/dl were considered normal. The severity and loudness of tinnitus, and the hearing thresholds of the normal zinc level and zinc-deficient groups, were compared. Twelve of 100 (12%) patients exhibited low zinc levels. The mean age of the zinc-deficient group was 65.41±12.77years. Serum zinc levels were significantly lower in group III (p<0.01). The severity and loudness of tinnitus were greater in zinc-deficient patients (p=0.011 and p=0.015, respectively). Moreover, the mean thresholds of air conduction were significantly higher in zinc-deficient patients (p=0.000). We observed that zinc levels decrease as age increases. In addition, there was a significant correlation between zinc level and the severity and loudness of tinnitus. Zinc deficiency was also associated with impairments in hearing thresholds. Copyright © 2015 Elsevier Inc. All rights reserved.

  1. Zinc deficiency mediates alcohol-induced apoptotic cell death in the liver of rats through activating ER and mitochondrial cell death pathways

    PubMed Central

    Sun, Qian; Zhong, Wei; Zhang, Wenliang; Li, Qiong; Sun, Xiuhua; Tan, Xiaobing; Sun, Xinguo; Dong, Daoyin

    2015-01-01

    Hepatic zinc deficiency has been well documented in alcoholic patients, but the mechanisms by which zinc deficiency mediates cell death have not been well defined. The objectives of this study were to determine whether alcohol perturbs subcellular zinc homeostasis and how organelle zinc depletion may link with cell death pathways. Wistar rats were pair-fed with the Lieber-DeCarli control or ethanol diet for 5 mo. Chronic alcohol exposure significantly reduced zinc level in isolated hepatic endoplasmic reticulum (ER) and mitochondria. Among the detected zinc transporters, ER Zrt/Irt-like protein (ZIP)13 and mitochondrial ZIP8, which transport zinc from ER and mitochondria to cytosol, were significantly increased. Mitochondrial zinc transporter (ZnT) 4, which transports zinc from cytosol to mitochondria, was also increased. ER phosphorylated eukaryotic initiation factor 2α, activating transcription factor 4, and C/EBP homologous protein were significantly upregulated, and mitochondrial cytochrome c release and Bax insertion were detected in association with caspase-3 activation and apoptotic cell death. To define the role of zinc deficiency in ER and mitochondrial stress, H4IIEC3 cells were treated with 3 μM N,N,N′,N′-tetrakis (2-pyridylmethyl) ethylenediamine for 6 h with or without supplementation with zinc or N-acetylcysteine (NAC). The results demonstrated that zinc deprivation induced caspase-3 activation and apoptosis in association with ER and mitochondria dysfunction, which were inhibited by zinc as low as 10 μM but not by 2 mM NAC. These results suggest that chronic ethanol exposure induced in ER and mitochondrial zinc deficiency might activate intrinsic cell death signaling pathway, which could not be effectively rescued by antioxidant treatment. PMID:25767260

  2. The cognitive impairment induced by zinc deficiency in rats aged 0∼2 months related to BDNF DNA methylation changes in the hippocampus.

    PubMed

    Hu, Yan-Dan; Pang, Wei; He, Cong-Cong; Lu, Hao; Liu, Wei; Wang, Zi-Yu; Liu, Yan-Qiang; Huang, Cheng-Yu; Jiang, Yu-Gang

    2017-11-01

    This study was carried out to understand the effects of zinc deficiency in rats aged 0∼2 months on learning and memory, and the brain-derived neurotrophic factor (BDNF) gene methylation status in the hippocampus. The lactating mother rats were randomly divided into three groups (n = 12): zinc-adequate group (ZA: zinc 30 mg/kg diet), zinc-deprived group (ZD: zinc 1 mg/kg diet), and a pair-fed group (PF: zinc 30 mg/kg diet), in which the rats were pair-fed to those in the ZD group. After weaning (on day 23), offspring were fed the same diets as their mothers. After 37 days, the zinc concentrations in the plasma and hippocampus were measured, and the behavioral function of the offspring rats was measured using the passive avoidance performance test. We then assessed the DNA methylation patterns of the exon IX of BDNF by methylation-specific quantitative real-time PCR and the mRNA expression of BDNF in the hippocampus by RT-PCR. Compared with the ZA and PF groups, rats in the ZD group had shorter latency period, lower zinc concentrations in the plasma and hippocampus (P < 0.05). Interestingly, the DNA methylation of the BDNF exon IX was significantly increased in the ZD group, compared with the ZA and PF groups, whereas the expression of the BDNF mRNA was decreased. In addition, the DNMT1 mRNA expression was significantly upregulated and DNMT3A was downregulated in the ZD group, but not in the ZA and PF groups. The learning and memory damage in offspring may be a result of the epigenetic changes of the BDNF genes in response to the zinc-deficient diet during 0∼2 month period. Furthermore, this work supports the speculative notion that altered DNA methylation of BDNF in the hippocampus is one of the main causes of cognitive impairment by zinc deficiency.

  3. Zinc Fortification Decreases ZIP1 Gene Expression of Some Adolescent Females with Appropriate Plasma Zinc Levels

    PubMed Central

    Méndez, Rosa O.; Santiago, Alejandra; Yepiz-Plascencia, Gloria; Peregrino-Uriarte, Alma B.; de la Barca, Ana M. Calderón; García, Hugo S.

    2014-01-01

    Zinc homeostasis is achieved after intake variation by changes in the expression levels of zinc transporters. The aim of this study was to evaluate dietary intake (by 24-h recall), absorption, plasma zinc (by absorption spectrophotometry) and the expression levels (by quantitative PCR), of the transporters ZIP1 (zinc importer) and ZnT1 (zinc exporter) in peripheral white blood cells from 24 adolescent girls before and after drinking zinc-fortified milk for 27 day. Zinc intake increased (p < 0.001) from 10.5 ± 3.9 mg/day to 17.6 ± 4.4 mg/day, and its estimated absorption from 3.1 ± 1.2 to 5.3 ± 1.3 mg/day. Mean plasma zinc concentration remained unchanged (p > 0.05) near 150 µg/dL, but increased by 31 µg/dL (p < 0.05) for 6/24 adolescents (group A) and decreased by 25 µg/dL (p < 0.05) for other 6/24 adolescents (group B). Expression of ZIP1 in blood leukocytes was reduced 1.4-fold (p < 0.006) in group A, while for the expression of ZnT1 there was no difference after intervention (p = 0.39). An increase of dietary zinc after 27-days consumption of fortified-milk did not increase (p > 0.05) the plasma level of adolescent girls but for 6/24 participants from group A in spite of the formerly appropriation, which cellular zinc uptake decreased as assessed by reduction of the expression of ZIP1. PMID:24922175

  4. Dietary Zinc Deficiency Affects Blood Linoleic Acid: Dihomo-γ-linolenic Acid (LA:DGLA) Ratio; a Sensitive Physiological Marker of Zinc Status in Vivo (Gallus gallus)

    PubMed Central

    Reed, Spenser; Qin, Xia; Ran-Ressler, Rinat; Brenna, James Thomas; Glahn, Raymond P.; Tako, Elad

    2014-01-01

    Zinc is a vital micronutrient used for over 300 enzymatic reactions and multiple biochemical and structural processes in the body. To date, sensitive and specific biological markers of zinc status are still needed. The aim of this study was to evaluate Gallus gallus as an in vivo model in the context of assessing the sensitivity of a previously unexplored potential zinc biomarker, the erythrocyte linoleic acid: dihomo-γ-linolenic acid (LA:DGLA) ratio. Diets identical in composition were formulated and two groups of birds (n = 12) were randomly separated upon hatching into two diets, Zn(+) (zinc adequate control, 42.3 μg/g zinc), and Zn(−) (zinc deficient, 2.5 μg/g zinc). Dietary zinc intake, body weight, serum zinc, and the erythrocyte fatty acid profile were measured weekly. At the conclusion of the study, tissues were collected for gene expression analysis. Body weight, feed consumption, zinc intake, and serum zinc were higher in the Zn(+) control versus Zn(−) group (p < 0.05). Hepatic TNF-α, IL-1β, and IL-6 gene expression were higher in the Zn(+) control group (p < 0.05), and hepatic Δ6 desaturase was significantly higher in the Zn(+) group (p < 0.001). The LA:DGLA ratio was significantly elevated in the Zn(−) group compared to the Zn(+) group (22.6 ± 0.5 and 18.5 ± 0.5, % w/w, respectively, p < 0.001). This study suggests erythrocyte LA:DGLA is able to differentiate zinc status between zinc adequate and zinc deficient birds, and may be a sensitive biomarker to assess dietary zinc manipulation. PMID:24658588

  5. The role of zinc deficiency-induced changes in the phospholipid-protein balance of blood serum in animal depression model by Raman, FTIR and UV-vis spectroscopy.

    PubMed

    Depciuch, J; Sowa-Kućma, M; Nowak, G; Szewczyk, B; Doboszewska, U; Parlinska-Wojtan, M

    2017-05-01

    Depression is a serious mental illness. To study the mechanisms of diseases and search for new, more effective therapies, animal models are used. Unfortunately, none of the available models does reflect all symptoms of depression. Zinc deficiency is proposed as a new animal model of depression. However, it has not been yet validated in a detailed manner. Recently, spectroscopic techniques are increasingly being used both in clinical and preclinical studies. Here we examined the effect of zinc deficiency and amitryptyline treatment on the phospholipid - protein balance in the blood serum of rats using Raman, Fourier Transform Infra Red (FTIR) and UV-vis technique. Male Sprague Dawley rats were fed with a zinc ample diet (ZnA, 50mg Zn/kg) or a zinc deficient diet (ZnD, 3mg Zn/kg) for 4 weeks. Then amitriptyline administration (AMI, 10mg/kg, i.p.) was started. After injecting the drug for 2-weeks, blood samples were collected and analyzed. It was found that zinc deficiency decreases both the level of phospholipids and proteins and also causes structural changes in their structures. In the ZnD group amitriptyline treatment influenced the protein level and structure. UV-vis spectroscopy combined with the second derivative calculated from the FTIR spectra provided information that the proteins in blood serum of rat fed with a low Zn diet regain their intact structure after amitriptyline medication. Simultaneously, the antidepressant therapy did not have any effect on the level of phospholipids in this group of rats. Additionally, our results show, that amitriptyline administration can change the structure of phospholipids in rats subjected to zinc ample diet. This altered structure of phospholipids was identified as shortening of carbon chains. Our findings indicate that the decreased level of zinc may be the cause of depressive disorders, as it leads to changes in the phospholipid-protein balance necessary for the proper functioning of the body. This study also shows

  6. Compound heterozygous mutations in SLC30A2/ZnT2 results in low milk zinc concentrations: a novel mechanism for zinc deficiency in a breast-fed infant.

    PubMed

    Itsumura, Naoya; Inamo, Yasuji; Okazaki, Fumiko; Teranishi, Fumie; Narita, Hiroshi; Kambe, Taiho; Kodama, Hiroko

    2013-01-01

    Zinc concentrations in breast milk are considerably higher than those of the maternal serum, to meet the infant's requirements for normal growth and development. Thus, effective mechanisms ensuring secretion of large amounts of zinc into the milk operate in mammary epithelial cells during lactation. ZnT2 was recently found to play an essential role in the secretion of zinc into milk. Heterozygous mutations of human ZnT2 (hZnT2), including H54R and G87R, in mothers result in low (>75% reduction) secretion of zinc into the breast milk, and infants fed on the milk develop transient neonatal zinc deficiency. We identified two novel missense mutations in the SLC30A2/ZnT2 gene in a Japanese mother with low milk zinc concentrations (>90% reduction) whose infant developed severe zinc deficiency; a T to C transition (c.454T>C) at exon 4, which substitutes a tryptophan residue with an arginine residue (W152R), and a C to T transition (c.887C>T) at exon 7, which substitutes a serine residue with a leucine residue (S296L). Biochemical characterization using zinc-sensitive DT40 cells indicated that the W152R mutation abolished the abilities to transport zinc and to form a dimer complex, indicating a loss-of-function mutation. The S296L mutation retained both abilities but was extremely destabilized. The two mutations were found on different alleles, indicating that the genotype of the mother with low milk zinc was compound heterozygous. These results show novel compound heterozygous mutations in the SLC30A2/ZnT2 gene causing zinc deficiency in a breast-fed infant.

  7. Compound Heterozygous Mutations in SLC30A2/ZnT2 Results in Low Milk Zinc Concentrations: A Novel Mechanism for Zinc Deficiency in a Breast-Fed Infant

    PubMed Central

    Itsumura, Naoya; Inamo, Yasuji; Okazaki, Fumiko; Teranishi, Fumie; Narita, Hiroshi; Kambe, Taiho; Kodama, Hiroko

    2013-01-01

    Zinc concentrations in breast milk are considerably higher than those of the maternal serum, to meet the infant's requirements for normal growth and development. Thus, effective mechanisms ensuring secretion of large amounts of zinc into the milk operate in mammary epithelial cells during lactation. ZnT2 was recently found to play an essential role in the secretion of zinc into milk. Heterozygous mutations of human ZnT2 (hZnT2), including H54R and G87R, in mothers result in low (>75% reduction) secretion of zinc into the breast milk, and infants fed on the milk develop transient neonatal zinc deficiency. We identified two novel missense mutations in the SLC30A2/ZnT2 gene in a Japanese mother with low milk zinc concentrations (>90% reduction) whose infant developed severe zinc deficiency; a T to C transition (c.454T>C) at exon 4, which substitutes a tryptophan residue with an arginine residue (W152R), and a C to T transition (c.887C>T) at exon 7, which substitutes a serine residue with a leucine residue (S296L). Biochemical characterization using zinc-sensitive DT40 cells indicated that the W152R mutation abolished the abilities to transport zinc and to form a dimer complex, indicating a loss-of-function mutation. The S296L mutation retained both abilities but was extremely destabilized. The two mutations were found on different alleles, indicating that the genotype of the mother with low milk zinc was compound heterozygous. These results show novel compound heterozygous mutations in the SLC30A2/ZnT2 gene causing zinc deficiency in a breast-fed infant. PMID:23741301

  8. Non-invasive detection of iron deficiency by fluorescence measurement of erythrocyte zinc protoporphyrin in the lip

    PubMed Central

    Hennig, Georg; Homann, Christian; Teksan, Ilknur; Hasbargen, Uwe; Hasmüller, Stephan; Holdt, Lesca M.; Khaled, Nadia; Sroka, Ronald; Stauch, Thomas; Stepp, Herbert; Vogeser, Michael; Brittenham, Gary M.

    2016-01-01

    Worldwide, more individuals have iron deficiency than any other health problem. Most of those affected are unaware of their lack of iron, in part because detection of iron deficiency has required a blood sample. Here we report a non-invasive method to optically measure an established indicator of iron status, red blood cell zinc protoporphyrin, in the microcirculation of the lower lip. An optical fibre probe is used to illuminate the lip and acquire fluorescence emission spectra in ∼1 min. Dual-wavelength excitation with spectral fitting is used to distinguish the faint zinc protoporphyrin fluorescence from the much greater tissue background fluorescence, providing immediate results. In 56 women, 35 of whom were iron-deficient, the sensitivity and specificity of optical non-invasive detection of iron deficiency were 97% and 90%, respectively. This fluorescence method potentially provides a rapid, easy to use means for point-of-care screening for iron deficiency in resource-limited settings lacking laboratory infrastructure. PMID:26883939

  9. [Interaction among the trace elements zinc, copper and iron after depletion and repletion of dairy cows with zinc].

    PubMed

    Kirchgessner, M; Schwarz, F J; Roth, H P; Schwarz, W A

    1978-12-01

    Imbalances in the supply with trace elements may be caused by the excessive administration of one or several elements or the insufficient administration in relation to other trace elements. This article deals with the interactions between the trace elements zinc and copper resp. zinc and iron under the conditions of the insufficient supply with Zn (6 mg per kg dry matter of the fodder) and the supply according to the demand with other trace elements (14 mg copper resp. 83 mg iron per dry matter of the fodder). For this purpose we investigated the copper, iron and zinc content of the milk and the serum of cows that were first depleted of zinc through a semi-synthetic zinc deficiency diet and then repleted with extra allowances of zinc. The closest connections exist between the copper and zinc content of the milk. Thus extreme Zn-deficiency feeding conditions the decreased Zn-content on the one hand and increased Cu-content on the other. In contrast to this, the cows' Zn-excretion in the milk increases after Zn-repletion whereas the Cu-content decreases. This shows a distinctly negative correlation. A loose connection could only be detected for the Cu- and Zn-content of the serum. Though the Zn-content changed considerably in dependence on the Zn-supply, the Cu-content remained largely uninfluenced. The Fe-content of both milk and serum shows no interaction with the nutritive Zn-supply. Only after 19 test weeks of extreme Zn-deficiency could a slight increase of the Fe-concentration be indicated.

  10. Overexpression of inducible nitric oxide synthase and cyclooxygenase-2 in rat zinc-deficient lung: Involvement of a NF-kappaB dependent pathway.

    PubMed

    Gomez, Nidia N; Davicino, Roberto C; Biaggio, Veronica S; Bianco, German A; Alvarez, Silvina M; Fischer, Patricia; Masnatta, Lucas; Rabinovich, Gabriel A; Gimenez, María S

    2006-02-01

    Reactive oxygen and nitrogen species have been implicated in the pathogenesis of pulmonary diseases. The goal of this study was to measure the response of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 enzymes (COX-2) in lung with moderate zinc deficiency. Adult male Wistar rats were divided into two groups receiving (1) a zinc-deficient diet (ZD) or (2) a zinc-adequate control diet. After 2 months of treatment, the zinc-deficient group showed a significant pulmonary edema. This was associated to a reduction of protein thiols and to a significant increase of metallothionein and glutathione disulfide levels. In addition, a higher serum and lung NO production in ZD group was positively related to the higher activity and expression of iNOS and COX-2 found in lungs. Western blot analysis revealed increased IkappaBalpha degradation, an indicator of NF-kappaB activation in ZD lungs. Anatomopathologic analysis of ZD lungs showed an increase of connective tissue fibers with an influx of polymorphonuclear cells. These cells and type II cells from the alveoli showed specific immunohistochemical signals for iNOS. The conclusion is that, during the development of zinc-deficiency, iNOS activity increases in lung and contributes to lung injury. Zinc deficiency implications must be taken into account to design therapies and public health interventions involving targeted zinc supplementation for high-risk subjects or certain diseases, such as asthma.

  11. The prevalence of low serum zinc and copper levels and dietary habits associated with serum zinc and copper in 12- to 36-month-old children from low-income families at risk for iron deficiency.

    PubMed

    Schneider, Julie M; Fujii, Mary L; Lamp, Catherine L; Lönnerdal, Bo; Zidenberg-Cherr, Sheri

    2007-11-01

    Iron and zinc share common food sources, and children at risk of iron deficiency may also develop zinc deficiency. We determined the prevalence of zinc and copper deficiency and examined factors associated with serum zinc and copper in young children from low-income families at risk of iron deficiency. A cross-sectional study design was used to assess serum zinc and copper, along with an interview-assisted survey to assess factors associated with serum zinc and copper in a convenience sample. Participants were 435 children aged 12 to 36 months recruited from select clinics of the Special Supplemental Nutrition Program for Women, Infants, and Children in Contra Costa and Tulare Counties, California. Frequencies were used to report prevalence. Multiple linear regressions were conducted to examine factors associated with serum zinc and copper, controlling for age, sex, and ethnicity. The prevalence of low serum zinc level (<70 microg/dL [<10.7 micromol/L]) was 42.8%, and low serum copper level (<90 microg/dL [<14.2 micromol/L]) was <1%. Mean+/-standard deviation of serum copper was 150+/-22 microg/dL (23.6+/-3.5 micromol/L) and 140+/-24 microg/dL (22.1+/-3.8 micromol/L) for anemic and non-anemic children, respectively (t test, P=0.026). In multiple linear regression consumption of sweetened beverages was negatively associated with serum zinc level, and consumption of >15 g/day meat was positively associated with serum zinc level, whereas current consumption of breast milk and >15 g/day beans were positively associated with serum copper level. The prevalence of low serum zinc concentration in the sample was high, and warrants further investigation amongst vulnerable populations.

  12. Micronutrient supplementation adherence and influence on the prevalences of anemia and iron, zinc and vitamin A deficiencies in preemies with a corrected age of six months

    PubMed Central

    de Freitas, Brunnella Alcantara Chagas; Lima, Luciana Moreira; Moreira, Maria Elisabeth Lopes; Priore, Silvia Eloiza; Henriques, Bruno David; Carlos, Carla Fernanda Lisboa Valente; Sabino, Jusceli Souza Nogueira; do Carmo Castro Franceschini, Sylvia

    2016-01-01

    OBJECTIVE: To analyze adherence to the recommended iron, zinc and multivitamin supplementation guidelines for preemies, the factors associated with this adherence, and the influence of adherence on the occurrence of anemia and iron, zinc and vitamin A deficiencies. METHODS: This prospective cohort study followed 58 preemies born in 2014 until they reached six months corrected age. The preemies were followed at a referral secondary health service and represented 63.7% of the preterm infants born that year. Outcomes of interest included high or low adherence to iron, zinc and multivitamin supplementation guidelines; prevalence of anemia; and prevalences of iron, zinc, and vitamin A deficiencies. The prevalence ratios were calculated by Poisson regression. RESULTS: Thirty-eight (65.5%) preemies presented high adherence to micronutrient supplementation guidelines. At six months of corrected age, no preemie had vitamin A deficiency. The prevalences of anemia, iron deficiency and zinc deficiency were higher in the low-adherence group but also concerning in the high-adherence group. Preemies with low adherence to micronutrient supplementation guidelines were 2.5 times more likely to develop anemia and 3.1 times more likely to develop zinc deficiency. Low maternal education level increased the likelihood of nonadherence to all three supplements by 2.2 times. CONCLUSIONS: Low maternal education level was independently associated with low adherence to iron, zinc and vitamin A supplementation guidelines in preemies, which impacted the prevalences of anemia and iron and zinc deficiencies at six months of corrected age. PMID:27626474

  13. Zinc deficiency exacerbates while zinc supplement attenuates cardiac hypertrophy in high-fat diet-induced obese mice through modulating p38 MAPK-dependent signaling.

    PubMed

    Wang, Shudong; Luo, Manyu; Zhang, Zhiguo; Gu, Junlian; Chen, Jing; Payne, Kristen McClung; Tan, Yi; Wang, Yuehui; Yin, Xia; Zhang, Xiang; Liu, Gilbert C; Wintergerst, Kupper; Liu, Quan; Zheng, Yang; Cai, Lu

    2016-09-06

    Childhood obesity often leads to cardiovascular diseases, such as obesity-related cardiac hypertrophy (ORCH), in adulthood, due to chronic cardiac inflammation. Zinc is structurally and functionally essential for many transcription factors; however, its role in ORCH and underlying mechanism(s) remain unclear and were explored here in mice with obesity induced with high-fat diet (HFD). Four week old mice were fed on either HFD (60%kcal fat) or normal diet (ND, 10% kcal fat) for 3 or 6 months, respectively. Either diet contained one of three different zinc quantities: deficiency (ZD, 10mg zinc per 4057kcal), normal (ZN, 30mg zinc per 4057kcal) or supplement (ZS, 90mg zinc per 4057kcal). HFD induced a time-dependent obesity and ORCH, which was accompanied by increased cardiac inflammation and p38 MAPK activation. These effects were worsened by ZD in HFD/ZD mice and attenuated by ZS in HFD/ZS group, respectively. Also, administration of a p38 MAPK specific inhibitor in HFD mice for 3 months did not affect HFD-induced obesity, but completely abolished HFD-induced, and zinc deficiency-worsened, ORCH and cardiac inflammation. In vitro exposure of adult cardiomyocytes to palmitate induced cell hypertrophy accompanied by increased p38 MAPK activation, which was heightened by zinc depletion with its chelator TPEN. Inhibition of p38 MAPK with its specific siRNA also prevented the effects of palmitate on cardiomyocytes. These findings demonstrate that ZS alleviates but ZD heightens cardiac hypertrophy in HFD-induced obese mice through suppressing p38 MAPK-dependent cardiac inflammatory and hypertrophic pathways. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

  14. Zinc deficiency reduces bone mineral density in the spine of young adult rats: a pilot study.

    PubMed

    Ryz, Natasha R; Weiler, Hope A; Taylor, Carla G

    2009-01-01

    The objective of this study was to investigate the effects of zinc deficiency initiated during adolescence on skeletal densitometry, serum markers of bone metabolism, femur minerals and morphometry in young adult rats. Ten-week-old male rats were fed a <1-mg Zn/kg diet (9ZD), a 5-mg Zn/kg diet (9MZD) or a 30-mg Zn/kg diet (9CTL) for up to 9 weeks. Analyses included bone mineral density, serum osteocalcin and C-terminal peptides of type I collagen, serum zinc, femur zinc, calcium and phosphorus, and femur morphometry. Bone mineral density was 14% lower in the spine of 9ZD, but was not altered in the whole body, tibia or femur, or in any of the aforementioned sites in 9MZD, compared to 9CTL. When adjusted for size, spine bone mineral apparent density was still 8% lower in 9ZD than 9CTL. Serum osteocalcin, a marker for bone formation, was approximately 33% lower in 9ZD compared to both 9MZD and 9CTL. The 9ZD and 9MZD had 57% lower femur zinc and 56-88% lower serum zinc concentrations compared to 9CTL. These findings indicate that severe zinc deficiency initiated during adolescence may have important implications for future bone health, especially with regards to bone consolidation in the spine. 2009 S. Karger AG, Basel.

  15. Relationship between zinc malnutrition and alterations in murine peripheral blood leukocytes

    SciTech Connect

    King, L.E.; Morford, L.A.; Fraker, P.J.

    1991-03-15

    Studies using a murine model have shown that the immune system responds rapidly and adversely to zinc deficiency. The extent of alteration of peripheral blood leukocytes (PBL) and immunoglobulin levels were investigated in four zinc dietary groups: zinc adequate (ZA); restricted fed zinc adequate (RZA); marginal zinc deficient (MZD, 72-76% of ZA mouse weight); and severely zinc deficient. The peripheral white blood cell count was 3.66 {plus minus} 1.08 {times} 10{sup 6} cells/ml for ZA mice decreasing by 21%, 28% and 54% for RZA, MZD and SZD mice respectively. An equally dramatic change in the flow cytometric light scatter profilemore » was found. ZA mice had 66% lymphocytes and 21% polymorphonuclear granulocytes (PMN) in their peripheral blood while MZD and SZD mice contained 43% and 30% lymphocytes and 40% and 60% PMNs respectively. Analysis of the phenotypic distribution of specific classes of lymphocytes revealed ZA blood contained 25% B-cells and 40% T-cells (CD5{sup +}). B-cells decreased 40-50% for RZA and MZD mice and 60-70% for SZD mice. The decline in CD5{sup +} T-cells was more modest at 30% and 45% for MZD and SZD mice. A nearly 40% decline in both T{sub h} and T{sub c/s} cells was noted for both MZD and SZD mice. Radioimmunoassay of serum for changes in IgM and IgG content revealed no change among dietary groups while serum zinc decreased 10% for RZA mice and 50% for both MZD and SZD mice. The authors conclude that peripheral blood differential counts in concert with total B and T-cell phenotype may serve as indicators of zinc status while serum zinc and Ig will not.« less

  16. Association of Mood Disorders with Serum Zinc Concentrations in Adolescent Female Students.

    PubMed

    Tahmasebi, Kobra; Amani, Reza; Nazari, Zahra; Ahmadi, Kambiz; Moazzen, Sara; Mostafavi, Seyed-Ali

    2017-08-01

    Among various factors influencing mood disorders, the impact of micronutrient deficiencies has attracted a great attention. Zinc deficiency is considered to play a crucial role in the onset and progression of mood disorders in different stages of life. The main objective of this study was to assess the correlation between serum zinc levels and mood disorders in high school female students. This cross-sectional study was conducted on a random sample of 100 representative high school female students. The participants completed 24-h food recall questionnaires to assess the daily zinc intakes. Serum zinc status was assessed using flame atomic absorption spectrometry, and zinc deficiency was defined accordingly. Mood disorders were estimated by calculating the sum of two test scores including Beck's depression inventory (BDI) and hospital anxiety depression scale (HADS) tests. General linear model (GLM) and Pearson's regression test were applied to show the correlation of serum zinc levels and mood disorder scores and the correlation between zinc serum levels and BDI scores, respectively. Dietary zinc intake was higher in subjects with normal zinc concentrations than that of zinc-deficient group (p = 0.001). Serum zinc levels were inversely correlated with BDI and HADS scores (p < 0.05). Each 10 μg/dL increment in serum zinc levels led to 0.3 and 0.01 decrease in depression and anxiety scores, respectively (p < 0.05). Serum zinc levels were inversely correlated with mood disorders including depression and anxiety in adolescent female students. Increasing serum levels of zinc in female students could improve their mood disorders.

  17. The Potential for Zinc Stable Isotope Techniques and Modelling to Determine Optimal Zinc Supplementation

    PubMed Central

    Tran, Cuong D.; Gopalsamy, Geetha L.; Mortimer, Elissa K.; Young, Graeme P.

    2015-01-01

    It is well recognised that zinc deficiency is a major global public health issue, particularly in young children in low-income countries with diarrhoea and environmental enteropathy. Zinc supplementation is regarded as a powerful tool to correct zinc deficiency as well as to treat a variety of physiologic and pathologic conditions. However, the dose and frequency of its use as well as the choice of zinc salt are not clearly defined regardless of whether it is used to treat a disease or correct a nutritional deficiency. We discuss the application of zinc stable isotope tracer techniques to assess zinc physiology, metabolism and homeostasis and how these can address knowledge gaps in zinc supplementation pharmacokinetics. This may help to resolve optimal dose, frequency, length of administration, timing of delivery to food intake and choice of zinc compound. It appears that long-term preventive supplementation can be administered much less frequently than daily but more research needs to be undertaken to better understand how best to intervene with zinc in children at risk of zinc deficiency. Stable isotope techniques, linked with saturation response and compartmental modelling, also have the potential to assist in the continued search for simple markers of zinc status in health, malnutrition and disease. PMID:26035248

  18. GC-MS analysis of headspace and liquid extracts for metabolomic differentiation of citrus Huanglongbing and zinc deficiency in leaves of 'Valencia' sweet orange from commercial groves.

    PubMed

    Cevallos-Cevallos, Juan Manuel; García-Torres, Rosalía; Etxeberria, Edgardo; Reyes-De-Corcuera, José Ignacio

    2011-01-01

    Citrus Huanglongbing (HLB) is considered the most destructive citrus disease worldwide. Symptoms-based detection of HLB is difficult due to similarities with zinc deficiency. To find metabolic differences between leaves from HLB-infected, zinc-deficient, and healthy 'Valencia' orange trees by using GC-MS based metabolomics. Analysis based on GC-MS methods for untargeted metabolite analysis of citrus leaves was developed and optimized. Sample extracts from healthy, zinc deficient, or HLB-infected sweet orange leaves were submitted to headspace solid phase micro-extraction (SPME) and derivatization treatments prior to GC-MS analysis. Principal components analysis achieved correct classification of all the derivatized liquid extracts. Analysis of variance revealed 6 possible biomarkers for HLB, of which 5 were identified as proline, β-elemene, (-)trans- caryophyllene, and α-humulene. Significant (P < 0.05) differences in oxo-butanedioic acid, arabitol, and neo-inositol were exclusively detected in samples from plants with zinc deficiency. Levels of isocaryophyllen, α-selinene, β-selinene, and fructose were significantly (P < 0.05) different in healthy leaves only. Results suggest the potential of using identified HLB biomarkers for rapid differentiation of HLB from zinc deficiency. Copyright © 2010 John Wiley & Sons, Ltd.

  19. Role of nutritional zinc in the prevention of osteoporosis.

    PubMed

    Yamaguchi, Masayoshi

    2010-05-01

    Zinc is known as an essential nutritional factor in the growth of the human and animals. Bone growth retardation is a common finding in various conditions associated with dietary zinc deficiency. Bone zinc content has been shown to decrease in aging, skeletal unloading, and postmenopausal conditions, suggesting its role in bone disorder. Zinc has been demonstrated to have a stimulatory effect on osteoblastic bone formation and mineralization; the metal directly activates aminoacyl-tRNA synthetase, a rate-limiting enzyme at translational process of protein synthesis, in the cells, and it stimulates cellular protein synthesis. Zinc has been shown to stimulate gene expression of the transcription factors runt-related transcription factor 2 (Runx2) that is related to differentiation into osteoblastic cells. Moreover, zinc has been shown to inhibit osteoclastic bone resorption due to inhibiting osteoclast-like cell formation from bone marrow cells and stimulating apoptotic cell death of mature osteoclasts. Zinc has a suppressive effect on the receptor activator of nuclear factor (NF)-kappaB ligand (RANKL)-induced osteoclastogenesis. Zinc transporter has been shown to express in osteoblastic and osteoclastic cells. Zinc protein is involved in transcription. The intake of dietary zinc causes an increase in bone mass. beta-Alanyl-L: -histidinato zinc (AHZ) is a zinc compound, in which zinc is chelated to beta-alanyl-L: -histidine. The stimulatory effect of AHZ on bone formation is more intensive than that of zinc sulfate. Zinc acexamate has also been shown to have a potent-anabolic effect on bone. The oral administration of AHZ or zinc acexamate has the restorative effect on bone loss under various pathophysiologic conditions including aging, skeletal unloading, aluminum bone toxicity, calcium- and vitamin D-deficiency, adjuvant arthritis, estrogen deficiency, diabetes, and fracture healing. Zinc compounds may be designed as new supplementation factor in the prevention and

  20. Effects of zinc deficiency and supplementation on leptin and leptin receptor expression in pregnant mice.

    PubMed

    Ueda, Hidenori; Nakai, Taketo; Konishi, Tatsuya; Tanaka, Keiichi; Sakazaki, Fumitoshi; Min, Kyong-Son

    2014-01-01

    Leptin is an adipose-derived hormone that primarily regulates energy balance in response to nutrition. Human placental cells produce leptin, whereas murine placental cells produce soluble leptin receptors (Ob-R). However, the roles of these proteins during pregnancy have not been elucidated completely. As an essential metal, zinc (Zn) is central to insulin biosynthesis and energy metabolism. In the present study, the effects of Zn deficiency and supplementation on maternal plasma leptin and soluble Ob-R regulation in pregnant mice placentas were examined using enzyme-linked immunosorbent assay, reverse transcription-polymerase chain reaction, and Western blotting. Nutritional Zn deficiency significantly reduced plasma insulin concentrations and fetal and placental weights in pregnant mice. Plasma leptin concentrations in pregnant mice also increased 20- to 40-fold compared with those in non-pregnant mice. Although dietary Zn deficiency and supplementation did not affect plasma leptin concentrations in non-pregnant mice, Zn-deficient pregnant mice had significantly reduced plasma leptin concentrations and adipose leptin mRNA expression. In contrast, Zn-supplemented pregnant mice had increased plasma leptin concentrations without increased adipose leptin mRNA expression. Placental soluble Ob-R mRNA expression also decreased in Zn-deficient mice and tended to increase in Zn-supplemented mice. These results indicate that Zn influences plasma leptin concentrations by modulating mRNA expression of soluble Ob-R in the placenta, and leptin in visceral fat during pregnancy. These data suggest that both adipose and placenta-derived leptin system are involved in the regulation of energy metabolism during fetal growth.

  1. Dietary zinc deficiency reduced growth performance, intestinal immune and physical barrier functions related to NF-κB, TOR, Nrf2, JNK and MLCK signaling pathway of young grass carp (Ctenopharyngodon idella).

    PubMed

    Song, Zheng-Xing; Jiang, Wei-Dan; Liu, Yang; Wu, Pei; Jiang, Jun; Zhou, Xiao-Qiu; Kuang, Sheng-Yao; Tang, Ling; Tang, Wu-Neng; Zhang, Yong-An; Feng, Lin

    2017-07-01

    Our study investigated the effects of dietary zinc (Zn) deficiency on growth performance, intestinal immune and physical barrier functions of young grass carp (Ctenopharyngodon idella). A total of 630 grass carp (244.14 ± 0.40 g) were fed graded levels of zinc lactate (10.71, 30.21, 49.84, 72.31, 92.56, 110.78 mg Zn/kg diet) and one zinc sulfate group (56.9 mg Zn/kg diet) for 60 days. At the end of the feeding trial, fish were challenged with Aeromonas hydrophila for 14 days. These results indicated that compared with optimal dietary Zn level, dietary Zn deficiency (10.71 mg/kg diet) decreased the production of antibacterial compounds, up-regulated pro-inflammatory cytokines related to nuclear factor kappa B (NF-κB) and down-regulated anti-inflammatory cytokines related to target of rapamycin (TOR) in three intestinal segments of young grass carp (P < 0.05), suggesting that dietary Zn deficiency could impair intestinal immune barrier of fish; decreased the activities and mRNA levels of antioxidant enzymes related to NF-E2-related factor 2 (Nrf2), up-regulated the mRNA levels of caspase-3, -7, -8, -9 related to p38 mitogen activated protein (p38 MAPK) and c-Jun N-terminal protein kinase (JNK), down-regulated the mRNA levels of tight junction complexes (TJs) related to myosin light chain kinase (MLCK) in three intestinal segments of young grass carp (P < 0.05), demonstrating that dietary Zn deficiency could injury intestinal physical barrier of fish. Besides, the Zn requirements (zinc lactate as Zn source) based on percent weight gain (PWG), against enteritis morbidity, acid phosphatase (ACP) activity in the proximal intestine (PI) and malondialdehyde (MDA) content in the PI of young grass carp was estimated to be 61.2, 61.4, 69.2 and 69.5 mg/kg diet, respectively. Finally, based on specific growth rate (SGR), feed efficiency (FE) and against enteritis morbidity of young grass carp, the efficacy of zinc lactate relative to zinc sulfate were 132.59%, 135

  2. Oral Zinc Supplementation Decreases the Serum Iron Concentration in Healthy Schoolchildren: A Pilot Study

    PubMed Central

    de Brito, Naira Josele Neves; de Medeiros Rocha, Érika Dantas; de Araújo Silva, Alfredo; Costa, João Batista Sousa; França, Mardone Cavalcante; das Graças Almeida, Maria; Brandão-Neto, José

    2014-01-01

    The recognized antagonistic actions between zinc and iron prompted us to study this subject in children. A convenience sample was used. Thirty healthy children between 8 and 9 years of age were studied with the aim of establishing the effect of a 3-mo oral zinc supplementation on iron status. Fifteen individuals were given a placebo (control group), and 15 were given 10 mg Zn/day (experimental group). Blood samples were collected at 0, 60, 120, 180 and 210 min after a 12-h overnight fast, before and after placebo or zinc supplementation. This supplementation was associated with significant improvements in energy, protein, fat, carbohydrate, fiber, calcium, iron, and zinc intake in accordance with the recommendations for age and sex. The basal serum zinc concentration significantly increased after oral zinc supplementation (p < 0.001). However, basal serum iron concentrations and area under the iron curves significantly decreased in the experimental group (p < 0.0001) and remained at the same level throughout the 210-min study. The values obtained for hemoglobin, mean corpuscular volume, ferritin, transferrin, transferrin saturation, ceruloplasmin and total protein were within normal reference ranges. In conclusion, the decrease in serum iron was likely due to the effects of chronic zinc administration, and the decrease in serum iron was not sufficient to cause anemia. PMID:25192026

  3. Zinc and Wound Healing: A Review of Zinc Physiology and Clinical Applications.

    PubMed

    Kogan, Samuel; Sood, Aditya; Garnick, Mark S

    2017-04-01

    Our understanding of the role of zinc in normal human physiology is constantly expanding, yet there are major gaps in our knowledge with regard to the function of zinc in wound healing. This review aims to provide the clinician with sufficient understanding of zinc biology and an up-to-date perspective on the role of zinc in wound healing. Zinc is an essential ion that is crucial for maintenance of normal physiology, and zinc deficiency has many manifestations ranging from delayed wound healing to immune dysfunction and impairment of multiple sensory systems. While consensus has been reached regarding the detrimental effects of zinc deficiency on wound healing, there is considerable discord in the literature on the optimal methods and true benefits of zinc supplementation.

  4. Galvanizing action: conclusions and next steps for mainstreaming zinc interventions in public health programs.

    PubMed

    Brown, Kenneth H; Baker, Shawn K

    2009-03-01

    This paper summarizes the results of the foregoing reviews of the impact of different intervention strategies designed to enhance zinc nutrition, including supplementation, fortification, and dietary diversification or modification. Current evidence indicates a beneficial impact of such interventions on zinc status and zinc-related functional outcomes. Preventive zinc supplementation reduces the incidence of diarrhea and acute lower respiratory tract infection among young children, decreases mortality of children over 12 months of age, and increases growth velocity. Therapeutic zinc supplementation during episodes of diarrhea reduces the duration and severity of illness. Zinc fortification increases zinc intake and total absorbed zinc, and recent studies are beginning to confirm a positive impact of zinc fortification on indicators of population zinc status. To assist with the development of zinc intervention programs, more information is needed on the prevalence of zinc deficiency in different countries, and rigorous evaluations of the effectiveness of large-scale zinc intervention programs should be planned. Recommended steps for scaling up zinc intervention programs, with or without other micronutrients, are described. In summary, there is now clear evidence of the benefit of selected interventions to reduce the risk of zinc deficiency, and a global commitment is urgently needed to conduct systematic assessments of population zinc status and to develop interventions to control zinc deficiency in the context of existing public health and nutrition programs.

  5. Interactions of iron with manganese, zinc, chromium, and selenium as related to prophylaxis and treatment of iron deficiency.

    PubMed

    Bjørklund, Geir; Aaseth, Jan; Skalny, Anatoly V; Suliburska, Joanna; Skalnaya, Margarita G; Nikonorov, Alexandr A; Tinkov, Alexey A

    2017-05-01

    Iron (Fe) deficiency is considered as the most common nutritional deficiency. Iron deficiency is usually associated with low Fe intake, blood loss, diseases, poor absorption, gastrointestinal parasites, or increased physiological demands as in pregnancy. Nutritional Fe deficiency is usually treated with Fe tablets, sometimes with Fe-containing multimineral tablets. Trace element interactions may have a significant impact on Fe status. Existing data demonstrate a tight interaction between manganese (Mn) and Fe, especially in Fe-deficient state. The influence of Mn on Fe homeostasis may be mediated through its influence on Fe absorption, circulating transporters like transferrin, and regulatory proteins. The existing data demonstrate that the influence of zinc (Zn) on Fe status may be related to their competition for metal transporters. Moreover, Zn may be involved in regulation of hepcidin production. At the same time, human data on the interplay between Fe and Zn especially in terms of Fe-deficiency and supplementation are contradictory, demonstrating both positive and negative influence of Zn on Fe status. Numerous data also demonstrate the possibility of competition between Fe and chromium (Cr) for transferrin binding. At the same time, human data on the interaction between these metals are contradictory. Therefore, while managing hypoferremia and Fe-deficiency anemia, it is recommended to assess the level of other trace elements in parallel with indices of Fe homeostasis. It is supposed that simultaneous correction of trace element status in Fe deficiency may help to decrease possible antagonistic or increase synergistic interactions. Copyright © 2017 Elsevier GmbH. All rights reserved.

  6. SLAP deficiency decreases dsDNA autoantibody production

    PubMed Central

    Peterson, Lisa K.; Pennington, Luke F.; Shaw, Laura A.; Brown, Meredith; Treacy, Eric C.; Friend, Samantha F.; Hatlevik, Øyvind; Rubtsova, Kira; Rubtsov, Anatoly V.; Dragone, Leonard L.

    2014-01-01

    Src-like adaptor protein (SLAP) adapts c-Cbl, an E3 ubiquitin ligase, to activated components of the BCR signaling complex regulating BCR levels and signaling in developing B cells. Based on this function, we asked whether SLAP deficiency could decrease the threshold for tolerance and eliminate development of autoreactive B cells in two models of autoantibody production. First, we sensitized mice with a dsDNA mimetope that causes an anti-dsDNA response. Despite equivalent production of anti-peptide antibodies compared to BALB/c controls, SLAP−/− mice did not produce anti-dsDNA. Second, we used the 56R tolerance model. SLAP−/− 56R mice had decreased levels of dsDNA-reactive antibodies compared to 56R mice due to skewed light chain usage. Thus, SLAP is a critical regulator of B-cell development and function and its deficiency leads to decreased autoreactive B cells that are otherwise maintained by inefficient receptor editing or failed negative selection. PMID:24440645

  7. SLAP deficiency decreases dsDNA autoantibody production.

    PubMed

    Peterson, Lisa K; Pennington, Luke F; Shaw, Laura A; Brown, Meredith; Treacy, Eric C; Friend, Samantha F; Hatlevik, Øyvind; Rubtsova, Kira; Rubtsov, Anatoly V; Dragone, Leonard L

    2014-02-01

    Src-like adaptor protein (SLAP) adapts c-Cbl, an E3 ubiquitin ligase, to activated components of the BCR signaling complex regulating BCR levels and signaling in developing B cells. Based on this function, we asked whether SLAP deficiency could decrease the threshold for tolerance and eliminate development of autoreactive B cells in two models of autoantibody production. First, we sensitized mice with a dsDNA mimetope that causes an anti-dsDNA response. Despite equivalent production of anti-peptide antibodies compared to BALB/c controls, SLAP(-/-) mice did not produce anti-dsDNA. Second, we used the 56R tolerance model. SLAP(-/-) 56R mice had decreased levels of dsDNA-reactive antibodies compared to 56R mice due to skewed light chain usage. Thus, SLAP is a critical regulator of B-cell development and function and its deficiency leads to decreased autoreactive B cells that are otherwise maintained by inefficient receptor editing or failed negative selection. Copyright © 2013 Elsevier Inc. All rights reserved.

  8. Zinc and its importance for human health: An integrative review

    PubMed Central

    Roohani, Nazanin; Hurrell, Richard; Kelishadi, Roya; Schulin, Rainer

    2013-01-01

    Since its first discovery in an Iranian male in 1961, zinc deficiency in humans is now known to be an important malnutrition problem world-wide. It is more prevalent in areas of high cereal and low animal food consumption. The diet may not necessarily be low in zinc, but its bio-availability plays a major role in its absorption. Phytic acid is the main known inhibitor of zinc. Compared to adults, infants, children, adolescents, pregnant, and lactating women have increased requirements for zinc and thus, are at increased risk of zinc depletion. Zinc deficiency during growth periods results in growth failure. Epidermal, gastrointestinal, central nervous, immune, skeletal, and reproductive systems are the organs most affected clinically by zinc deficiency. Clinical diagnosis of marginal Zn deficiency in humans remains problematic. So far, blood plasma/serum zinc concentration, dietary intake, and stunting prevalence are the best known indicators of zinc deficiency. Four main intervention strategies for combating zinc deficiency include dietary modification/diversification, supplementation, fortification, and bio-fortification. The choice of each method depends on the availability of resources, technical feasibility, target group, and social acceptance. In this paper, we provide a review on zinc biochemical and physiological functions, metabolism including, absorption, excretion, and homeostasis, zinc bio-availability (inhibitors and enhancers), human requirement, groups at high-risk, consequences and causes of zinc deficiency, evaluation of zinc status, and prevention strategies of zinc deficiency. PMID:23914218

  9. Silicon addition to soybean (Glycine max L.) plants alleviate zinc deficiency.

    PubMed

    Pascual, Ma Blanca; Echevarria, Virginia; Gonzalo, Ma José; Hernández-Apaolaza, Lourdes

    2016-11-01

    It is well established the beneficial role of silicon (Si) in alleviating abiotic stress. However, it remains poorly understood the mechanisms of the Si-mediated protection against metal deficiency, especially the zinc (Zn) one. Recently, it has been proposed that Si may act by an interaction with this biometal in the root apoplast contributing to its movement through the plant, as in the case of Fe deficiency. In the present work, the effect of initial or continuous Si doses in soybean Zn deficient plants has been studied. For that purpose, plants grown in hydroponic culture were treated with different Si doses (0.0, 0.5 and 1.0 mM) under Zn limiting conditions. SPAD index in leaves, several growth parameters, mineral content in the whole plant and the formation of Zn pools in roots were determined. An initial addition of 0.5 mM of Si to the nutrient solution led to an enhancement of plants growth, Zn and Si content in leaves, and a higher storage of Zn in the root apoplast. The results suggest that this treatment enhanced Zn accumulation on roots and its movement to shoots when needed, mitigating Zn deficiency symptoms. Copyright © 2016 Elsevier Masson SAS. All rights reserved.

  10. Characterization of the response to zinc deficiency in the cyanobacterium Anabaena sp. strain PCC 7120.

    PubMed

    Napolitano, Mauro; Rubio, Miguel Ángel; Santamaría-Gómez, Javier; Olmedo-Verd, Elvira; Robinson, Nigel J; Luque, Ignacio

    2012-05-01

    Zur regulators control zinc homeostasis by repressing target genes under zinc-sufficient conditions in a wide variety of bacteria. This paper describes how part of a survey of duplicated genes led to the identification of the open reading frame all2473 as the gene encoding the Zur regulator of the cyanobacterium Anabaena sp. strain PCC 7120. All2473 binds to DNA in a zinc-dependent manner, and its DNA-binding sequence was characterized, which allowed us to determine the relative contribution of particular nucleotides to Zur binding. A zur mutant was found to be impaired in the regulation of zinc homeostasis, showing sensitivity to elevated concentrations of zinc but not other metals. In an effort to characterize the Zur regulon in Anabaena, 23 genes containing upstream putative Zur-binding sequences were identified and found to be regulated by Zur. These genes are organized in six single transcriptional units and six operons, some of them containing multiple Zur-regulated promoters. The identities of genes of the Zur regulon indicate that Anabaena adapts to conditions of zinc deficiency by replacing zinc metalloproteins with paralogues that fulfill the same function but presumably with a lower zinc demand, and with inducing putative metallochaperones and membrane transport systems likely being involved in the scavenging of extracellular zinc, including plasma membrane ABC transport systems and outer membrane TonB-dependent receptors. Among the Zur-regulated genes, the ones showing the highest induction level encode proteins of the outer membrane, suggesting a primary role for components of this cell compartment in the capture of zinc cations from the extracellular medium.

  11. Release of iron, zinc, and lead from common iron construction bars and zinc metallic bars in water solutions and meals.

    PubMed

    Lechtig, Aarón; Lòpez de Romaña, Daniel; Boy, Erick; Vargas, Alejandro; Rosas del Portal, Mauricio; Huaylinos, María Luisa

    2007-12-01

    The use of iron pots has decreased the prevalence of anemia. To investigate the release of iron, zinc, and lead from metallic iron and zinc bars incubated in water and in meals. Iron, zinc, and lead concentrations were measured at different incubation conditions in water and in meals. The iron concentration in water was 1.26 mg/L after incubation with one iron bar at pH 7 and 100 degrees C for 20 minutes and in meals was 0.97 mg per 100 g of wet meals, rich in phytate, cooking at 100 degrees C during 20 minutes. The maximum contents were 7720 mg/L of iron and 1826 mg/L of zinc in vinegar at pH 3 and 20 degrees C after 90 and 32 days, respectively. Lead was released from the bars, but at concentrations well below the upper tolerable limits. In outreach populations, the use of iron and zinc metallic bars in water and meals could contribute to sustainable, very low-cost prevention of iron and zinc deficiencies, and home-fortified vinegar could be used for treatment of both deficiencies. Field trials should be performed to determine the impact that the use of iron and zinc metallic bars in water and meals might have on the iron and zinc status of population groups.

  12. Zinc Absorption by Young Adults from Supplemental Zinc Citrate Is Comparable with That from Zinc Gluconate and Higher than from Zinc Oxide123

    PubMed Central

    Wegmüller, Rita; Tay, Fabian; Zeder, Christophe; Brnić, Marica; Hurrell, Richard F.

    2014-01-01

    The water-soluble zinc salts gluconate, sulfate, and acetate are commonly used as supplements in tablet or syrup form to prevent zinc deficiency and to treat diarrhea in children in combination with oral rehydration. Zinc citrate is an alternative compound with high zinc content, slightly soluble in water, which has better sensory properties in syrups but no absorption data in humans. We used the double-isotope tracer method with 67Zn and 70Zn to measure zinc absorption from zinc citrate given as supplements containing 10 mg of zinc to 15 healthy adults without food and compared absorption with that from zinc gluconate and zinc oxide (insoluble in water) using a randomized, double-masked, 3-way crossover design. Median (IQR) fractional absorption of zinc from zinc citrate was 61.3% (56.6–71.0) and was not different from that from zinc gluconate with 60.9% (50.6–71.7). Absorption from zinc oxide at 49.9% (40.9–57.7) was significantly lower than from both other supplements (P < 0.01). Three participants had little or no absorption from zinc oxide. We conclude that zinc citrate, given as a supplement without food, is as well absorbed by healthy adults as zinc gluconate and may thus be a useful alternative for preventing zinc deficiency and treating diarrhea. The more insoluble zinc oxide is less well absorbed when given as a supplement without food and may be minimally absorbed by some individuals. This trial was registered at clinicaltrials.gov as NCT01576627. PMID:24259556

  13. Leptin and zinc relation: In regulation of food intake and immunity

    PubMed Central

    Baltaci, Abdulkerim Kasim; Mogulkoc, Rasim

    2012-01-01

    Leptin is synthesized and released by the adipose tissue. Leptin, which carries the information about energy reserves of the body to the brain, controls food intake by acting on neuropeptide Y (NPY), which exercises a food-intake-increasing effect through relevant receptors in the hypothalamus. Zinc deficiency is claimed to result in anorexia, weight loss, poor food efficiency, and growth impairment. The fact that obese individuals have low zinc and high leptin levels suggests that there is a relation between zinc and nutrition, and consequently also between zinc and leptin. Leptin deficiency increases the predisposition to infections and this increase is associated with the impairments in the production of cytokines. Zinc has a key role in the sustenance of immune resistance against infections. Dietary zinc deficiency negatively affects CD+4 cells, Th functions, and consequently, cell-mediated immunity by causing a decrease in the production of IL-2, IF-γ, and TNF-α, which are Th1 products. The relation between zinc and the concerned cytokines in particular, and the fact that leptin has a part in the immune responses mediated by these cytokines demonstrate that an interaction among cellular immunity, leptin and zinc is inevitable. An overall evaluation of the information presented above suggests that there are complex relations among food intake, leptin and zinc on one hand and among cellular immunity, leptin and zinc on the other. The aim of the present review was to draw attention to the possible relation between zinc and leptin in dietary regulation and cellular immunity. PMID:23565497

  14. Association between Maternal Zinc Status, Dietary Zinc Intake and Pregnancy Complications: A Systematic Review

    PubMed Central

    Wilson, Rebecca L.; Grieger, Jessica A.; Bianco-Miotto, Tina; Roberts, Claire T.

    2016-01-01

    Adequate zinc stores in the body are extremely important during periods of accelerated growth. However, zinc deficiency is common in developing countries and low maternal circulating zinc concentrations have previously been associated with pregnancy complications. We reviewed current literature assessing circulating zinc and dietary zinc intake during pregnancy and the associations with preeclampsia (PE); spontaneous preterm birth (sPTB); low birthweight (LBW); and gestational diabetes (GDM). Searches of MEDLINE; CINAHL and Scopus databases identified 639 articles and 64 studies were reviewed. In 10 out of 16 studies a difference was reported with respect to circulating zinc between women who gave birth to a LBW infant (≤2500 g) and those who gave birth to an infant of adequate weight (>2500 g), particularly in populations where inadequate zinc intake is prevalent. In 16 of our 33 studies an association was found between hypertensive disorders of pregnancy and circulating zinc; particularly in women with severe PE (blood pressure ≥160/110 mmHg). No association between maternal zinc status and sPTB or GDM was seen; however; direct comparisons between the studies was difficult. Furthermore; only a small number of studies were based on women from populations where there is a high risk of zinc deficiency. Therefore; the link between maternal zinc status and pregnancy success in these populations cannot be established. Future studies should focus on those vulnerable to zinc deficiency and include dietary zinc intake as a measure of zinc status. PMID:27754451

  15. Diabetes-induced hepatic pathogenic damage, inflammation, oxidative stress, and insulin resistance was exacerbated in zinc deficient mouse model.

    PubMed

    Zhang, Chi; Lu, Xuemian; Tan, Yi; Li, Bing; Miao, Xiao; Jin, Litai; Shi, Xue; Zhang, Xiang; Miao, Lining; Li, Xiaokun; Cai, Lu

    2012-01-01

    Zinc (Zn) deficiency often occurs in the patients with diabetes. Effects of Zn deficiency on diabetes-induced hepatic injury were investigated. Type 1 diabetes was induced in FVB mice with multiple low-dose streptozotocin. Hyperglycemic and age-matched control mice were treated with and without Zn chelator, N,N,N',N'-tetrakis (2-pyridylemethyl) ethylenediamine (TPEN), at 5 mg/kg body-weight daily for 4 months. Hepatic injury was examined by serum alanine aminotransferase (ALT) level and liver histopathological and biochemical changes. Hepatic Zn deficiency (lower than control level, p<0.05) was seen in the mice with either diabetes or TPEN treatment and more evident in the mice with both diabetes and TPEN. Zn deficiency exacerbated hepatic injuries, shown by further increased serum ALT, hepatic lipid accumulation, inflammation, oxidative damage, and endoplasmic reticulum stress-related cell death in Diabetes/TPEN group compared to Diabetes alone. Diabetes/TPEN group also showed a significant decrease in nuclear factor-erythroid 2-related factor 2 (Nrf2) expression and transcription action along with significant increases in Akt negative regulators, decrease in Akt and GSK-3β phosphorylation, and increase in nuclear accumulation of Fyn (a Nrf2 negative regulator). In vitro study with HepG2 cells showed that apoptotic effect of TPEN at 0.5-1.0 µM could be completely prevented by simultaneous Zn supplementation at the dose range of 30-50 µM. Zn is required for maintaining Akt activation by inhibiting the expression of Akt negative regulators; Akt activation can inhibit Fyn nuclear translocation to export nuclear Nrf2 to cytoplasm for degradation. Zn deficiency significantly enhanced diabetes-induced hepatic injury likely through down-regulation of Nrf2 function.

  16. Zinc status in South Asian populations--an update.

    PubMed

    Akhtar, Saeed

    2013-06-01

    This article attempts to highlight the prevalence of zinc deficiency and its health and economic consequences in South Asian developing countries and to shed light on possible approaches to combating zinc deficiency. A computer-based search was performed on PubMed, Google, and ScienceDirect.com to retrieve relevant scientific literature published between 2000 and 2012. The search yielded 194 articles, of which 71 were culled. Studies were further screened on the basis of population groups, age and sex, pregnancy, and lactation. The most relevant articles were included in the review. Cutoffs for serum zinc concentration defined for zinc deficiency were 65 microg/dL for males and females aged < 10 years, 66 microg/dL for non-pregnant females, and 70 microg/dL for males aged > or = 10 years. Population segments from rural and urban areas of South Asian developing countries were included in the analysis. They comprised pregnant and lactating women, preschool and school children. The analysis reveals that zinc deficiency is high among children, pregnant and lactating women in India, Pakistan, Bangladesh, Sri Lanka, and Nepal. Diarrhoea has been established as a leading cause to intensify zinc deficiency in Bangladesh. Little has been done in Sri Lanka and Nepal to estimate the prevalence of zinc deficiency precisely. A substantial population segment of the South Asian developing countries is predisposed to zinc deficiency which is further provoked by increased requirements for zinc under certain physiological conditions. Supplementation, fortification, and dietary diversification are the most viable strategies to enhancing zinc status among various population groups.

  17. Transient symptomatic zinc deficiency resembling acrodermatitis enteropathica in a breast-fed premature infant: case report and brief review of the literature.

    PubMed

    Zattra, E; Belloni Fortina, A

    2013-12-01

    Transient symptomatic zinc deficiency is a rare disorder clinically indistinguishable from acrodermatitis enteropathica characterized by periorificial and acral dermatitis that usually occurs in exclusively breast-fed infant especially if preterm. We describe a three-month-old breast-fed preterm boy who developed the typical skin lesions. Maternal breast milk zinc was lower than the levels from other 2 mothers of infants at the same gestational age. The disease improved and serum zinc level became normal with oral supplementation of zinc. No recurrence of the dermatosis was observed when the treatment was stopped after weaning.

  18. Effects of cooking methods on the iron and zinc contents in cowpea (Vigna unguiculata) to combat nutritional deficiencies in Brazil

    PubMed Central

    Pereira, Elenilda J.; Carvalho, Lucia M. J.; Dellamora-Ortiz, Gisela M.; Cardoso, Flávio S. N.; Carvalho, José L. V.; Viana, Daniela S.; Freitas, Sidinea C.; Rocha, Maurisrael M.

    2014-01-01

    Background Because iron deficiency anemia is prevalent in developing countries, determining the levels of iron and zinc in beans, the second most consumed staple food in Brazil, is essential, especially for the low-income people who experience a deficiency of these minerals in their diet. Objectives This study aimed to evaluate the effect of cooking methods by measuring the iron and zinc contents in cowpea cultivars before and after soaking to determine the retention of these minerals. Methods The samples were cooked in both regular pans and pressure cookers with and without previous soaking. Mineral analyses were carried out by Spectrometry of Inductively Coupled Plasma (ICP). Results The results showed high contents of iron and zinc in raw samples as well as in cooked ones, with the use of regular pan resulting in greater percentage of iron retention and the use of pressure cooker ensuring higher retention of zinc. Conclusions The best retention of iron was found in the BRS Aracê cultivar prepared in a regular pan with previous soaking. This cultivar may be indicated for cultivation and human consumption. The best retention of zinc was found for the BRS Tumucumaque cultivar prepared in a pressure cooker without previous soaking. PMID:24624050

  19. Induction of nitric oxide synthase in rat intestine by interleukin-1alpha may explain diarrhea associated with zinc deficiency.

    PubMed

    Cui, L; Takagi, Y; Wasa, M; Iiboshi, Y; Khan, J; Nezu, R; Okada, A

    1997-09-01

    Synthesis of inducible nitric oxide synthase (iNOS) in the intestine may result in local tissue damage. We investigated whether a challenge with interleukin-1alpha could give rise to intestinal iNOS expression and diarrhea in rats of differing zinc status. Weaning male rats were fed a zinc-deficient (ZD) diet (2 mg zinc/kg) for 4 wk to induce zinc deficiency or a zinc-supplemented diet [50.8 mg zinc/kg; controls, including pair-fed (PF ) and ad libitum (AL) consumption groups], and then subcutaneously injected with interleukin-1alpha (2 x 10(7) units/kg body wt). Without the interleukin-1alpha challenge, ZD rats had significantly lower plasma zinc concentration than the other groups. Intestinal metallothionein-1 mRNA abundance was lower in ZD rats than in AL rats. iNOS was expressed in the intestine of ZD rats but not in the others. None of the rats experienced diarrhea during the feeding period. Interleukin-1alpha led to a reduction in plasma zinc concentration, enhancement in intestinal metallothionein-1 mRNA levels, and expression of the intestinal iNOS gene in all groups. However, the abundance of iNOS mRNA was significantly higher in ZD rats than in the other groups. The presence of iNOS protein was demonstrated by immunohistochemical staining in the intestine of ZD rats that had been treated with interleukin-1alpha 12 h earlier. In addition, diarrhea occurred in most of the ZD rats and some of the PF rats but not in AL rats after interleukin-1alpha treatment. We conclude that ZD rats respond to interleukin-1alpha challenge more severely than controls, reflected by a more marked and prolonged iNOS expression and a greater incidence of diarrhea.

  20. Modulation of intestinal gene expression by dietary zinc status: Effectiveness of cDNA arrays for expression profiling of a single nutrient deficiency

    PubMed Central

    Blanchard, Raymond K.; Moore, J. Bernadette; Green, Calvert L.; Cousins, Robert J.

    2001-01-01

    Mammalian nutritional status affects the homeostatic balance of multiple physiological processes and their associated gene expression. Although DNA array analysis can monitor large numbers of genes, there are no reports of expression profiling of a micronutrient deficiency in an intact animal system. In this report, we have tested the feasibility of using cDNA arrays to compare the global changes in expression of genes of known function that occur in the early stages of rodent zinc deficiency. The gene-modulating effects of this deficiency were demonstrated by real-time quantitative PCR measurements of altered mRNA levels for metallothionein 1, zinc transporter 2, and uroguanylin, all of which have been previously documented as zinc-regulated genes. As a result of the low level of inherent noise within this model system and application of a recently reported statistical tool for statistical analysis of microarrays [Tusher, V.G., Tibshirani, R. & Chu, G. (2001) Proc. Natl. Acad. Sci. USA 98, 5116–5121], we demonstrate the ability to reproducibly identify the modest changes in mRNA abundance produced by this single micronutrient deficiency. Among the genes identified by this array profile are intestinal genes that influence signaling pathways, growth, transcription, redox, and energy utilization. Additionally, the influence of dietary zinc supply on the expression of some of these genes was confirmed by real-time quantitative PCR. Overall, these data support the effectiveness of cDNA array expression profiling to investigate the pleiotropic effects of specific nutrients and may provide an approach to establishing markers for assessment of nutritional status. PMID:11717422

  1. Zinc in denture adhesive: a rare cause of copper deficiency in a patient on home parenteral nutrition

    PubMed Central

    Prasad, Rakesh; Hawthorne, Barney; Durai, Dharmaraj; McDowell, Ian

    2015-01-01

    A 65-year-old woman with Crohn's disease, who had been on home parenteral nutrition for many years, presented with perioral paraesthesia and a burning sensation in the mouth. Initial blood tests including serum ferritin, vitamin B12 and folate, were normal apart from mild pancytopaenia. Serum copper was low, in spite of receiving regular copper in her parenteral feeds. The copper in her parenteral feeds was increased initially, but when it did not improve, she was started on weekly intravenous copper infusions. She was using dental adhesive, which had zinc in it, and a possibility that this was causing her copper deficiency was raised. Serum zinc levels were normal, but urinary zinc was very high. The patient was advised to use zinc-free dental adhesive and her copper level returned to normal within a few months with normalisation of her pancytopaenia, and partial resolution of her oral paraesthesia. PMID:26452740

  2. The relevance of the colon to zinc nutrition

    USDA-ARS?s Scientific Manuscript database

    Globally, zinc deficiency is widespread, despite decades of research highlighting its negative effects on health, and in particular upon child health in low-income countries. Apart from inadequate dietary intake of bioavailable zinc, other significant contributors to zinc deficiency include the exce...

  3. Zinc in Infection and Inflammation.

    PubMed

    Gammoh, Nour Zahi; Rink, Lothar

    2017-06-17

    Micronutrient homeostasis is a key factor in maintaining a healthy immune system. Zinc is an essential micronutrient that is involved in the regulation of the innate and adaptive immune responses. The main cause of zinc deficiency is malnutrition. Zinc deficiency leads to cell-mediated immune dysfunctions among other manifestations. Consequently, such dysfunctions lead to a worse outcome in the response towards bacterial infection and sepsis. For instance, zinc is an essential component of the pathogen-eliminating signal transduction pathways leading to neutrophil extracellular traps (NET) formation, as well as inducing cell-mediated immunity over humoral immunity by regulating specific factors of differentiation. Additionally, zinc deficiency plays a role in inflammation, mainly elevating inflammatory response as well as damage to host tissue. Zinc is involved in the modulation of the proinflammatory response by targeting Nuclear Factor Kappa B (NF-κB), a transcription factor that is the master regulator of proinflammatory responses. It is also involved in controlling oxidative stress and regulating inflammatory cytokines. Zinc plays an intricate function during an immune response and its homeostasis is critical for sustaining proper immune function. This review will summarize the latest findings concerning the role of this micronutrient during the course of infections and inflammatory response and how the immune system modulates zinc depending on different stimuli.

  4. Maternal Zinc Intakes and Homeostatic Adjustments during Pregnancy and Lactation

    PubMed Central

    Donangelo, Carmen Marino; King, Janet C.

    2012-01-01

    Zinc plays critical roles during embryogenesis, fetal growth, and milk secretion, which increase the zinc need for pregnancy and lactation. Increased needs can be met by increasing the dietary zinc intake, along with making homeostatic adjustments in zinc utilization. Potential homeostatic adjustments include changes in circulating zinc, increased zinc absorption, decreased zinc losses, and changes in whole body zinc kinetics. Although severe zinc deficiency during pregnancy has devastating effects, systematic reviews and meta-analysis of the effect of maternal zinc supplementation on pregnancy outcomes have consistently shown a limited benefit. We hypothesize, therefore, that zinc homeostatic adjustments during pregnancy and lactation improve zinc utilization sufficiently to provide the increased zinc needs in these stages and, therefore, mitigate immediate detrimental effects due to a low zinc intake. The specific questions addressed are the following: How is zinc utilization altered during pregnancy and lactation? Are those homeostatic adjustments influenced by maternal zinc status, dietary zinc, or zinc supplementation? These questions are addressed by critically reviewing results from published human studies on zinc homeostasis during pregnancy and lactation carried out in different populations worldwide. PMID:22852063

  5. Deficiency in Nrf2 transcription factor decreases adipose tissue mass and hepatic lipid accumulation in leptin-deficient mice.

    PubMed

    Xu, Jialin; Donepudi, Ajay C; More, Vijay R; Kulkarni, Supriya R; Li, Liya; Guo, Liangran; Yan, Bingfang; Chatterjee, Tapan; Weintraub, Neal; Slitt, Angela L

    2015-02-01

    To evaluate whether Nrf2 deficiency impacts insulin resistance and lipid accumulation in liver and white adipose tissue. Lep(ob/ob) mice (OB) with targeted Nrf2 deletion (OB-Nrf2KO) were generated. Pathogenesis of obesity and type 2 diabetes was measured in C57BL/6J, Nrf2KO, OB, and OB-Nrf2KO mice. Hepatic lipid content, lipid clearance, and very low-density lipoprotein (VLDL) secretion were determined between OB and OB-Nrf2KO mice. OB-Nrf2KO mice exhibited decreased white adipose tissue mass and decreased adipogenic and lipogenic gene expression compared with OB mice. Nrf2 deficiency prolonged hyperglycemia in response to glucose challenge, which was paralleled by reduced insulin-stimulated Akt phosphorylation. In OB mice, Nrf2 deficiency decreased hepatic lipid accumulation, decreased peroxisome proliferator-activated receptor γ expression and nicotinamide adenine dinucleotide phosphate (NADPH) content, and enhanced VLDL secretion. However, this observation was opposite in lean mice. Additionally, OB-Nrf2KO mice exhibited increased plasma triglyceride content, decreased HDL-cholesterol content, and enhanced apolipoprotein B expression, suggesting Nrf2 deficiency caused dyslipidemia in these mice. Nrf2 deficiency in Lep(ob/ob) mice reduced white adipose tissue mass and prevented hepatic lipid accumulation but induced insulin resistance and dyslipidemia. This study indicates a dual role of Nrf2 during metabolic dysregulation-increasing lipid accumulation in liver and white adipose tissue but preventing lipid accumulation in obese mice. © 2014 The Obesity Society.

  6. Phosphatidate Phosphatase Plays Role in Zinc-mediated Regulation of Phospholipid Synthesis in Yeast*

    PubMed Central

    Soto-Cardalda, Aníbal; Fakas, Stylianos; Pascual, Florencia; Choi, Hyeon-Son; Carman, George M.

    2012-01-01

    In the yeast Saccharomyces cerevisiae, the synthesis of phospholipids is coordinately regulated by mechanisms that control the homeostasis of the essential mineral zinc (Carman, G.M., and Han, G. S. (2007) Regulation of phospholipid synthesis in Saccharomyces cerevisiae by zinc depletion. Biochim. Biophys. Acta 1771, 322–330; Eide, D. J. (2009) Homeostatic and adaptive responses to zinc deficiency in Saccharomyces cerevisiae. J. Biol. Chem. 284, 18565–18569). The synthesis of phosphatidylcholine is balanced by the repression of CDP-diacylglycerol pathway enzymes and the induction of Kennedy pathway enzymes. PAH1-encoded phosphatidate phosphatase catalyzes the penultimate step in triacylglycerol synthesis, and the diacylglycerol generated in the reaction may also be used for phosphatidylcholine synthesis via the Kennedy pathway. In this work, we showed that the expression of PAH1-encoded phosphatidate phosphatase was induced by zinc deficiency through a mechanism that involved interaction of the Zap1p zinc-responsive transcription factor with putative upstream activating sequence zinc-responsive elements in the PAH1 promoter. The pah1Δ mutation resulted in the derepression of the CHO1-encoded phosphatidylserine synthase (CDP-diacylglycerol pathway enzyme) and loss of the zinc-mediated regulation of the enzyme. Loss of phosphatidate phosphatase also resulted in the derepression of the CKI1-encoded choline kinase (Kennedy pathway enzyme) but decreased the synthesis of phosphatidylcholine when cells were deficient of zinc. This result confirmed the role phosphatidate phosphatase plays in phosphatidylcholine synthesis via the Kennedy pathway. PMID:22128164

  7. Genomic analysis, cytokine expression, and microRNA profiling reveal biomarkers of human dietary zinc depletion and homeostasis.

    PubMed

    Ryu, Moon-Suhn; Langkamp-Henken, Bobbi; Chang, Shou-Mei; Shankar, Meena N; Cousins, Robert J

    2011-12-27

    Implementation of zinc interventions for subjects suspected of being zinc-deficient is a global need, but is limited due to the absence of reliable biomarkers. To discover molecular signatures of human zinc deficiency, a combination of transcriptome, cytokine, and microRNA analyses was applied to a dietary zinc depletion/repletion protocol with young male human subjects. Concomitant with a decrease in serum zinc concentration, changes in buccal and blood gene transcripts related to zinc homeostasis occurred with zinc depletion. Microarray analyses of whole blood RNA revealed zinc-responsive genes, particularly, those associated with cell cycle regulation and immunity. Responses of potential signature genes of dietary zinc depletion were further assessed by quantitative real-time PCR. The diagnostic properties of specific serum microRNAs for dietary zinc deficiency were identified by acute responses to zinc depletion, which were reversible by subsequent zinc repletion. Depression of immune-stimulated TNFα secretion by blood cells was observed after low zinc consumption and may serve as a functional biomarker. Our findings introduce numerous novel candidate biomarkers for dietary zinc status assessment using a variety of contemporary technologies and which identify changes that occur prior to or with greater sensitivity than the serum zinc concentration which represents the current zinc status assessment marker. In addition, the results of gene network analysis reveal potential clinical outcomes attributable to suboptimal zinc intake including immune function defects and predisposition to cancer. These demonstrate through a controlled depletion/repletion dietary protocol that the illusive zinc biomarker(s) can be identified and applied to assessment and intervention strategies.

  8. Zinc treatment increases the titre of 'Candidatus Liberibacter asiaticus' in huanglongbing-affected citrus plants while affecting the bacterial microbiomes.

    PubMed

    Zhang, M Q; Guo, Y; Powell, C A; Doud, M S; Yang, C Y; Zhou, H; Duan, Y P

    2016-06-01

    Huanglongbing (HLB)-affected citrus often display zinc deficiency symptoms. In this study, supplemental zinc was applied to citrus to determine its effect on Candidatus Liberibacter asiaticus (Las) titre, HLB symptoms, and leaf microbiome. HLB-affected citrus were treated with various amounts of zinc. The treatments promoted Las growth and affected microbiomes in citrus leaves. Phylochip(™) -based results indicated that 5475 of over 50 000 known Operational Taxonomic Units (OTUs) in 52 phyla were detected in the midribs of HLB-affected citrus, of which Proteobacteria was the most abundant, followed by Firmicutes and Actinobacteria. In comparison, the microbiomes of zinc-treated diseased plants had overall more OTUs with higher amounts of Proteobacteria, but decreased percentages of Firmicutes and Actinobacteria. In addition, more OTUs of siderophore-producing bacteria were present. Only zinc-sensitive Staphylococcaceae had higher OTU's in the diseased plants without zinc treatments. Although HLB-affected citrus appear zinc deficient, zinc amendments increased the pathogen levels and shifted the microbiome. HLB is currently the most devastating disease of citrus worldwide. Zinc is often applied to HLB-affected citrus due to zinc deficiency symptoms. This study provided new insights into the potential effects of zinc on HLB and the microbial ecology of citrus. © 2016 The Society for Applied Microbiology.

  9. [Zinc and chronic enteropathies].

    PubMed

    Giorgi, P L; Catassi, C; Guerrieri, A

    1984-01-01

    In recent years the nutritional importance of zinc has been well established; its deficiency and its symptoms have also been recognized in humans. Furthermore, Acrodermatitis Enteropathica has been isolated, a rare but severe disease, of which skin lesions, chronic diarrhoea and recurring infections are the main symptoms. The disease is related to the malfunctioning of intestinal absorption of zinc and can be treated by administering pharmacological doses of zinc orally. Good dietary sources of zinc are meat, fish and, to a less extent, human milk. The amount of zinc absorbed in the small intestine is influenced by other nutrients: some compounds inhibit this process (dietary fiber, phytate) while others (picolinic acid, citric acid), referred to as Zn-binding ligands (ZnBL) facilitate it. Citric acid is thought to be the ligand which accounts for the high level of bioavailability of zinc in human milk. zinc absorption occurs throughout the small intestine, not only in the prossimal tract (duodenum and jejunum) but also in the distal tract (ileum). Diarrhoea is one of the clinical manifestations of zinc deficiency, thus many illnesses distinguished by chronic diarrhoea entail a bad absorption of zinc. In fact, in some cases of chronic enteropathies in infants, like coeliac disease and seldom cystic fibrosis, a deficiency of zinc has been isolated. Some of the symptoms of Crohn's disease, like retarded growth and hypogonadism, have been related to hypozinchemia which is present in this illness. Finally, it is possible that some of the dietary treatments frequently used for persistent post-enteritis diarrhoea (i.e. cow's milk exclusion, abuse and misuse of dietary fiber like carrot and carub powder, use of soy formula) can constitute a scarce supply of zinc and therefore could promote the persistency of diarrhoea itself.

  10. Zinc in Infection and Inflammation

    PubMed Central

    Gammoh, Nour Zahi; Rink, Lothar

    2017-01-01

    Micronutrient homeostasis is a key factor in maintaining a healthy immune system. Zinc is an essential micronutrient that is involved in the regulation of the innate and adaptive immune responses. The main cause of zinc deficiency is malnutrition. Zinc deficiency leads to cell-mediated immune dysfunctions among other manifestations. Consequently, such dysfunctions lead to a worse outcome in the response towards bacterial infection and sepsis. For instance, zinc is an essential component of the pathogen-eliminating signal transduction pathways leading to neutrophil extracellular traps (NET) formation, as well as inducing cell-mediated immunity over humoral immunity by regulating specific factors of differentiation. Additionally, zinc deficiency plays a role in inflammation, mainly elevating inflammatory response as well as damage to host tissue. Zinc is involved in the modulation of the proinflammatory response by targeting Nuclear Factor Kappa B (NF-κB), a transcription factor that is the master regulator of proinflammatory responses. It is also involved in controlling oxidative stress and regulating inflammatory cytokines. Zinc plays an intricate function during an immune response and its homeostasis is critical for sustaining proper immune function. This review will summarize the latest findings concerning the role of this micronutrient during the course of infections and inflammatory response and how the immune system modulates zinc depending on different stimuli. PMID:28629136

  11. Effect of resveratrol and zinc on intracellular zinc status in normal human prostate epithelial cells

    USDA-ARS?s Scientific Manuscript database

    To evaluate the influence of resveratrol on cellular zinc status, normal human prostate epithelial (NHPrE) cells were treated with 6 levels of resveratrol (0, 0.5, 1, 2.5, 5 and 10 microM) and 4 levels of zinc [0, 4, 16, and 32 microM for zinc-deficient (ZD), zinc-normal (ZN), zinc-adequate (ZA), an...

  12. Iron, zinc, and copper in retinal physiology and disease.

    PubMed

    Ugarte, Marta; Osborne, Neville N; Brown, Laurence A; Bishop, Paul N

    2013-01-01

    The essential trace metals iron, zinc, and copper play important roles both in retinal physiology and disease. They are involved in various retinal functions such as phototransduction, the visual cycle, and the process of neurotransmission, being tightly bound to proteins and other molecules to regulate their structure and/or function or as unbound free metal ions. Elevated levels of "free" or loosely bound metal ions can exert toxic effects, and in order to maintain homeostatic levels to protect retinal cells from their toxicity, appropriate mechanisms exist such as metal transporters, chaperones, and the presence of certain storage molecules that tightly bind metals to form nontoxic products. The pathways to maintain homeostatic levels of metals are closely interlinked, with various metabolic pathways directly and/or indirectly affecting their concentrations, compartmentalization, and oxidation/reduction states. Retinal deficiency or excess of these metals can result from systemic depletion and/or overload or from mutations in genes involved in maintaining retinal metal homeostasis, and this is associated with retinal dysfunction and pathology. Iron accumulation in the retina, a characteristic of aging, may be involved in the pathogenesis of retinal diseases such as age-related macular degeneration (AMD). Zinc deficiency is associated with poor dark adaptation. Zinc levels in the human retina and RPE decrease with age in AMD. Copper deficiency is associated with optic neuropathy, but retinal function is maintained. The changes in iron and zinc homeostasis in AMD have led to the speculation that iron chelation and/or zinc supplements may help in its treatment. Copyright © 2013 Elsevier Inc. All rights reserved.

  13. Plasma zinc's alter ego is a low-molecular-weight humoral factor.

    PubMed

    Ou, Ou; Allen-Redpath, Keith; Urgast, Dagmar; Gordon, Margaret-Jane; Campbell, Gill; Feldmann, Jörg; Nixon, Graeme F; Mayer, Claus-Dieter; Kwun, In-Sook; Beattie, John H

    2013-09-01

    Mild dietary zinc deprivation in humans and rodents has little effect on blood plasma zinc levels, and yet cellular consequences of zinc depletion can be detected in vascular and other tissues. We proposed that a zinc-regulated humoral factor might mediate the effects of zinc deprivation. Using a novel approach, primary rat vascular smooth muscle cells (VSMCs) were treated with plasma from zinc-deficient (<1 mg Zn/kg) or zinc-adequate (35 mg Zn/kg, pair-fed) adult male rats, and zinc levels were manipulated to distinguish direct and indirect effects of plasma zinc. Gene expression changes were analyzed by microarray and qPCR, and incubation of VSMCs with blood plasma from zinc-deficient rats strongly changed the expression of >2500 genes, compared to incubation of cells with zinc-adequate rat plasma. We demonstrated that this effect was caused by a low-molecular-weight (∼2-kDa) zinc-regulated humoral factor but that changes in gene expression were mostly reversed by adding zinc back to zinc-deficient plasma. Strongly regulated genes were overrepresented in pathways associated with immune function and development. We conclude that zinc deficiency induces the production of a low-molecular-weight humoral factor whose influence on VSMC gene expression is blocked by plasma zinc. This factor is therefore under dual control by zinc.

  14. Zinc and gastrointestinal disease

    PubMed Central

    Skrovanek, Sonja; DiGuilio, Katherine; Bailey, Robert; Huntington, William; Urbas, Ryan; Mayilvaganan, Barani; Mercogliano, Giancarlo; Mullin, James M

    2014-01-01

    This review is a current summary of the role that both zinc deficiency and zinc supplementation can play in the etiology and therapy of a wide range of gastrointestinal diseases. The recent literature describing zinc action on gastrointestinal epithelial tight junctions and epithelial barrier function is described. Zinc enhancement of gastrointestinal epithelial barrier function may figure prominently in its potential therapeutic action in several gastrointestinal diseases. PMID:25400994

  15. Copper and Zinc Deficiency in a Patient Receiving Long-Term Parenteral Nutrition During a Shortage of Parenteral Trace Element Products.

    PubMed

    Palm, Eric; Dotson, Bryan

    2015-11-01

    Drug shortages in the United States, including parenteral nutrition (PN) components, have been common in recent years and can adversely affect patient care. Here we report a case of copper and zinc deficiency in a patient receiving PN during a shortage of parenteral trace element products. The management of the patient's deficiencies, including the use of an imported parenteral multi-trace element product, is described. © 2014 American Society for Parenteral and Enteral Nutrition.

  16. Zinc supplementation in public health.

    PubMed

    Penny, Mary Edith

    2013-01-01

    Zinc is necessary for physiological processes including defense against infections. Zinc deficiency is responsible for 4% of global child morbidity and mortality. Zinc supplements given for 10-14 days together with low-osmolarity oral rehydration solution (Lo-ORS) are recommended for the treatment of childhood diarrhea. In children aged ≥ 6 months, daily zinc supplements reduce the duration of acute diarrhea episodes by 12 h and persistent diarrhea by 17 h. Zinc supplements could reduce diarrhea mortality in children aged 12-59 months by an estimated 23%; they are very safe but are associated with an increase in vomiting especially with the first dose. Heterogeneity between the results of trials is not understood but may be related to dose and the etiology of the diarrhea infection. Integration of zinc and Lo-ORS into national programs is underway but slowly, procurement problems are being overcome and the greatest challenge is changing health provider and caregiver attitudes to diarrhea management. Fewer trials have been conducted of zinc adjunct therapy in severe respiratory tract infections and there is as yet insufficient evidence to recommend addition of zinc to antibiotic therapy. Daily zinc supplements for all children >12 months of age in zinc deficient populations are estimated to reduce diarrhea incidence by 11-23%. The greatest impact is in reducing multiple episodes of diarrhea. The effect on duration of diarrheal episodes is less clear, but there may be up to 9% reduction. Zinc is also efficacious in reducing dysentery and persistent diarrhea. Zinc supplements may also prevent pneumonia by about 19%, but heterogeneity across studies has not yet been explained. When analyses are restricted to better quality studies using CHERG (Child Health Epidemiology Reference Group) methodology, zinc supplements are estimated to reduce diarrheal deaths by 13% and pneumonia deaths by 20%. National-level programs to combat childhood zinc deficiency should be

  17. Zinc: an essential but elusive nutrient123

    PubMed Central

    King, Janet C

    2011-01-01

    Zinc is essential for multiple aspects of metabolism. Physiologic signs of zinc depletion are linked with diverse biochemical functions rather than with a specific function, which makes it difficult to identify biomarkers of zinc nutrition. Nutrients, such as zinc, that are required for general metabolism are called type 2 nutrients. Protein and magnesium are examples of other type 2 nutrients. Type 1 nutrients are required for one or more specific functions: examples include iron, vitamin A, iodine, folate, and copper. When dietary zinc is insufficient, a marked reduction in endogenous zinc loss occurs immediately to conserve the nutrient. If zinc balance is not reestablished, other metabolic adjustments occur to mobilize zinc from small body pools. The location of those pools is not known, but all cells probably have a small zinc reserve that includes zinc bound to metallothionein or zinc stored in the Golgi or in other organelles. Plasma zinc is also part of this small zinc pool that is vulnerable to insufficient intakes. Plasma zinc concentrations decline rapidly with severe deficiencies and more moderately with marginal depletion. Unfortunately, plasma zinc concentrations also decrease with a number of conditions (eg, infection, trauma, stress, steroid use, after a meal) due to a metabolic redistribution of zinc from the plasma to the tissues. This redistribution confounds the interpretation of low plasma zinc concentrations. Biomarkers of metabolic zinc redistribution are needed to determine whether this redistribution is the cause of a low plasma zinc rather than poor nutrition. Measures of metallothionein or cellular zinc transporters may fulfill that role. PMID:21715515

  18. Genomic instability related to zinc deficiency and excess in an in vitro model: is the upper estimate of the physiological requirements recommended for children safe?

    PubMed

    Padula, Gisel; Ponzinibbio, María Virginia; Gambaro, Rocío Celeste; Seoane, Analía Isabel

    2017-08-01

    Micronutrients are important for the prevention of degenerative diseases due to their role in maintaining genomic stability. Therefore, there is international concern about the need to redefine the optimal mineral and vitamin requirements to prevent DNA damage. We analyzed the cytostatic, cytotoxic, and genotoxic effect of in vitro zinc supplementation to determine the effects of zinc deficiency and excess and whether the upper estimate of the physiological requirement recommended for children is safe. To achieve zinc deficiency, DMEM/Ham's F12 medium (HF12) was chelated (HF12Q). Lymphocytes were isolated from healthy female donors (age range, 5-10 yr) and cultured for 7 d as follows: negative control (HF12, 60 μg/dl ZnSO 4 ); deficient (HF12Q, 12 μg/dl ZnSO 4 ); lower level (HF12Q + 80 μg/dl ZnSO 4 ); average level (HF12Q + 180 μg/dl ZnSO 4 ); upper limit (HF12Q + 280 μg/dl ZnSO 4 ); and excess (HF12Q + 380 μg/dl ZnSO 4 ). The comet (quantitative analysis) and cytokinesis-block micronucleus cytome assays were used. Differences were evaluated with Kruskal-Wallis and ANOVA (p < 0.05). Olive tail moment, tail length, micronuclei frequency, and apoptotic and necrotic percentages were significantly higher in the deficient, upper limit, and excess cultures compared with the negative control, lower, and average limit ones. In vitro zinc supplementation at the lower and average limit (80 and 180 μg/dl ZnSO 4 ) of the physiological requirement recommended for children proved to be the most beneficial in avoiding genomic instability, whereas the deficient, upper limit, and excess (12, 280, and 380 μg/dl) cultures increased DNA and chromosomal damage and apoptotic and necrotic frequencies.

  19. Biomarkers of Nutrition for Development (BOND)—Zinc Review12345

    PubMed Central

    King, Janet C; Brown, Kenneth H; Gibson, Rosalind S; Krebs, Nancy F; Lowe, Nicola M; Siekmann, Jonathan H; Raiten, Daniel J

    2016-01-01

    Zinc is required for multiple metabolic processes as a structural, regulatory, or catalytic ion. Cellular, tissue, and whole-body zinc homeostasis is tightly controlled to sustain metabolic functions over a wide range of zinc intakes, making it difficult to assess zinc insufficiency or excess. The BOND (Biomarkers of Nutrition for Development) Zinc Expert Panel recommends 3 measurements for estimating zinc status: dietary zinc intake, plasma zinc concentration (PZC), and height-for-age of growing infants and children. The amount of dietary zinc potentially available for absorption, which requires an estimate of dietary zinc and phytate, can be used to identify individuals and populations at risk of zinc deficiency. PZCs respond to severe dietary zinc restriction and to zinc supplementation; they also change with shifts in whole-body zinc balance and clinical signs of zinc deficiency. PZC cutoffs are available to identify individuals and populations at risk of zinc deficiency. However, there are limitations in using the PZC to assess zinc status. PZCs respond less to additional zinc provided in food than to a supplement administered between meals, there is considerable interindividual variability in PZCs with changes in dietary zinc, and PZCs are influenced by recent meal consumption, the time of day, inflammation, and certain drugs and hormones. Insufficient data are available on hair, urinary, nail, and blood cell zinc responses to changes in dietary zinc to recommend these biomarkers for assessing zinc status. Of the potential functional indicators of zinc, growth is the only one that is recommended. Because pharmacologic zinc doses are unlikely to enhance growth, a growth response to supplemental zinc is interpreted as indicating pre-existing zinc deficiency. Other functional indicators reviewed but not recommended for assessing zinc nutrition in clinical or field settings because of insufficient information are the activity or amounts of zinc-dependent enzymes

  20. History of zinc in agriculture

    USDA-ARS?s Scientific Manuscript database

    Zinc was established as essential for green plants in 1926 and for mammals in 1934. However, over 20 years would past before the first descriptions of zinc deficiencies in farm animals appeared. In 1955, it was reported that zinc supplementation would cure a parakeratosis in swine. In 1958, it wa...

  1. Iron, zinc and iodide status in Mexican children under 12 years and women 12-49 years of age. A probabilistic national survey.

    PubMed

    Villalpando, Salvador; García-Guerra, Armando; Ramírez-Silva, Claudia Ivonne; Mejía-Rodríguez, Fabiola; Matute, Guadalupe; Shamah-Levy, Teresa; Rivera, Juan A

    2003-01-01

    To describe the epidemiology of iron, zinc and iodide deficiencies in a probabilistic sample of Mexican women and children and explore its association with some dietary and socio-demographic variables. We carried out in 1999 an epidemiological description of iron (percent transferrin saturation, PTS, < 16%), serum zinc (< 65 ug/dl) and iodide (< 50 ug/l urine) deficiencies in a probabilistic sample of 1,363 Mexican children under 12 years and of 731 women of child-bearing age. Serum iron, Total Iron Binding Capacity (TIBC) and zinc were measured by atomic absorption spectrometry, and urinary iodide by a colorimetric method. Logistic regression models explored determinants for such micromineral deficiencies. Iron deficiency was higher (67%) in infants < 2 years of age. Prevalence declined (34-39%) at school age. The prevalence for iron deficiency in women was 40%. Zinc deficiency was higher in infants < 2 years of age (34%) than in school-age children (19-24%). Prevalence in women was 30%, with no rural/urban difference. In women the likelihood of iron deficiency decreased as SEL improved (p = 0.04) and increased with the intake of cereals (p = 0.01). The likelihood of low serum zinc levels was greater in women and children of low socioeconomic level (SEL) (p < 0.02 and p = 0.001) iodide deficiency was negligible in both children and women. The data shows high prevalence of iron deficiency-specially in infants 12 to 24 months of age. It is suggested that in older children and women 12 to 49 years of age that iron bioavailability is low. The prevalence of zinc deficiency was also very high. The English version of this paper is available too at: http://www.insp.mx/salud/index.html.

  2. Brain Lateralization in Mice Is Associated with Zinc Signaling and Altered in Prenatal Zinc Deficient Mice That Display Features of Autism Spectrum Disorder

    PubMed Central

    Grabrucker, Stefanie; Haderspeck, Jasmin C.; Sauer, Ann Katrin; Kittelberger, Nadine; Asoglu, Harun; Abaei, Alireza; Rasche, Volker; Schön, Michael; Boeckers, Tobias M.; Grabrucker, Andreas M.

    2018-01-01

    A number of studies have reported changes in the hemispheric dominance in autism spectrum disorder (ASD) patients on functional, biochemical, and morphological level. Since asymmetry of the brain is also found in many vertebrates, we analyzed whether prenatal zinc deficient (PZD) mice, a mouse model with ASD like behavior, show alterations regarding brain lateralization on molecular and behavioral level. Our results show that hemisphere-specific expression of marker genes is abolished in PZD mice on mRNA and protein level. Using magnetic resonance imaging, we found an increased striatal volume in PZD mice with no change in total brain volume. Moreover, behavioral patterns associated with striatal lateralization are altered and the lateralized expression of dopamine receptor 1 (DR1) in the striatum of PZD mice was changed. We conclude that zinc signaling during brain development has a critical role in the establishment of brain lateralization in mice. PMID:29379414

  3. Zinc as a Gatekeeper of Immune Function

    PubMed Central

    Wessels, Inga; Maywald, Martina; Rink, Lothar

    2017-01-01

    After the discovery of zinc deficiency in the 1960s, it soon became clear that zinc is essential for the function of the immune system. Zinc ions are involved in regulating intracellular signaling pathways in innate and adaptive immune cells. Zinc homeostasis is largely controlled via the expression and action of zinc “importers” (ZIP 1–14), zinc “exporters” (ZnT 1–10), and zinc-binding proteins. Anti-inflammatory and anti-oxidant properties of zinc have long been documented, however, underlying mechanisms are still not entirely clear. Here, we report molecular mechanisms underlying the development of a pro-inflammatory phenotype during zinc deficiency. Furthermore, we describe links between altered zinc homeostasis and disease development. Consequently, the benefits of zinc supplementation for a malfunctioning immune system become clear. This article will focus on underlying mechanisms responsible for the regulation of cellular signaling by alterations in zinc homeostasis. Effects of fast zinc flux, intermediate “zinc waves”, and late homeostatic zinc signals will be discriminated. Description of zinc homeostasis-related effects on the activation of key signaling molecules, as well as on epigenetic modifications, are included to emphasize the role of zinc as a gatekeeper of immune function. PMID:29186856

  4. Levels of semenogelin in human spermatozoa decrease during capacitation: involvement of reactive oxygen species and zinc.

    PubMed

    de Lamirande, E; Lamothe, G

    2010-07-01

    Semenogelin (Sg), the main protein of human semen coagulum, prevents sperm capacitation. The objective of this study was to examine the role of Sg and its mechanism of action. Sg blocked sperm capacitation triggered by various stimuli, via inhibition of superoxide anion (O(2)*-; luminescence assay) and nitric oxide (NO*; tested using diaminofluorescein) generation. Triton-soluble and -insoluble sperm fractions contained Sg and Sg peptides (immunoblotting), the level of which decreased with initiation of capacitation. This drop was prevented by superoxide dismutase and NO* synthase inhibitor and was reproduced by addition of O(2)*- and NO*. Zinc (Zn(2+)) blocked and a zinc chelator (TPEN) promoted the decline in Sg levels. There was a decreased labelling of Sg on the head in capacitating spermatozoa with the two fixation techniques tested (immunocytochemistry). Reactive oxygen species (ROS) (O(2)*- and NO*) caused, these changes, and zinc prevented them. Spermatozoa quickly internalized Sg upon incubation and Sg was then rapidly degraded in a zinc-inhibitable manner. Sg blocked capacitation mainly via inhibition of ROS generation. Spermatozoa appeared permeable to Sg and processed Sg in a zinc-inhibitable fashion. ROS themselves could promote sperm disposal of Sg which maybe one of the mechanisms that allows initiation of capacitation.

  5. Effects of zinc deficiency and zinc supplementation on homocysteine levels and related enzyme expression in rats.

    PubMed

    Jing, Mingyan; Rech, Leslie; Wu, Yinghong; Goltz, Douglas; Taylor, Carla G; House, James D

    2015-04-01

    Methionine synthase (MS) and betaine-homocysteine methyltransferase (BHMT) are both zinc (Zn)-dependent methyltransferases and involved in the methylation of homocysteine. The objective of this study was to investigate the effects of dietary Zn supply on homocysteine levels and expression of the two enzymes in growing rats. Male weanling Sprague-Dawley rats were assigned randomly to four dietary groups (n=8/group) for 3 weeks: Zn deficient (ZD; <1mg Zn/kg); Zn control (ZC; 30mg Zn/kg); Zn supplemented (ZS; 300mg Zn/kg); pair fed (PF; 30mg Zn/kg) to the ZD group. Serum and femur Zn concentrations were 83% and 58% lower in ZD, and 49% and 62% higher in ZS compared to ZC (P<0.001), respectively. The ZD rats had lower feed intake (37%), body weight gains (45%), liver (43%) and kidney (31%) weights than those of ZC (P<0.001), but these parameters in ZD were not significantly different from the PF controls. Serum homocysteine concentrations were 65% higher in ZD compared to PF (P<0.05), and there was no significant difference in serum folate levels between ZD and PF groups. The mRNA expression of liver and kidney MS was 57% and 38% lower in ZD than PF (P<0.001), respectively. Hepatic and renal BHMT mRNA levels were not altered in ZD compared to controls. The aforementioned measurements were not significantly different between ZS and ZC groups, except Zn levels. These results demonstrated that homocysteine homeostasis appeared to be disturbed by Zn deficiency but not Zn supplementation, and elevated serum homocysteine might be due to reduced expression of MS during Zn deficiency. Copyright © 2014 Elsevier GmbH. All rights reserved.

  6. Zinc in Early Life: A Key Element in the Fetus and Preterm Neonate

    PubMed Central

    Terrin, Gianluca; Berni Canani, Roberto; Di Chiara, Maria; Pietravalle, Andrea; Aleandri, Vincenzo; Conte, Francesca; De Curtis, Mario

    2015-01-01

    Zinc is a key element for growth and development. In this narrative review, we focus on the role of dietary zinc in early life (including embryo, fetus and preterm neonate), analyzing consequences of zinc deficiency and adequacy of current recommendations on dietary zinc. We performed a systematic search of articles on the role of zinc in early life. We selected and analyzed 81 studies. Results of this analysis showed that preservation of zinc balance is of critical importance for the avoidance of possible consequences of low zinc levels on pre- and post-natal life. Insufficient quantities of zinc during embryogenesis may influence the final phenotype of all organs. Maternal zinc restriction during pregnancy influences fetal growth, while adequate zinc supplementation during pregnancy may result in a reduction of the risk of preterm birth. Preterm neonates are at particular risk to develop zinc deficiency due to a combination of different factors: (i) low body stores due to reduced time for placental transfer of zinc; (ii) increased endogenous losses; and (iii) marginal intake. Early diagnosis of zinc deficiency, through the measurement of serum zinc concentrations, may be essential to avoid severe prenatal and postnatal consequences in these patients. Typical clinical manifestations of zinc deficiency are growth impairment and dermatitis. Increasing data suggest that moderate zinc deficiency may have significant subclinical effects, increasing the risk of several complications typical of preterm neonates (i.e., necrotizing enterocolitis, chronic lung disease, and retinopathy), and that current recommended intakes should be revised to meet zinc requirements of extremely preterm neonates. Future studies evaluating the adequacy of current recommendations are advocated. PMID:26690476

  7. Relationship of /sup 65/Zn absorption kinetics to intestinal metallothionein in rats: effects of zinc depletion and fasting

    SciTech Connect

    Hoadley, J.E.; Leinart, A.S.; Cousins, R.J.

    1988-04-01

    Intestinal 65Zn transport and metallothionein levels were examined in rats fed zinc-adequate and zinc-deficient diets and in rats subjected to an overnight fast. 65Zn uptake by intestines perfused with 1.5 microM 65Zn was greater in both zinc-deficient and fasted groups than in the control group. Mucosal retention of 65Zn was also greater in the zinc-deficient group but not in the fasted group. The greater 65Zn uptake in the fasted group was associated with a compartment that readily released 65Zn back into the lumen. Kinetic analysis of the rate of 65Zn transfer to the vascular space (absorption) showed that 65Zn absorptionmore » involved approximately 3% of mucosal 65Zn in a 40-min perfusion period. The half-life (t1/2) of this mucosal 65Zn rapid transport pool corresponded directly to changes in intestinal metallothionein levels. Both metallothionein and t1/2 were higher in the fasted group and lower in the zinc-deficient group than in controls. While the rate of 65Zn transport from this rapid transport pool decreased with increasing metallothionein level, the predicted pool size increased when the metallothionein level was elevated by fasting. These results indicate that the rate of zinc absorption is inversely related to intestinal metallothionein levels, but the portion of mucosal 65Zn available for absorption is directly related to intestinal metallothionein.« less

  8. Zinc and Regulation of Inflammatory Cytokines: Implications for Cardiometabolic Disease

    PubMed Central

    Foster, Meika; Samman, Samir

    2012-01-01

    In atherosclerosis and diabetes mellitus, the concomitant presence of low-grade systemic inflammation and mild zinc deficiency highlights a role for zinc nutrition in the management of chronic disease. This review aims to evaluate the literature that reports on the interactions of zinc and cytokines. In humans, inflammatory cytokines have been shown both to up- and down-regulate the expression of specific cellular zinc transporters in response to an increased demand for zinc in inflammatory conditions. The acute phase response includes a rapid decline in the plasma zinc concentration as a result of the redistribution of zinc into cellular compartments. Zinc deficiency influences the generation of cytokines, including IL-1β, IL-2, IL-6, and TNF-α, and in response to zinc supplementation plasma cytokines exhibit a dose-dependent response. The mechanism of action may reflect the ability of zinc to either induce or inhibit the activation of NF-κB. Confounders in understanding the zinc-cytokine relationship on the basis of in vitro experimentation include methodological issues such as the cell type and the means of activating cells in culture. Impaired zinc homeostasis and chronic inflammation feature prominently in a number of cardiometabolic diseases. Given the high prevalence of zinc deficiency and chronic disease globally, the interplay of zinc and inflammation warrants further examination. PMID:22852057

  9. Measurements of zinc absorption: application and interpretation in research designed to improve human zinc nutriture.

    PubMed

    Hambidge, K Michael; Miller, Leland V; Tran, Cuong D; Krebs, Nancy F

    2005-11-01

    The focus of this paper is on the application of measurements of zinc absorption in human research, especially studies designed to assess the efficacy of intervention strategies to prevent and manage zinc deficiency in populations. Emphasis is given to the measurement of quantities of zinc absorbed rather than restricting investigations to measurements of fractional absorption of zinc. This is especially important when determining absorption of zinc from the diet, whether it be the habitual diet or an intervention diet under evaluation. Moreover, measurements should encompass all meals for a minimum of one day with the exception of some pilot studies. Zinc absorption is primarily via an active saturable transport process into the enterocytes of the proximal small intestine. The relationship between quantity of zinc absorbed and the quantity ingested is best characterized by saturable binding models. When applied to human studies that have sufficient data to examine dose-response relationships, efficiency of absorption is high until approximately 50-60% maximal absorption is achieved, even with moderate phytate intakes. This also coincides approximately with the quantity of absorbed zinc necessary to meet physiologic requirements. Efficiency of absorption with intakes that exceed this level is low or very low. These observations have important practical implications for the design and interpretation of intervention studies to prevent zinc deficiency. They also suggest the potential utility of measurements of the quantity of zinc absorbed when evaluating the zinc status of populations.

  10. Prediction of Serum Zinc Levels in Mexican Children at 2 Years of Age Using a Food Frequency Questionnaire and Different Zinc Bioavailability Criteria

    PubMed Central

    Cantoral, Alejandra; Téllez-Rojo, Martha; Shamah-Levy, Teresa; Schnaas, Lourdes; Hernández-Ávila, Mauricio; Peterson, Karen; Ettinger, Adrienne

    2017-01-01

    Background The 2006 Mexican National Health and Nutrition Survey documented a prevalence of zinc deficiency of almost 30% in children aged one to two years old. Objective We sought to validate a Food Frequency Questionnaire (FFQ) for quantifying dietary bioavailable zinc intake in two-year old Mexican children accounting for phytic acid intake and using serum zinc as a reference. Methods This cross-sectional study was nested within a longitudinal birth cohort of 333 young children in Mexico City. Non-fasting serum zinc concentration was measured and dietary zinc intake was calculated on the basis of a semi-quantitative FFQ administered to their mothers. The relationship between dietary zinc intake and serum zinc was assessed using linear regression, adjusting for phytic acid intake, and analyzed according to two distinct international criteria to estimate bioavailable zinc. Models were stratified by zinc deficiency status. Results Dietary zinc, adjusted for phytic acid intake, explained the greatest proportion of the variance of serum zinc. For each mg of dietary zinc intake, serum zinc increased on average by 0.95 μg/dL (0.15 μmol/L) (p=0.06). When stratified by zinc status, this increase was 0.74 μg/dL (p=0.12) for each milligram of zinc consumed among children with adequate serum zinc (N=276) whereas among those children with zinc deficiency (N=57), serum zinc increased by only 0.11 μg/dL (p=0.82). Conclusion A semi-quantitative FFQ can be used for predicting serum zinc in relation to dietary intake in young children, particularly among those who are zinc-replete, and when phytic acid/phytate intake is considered. Future studies should be conducted accounting for both zinc status and dietary zinc inhibitors to further elucidate and validate these findings. PMID:26121697

  11. Prevalence of prenatal zinc deficiency and its association with socio-demographic, dietary and health care related factors in Rural Sidama, Southern Ethiopia: A cross-sectional study

    PubMed Central

    2011-01-01

    Background Several studies witnessed that prenatal zinc deficiency (ZD) predisposes to diverse pregnancy complications. However, scientific evidences on the determinants of prenatal ZD are scanty and inconclusive. The purpose of the present study was to assess the prevalence and determinants of prenatal ZD in Sidama zone, Southern Ethiopia. Methods A community based, cross-sectional study was conducted in Sidama zone in January and February 2011. Randomly selected 700 pregnant women were included in the study. Data on potential determinants of ZD were gathered using a structured questionnaire. Serum zinc concentration was measured using Atomic Absorption Spectrometry. Statistical analysis was done using logistic regression and linear regression. Results The mean serum zinc concentration was 52.4 (+/-9.9) μg/dl (95% CI: 51.6-53.1 μg/dl). About 53.0% (95% CI: 49.3-56.7%) of the subjects were zinc deficient. The majority of the explained variability of serum zinc was due to dietary factors like household food insecurity level, dietary diversity and consumption of animal source foods. The risk of ZD was 1.65 (95% CI: 1.02-2.67) times higher among women from maize staple diet category compared to Enset staple diet category. Compared to pregnant women aged 15-24 years, those aged 25-34 and 35-49 years had 1.57 (95% CI: 1.04-2.34) and 2.18 (95% CI: 1.25-3.63) times higher risk of ZD, respectively. Women devoid of self income had 1.74 (95% CI: 1.11-2.74) time increased risk than their counterparts. Maternal education was positively associated to zinc status. Grand multiparas were 1.74 (95% CI: 1.09-3.23) times more likely to be zinc deficient than nulliparas. Frequency of coffee intake was negatively association to serum zinc level. Positive association was noted between serum zinc and hemoglobin concentrations. Altitude, history of iron supplementation, maternal workload, physical access to health service, antenatal care and nutrition education were not associated to

  12. Observation of decreasing resistivity of amorphous indium gallium zinc oxide thin films with an increasing oxygen partial pressure

    NASA Astrophysics Data System (ADS)

    Singh, Anup K.; Adhikari, Sonachand; Gupta, Rajeev; Deepak

    2017-01-01

    We have investigated the electrical resistivity behavior in amorphous indium gallium zinc oxide (a-IGZO) thin films. It is well known that resistivity increases as the film is deposited at a higher and higher oxygen partial pressure; we also record the same. However, in process we have discovered a remarkable region, in the oxygen deficient condition, that the resistivity shows an inverse behavior. This leads to the possibility that resistive films, suitable for thin film transistors, can also be obtained in oxygen deficient deposition conditions. Optical spectroscopic investigation could discern between a-IGZO films grown in oxygen deficient and oxygen rich conditions. The related resistivity behavior could be correlated to the presence of sub-bandgap states in films deposited in oxygen deficiency. These subgap states appear to be due to defects arising from local variations around the cations or oxygen atoms. The likely cause is an increase in Ga relative to In around O atom and the nature of cation-cation interaction when an oxygen atom is missing.

  13. High incidence of zinc deficiency among Filipino children with compensated and decompensated liver disease.

    PubMed

    Umusig-Quitain, Perlina; Gregorio, Germana V

    2010-02-01

    The role of zinc in the nutrition and growth of children with chronic liver disease is poorly defined. The present study determined the serum zinc levels of children with compensated liver disease (CLD) and decompensated liver disease (DLD) and compared this with healthy children. Zinc levels were also correlated with the severity of liver disease as measured by Child-Pugh scores. The study comprised of 60 children 0-10 years of age with chronic liver disease, defined as CLD (n = 30) if the Child-Pugh score was < 6, and DLD (n = 30) if the Child-Pugh score was > or = 6. Thirty healthy children 0-10 years served as controls. Serum zinc levels were measured by atomic absorption spectrometry. The 90 patients included 30 with CLD (mean age: 4.54 years: 21 boys; mean Child-Pugh score: 5.83), 30 with DLD (mean age: 1.39 years; 17 boys; mean Child-Pugh score: 9.53) and 30 healthy children (mean age: 4.6; 16 boys). Zinc levels of patients with CLD were significantly lower compared with the healthy controls (Mean [standard deviation]: 68.07 [31.55]vs 89.9 [25.9]microg/dL, P = 0.000), but significantly higher compared to the patients with DLD (48.8 [26.8]microg/dL). Correlation studies showed that the higher the Child-Pugh score, the lower the zinc levels (r = -0.460) Children with chronic liver disease, whether in a compensated or decompensated state, had lower serum zinc levels compared with the healthy controls. As the severity of liver disease worsened, the zinc levels decreased. The study suggests that zinc supplementation should constitute part of the micronutrient intake of children with chronic liver disease.

  14. Zinc Signals and Immunity.

    PubMed

    Maywald, Martina; Wessels, Inga; Rink, Lothar

    2017-10-24

    Zinc homeostasis is crucial for an adequate function of the immune system. Zinc deficiency as well as zinc excess result in severe disturbances in immune cell numbers and activities, which can result in increased susceptibility to infections and development of especially inflammatory diseases. This review focuses on the role of zinc in regulating intracellular signaling pathways in innate as well as adaptive immune cells. Main underlying molecular mechanisms and targets affected by altered zinc homeostasis, including kinases, caspases, phosphatases, and phosphodiesterases, will be highlighted in this article. In addition, the interplay of zinc homeostasis and the redox metabolism in affecting intracellular signaling will be emphasized. Key signaling pathways will be described in detail for the different cell types of the immune system. In this, effects of fast zinc flux, taking place within a few seconds to minutes will be distinguish from slower types of zinc signals, also designated as "zinc waves", and late homeostatic zinc signals regarding prolonged changes in intracellular zinc.

  15. Zinc Signals and Immunity

    PubMed Central

    Maywald, Martina; Wessels, Inga; Rink, Lothar

    2017-01-01

    Zinc homeostasis is crucial for an adequate function of the immune system. Zinc deficiency as well as zinc excess result in severe disturbances in immune cell numbers and activities, which can result in increased susceptibility to infections and development of especially inflammatory diseases. This review focuses on the role of zinc in regulating intracellular signaling pathways in innate as well as adaptive immune cells. Main underlying molecular mechanisms and targets affected by altered zinc homeostasis, including kinases, caspases, phosphatases, and phosphodiesterases, will be highlighted in this article. In addition, the interplay of zinc homeostasis and the redox metabolism in affecting intracellular signaling will be emphasized. Key signaling pathways will be described in detail for the different cell types of the immune system. In this, effects of fast zinc flux, taking place within a few seconds to minutes will be distinguish from slower types of zinc signals, also designated as “zinc waves”, and late homeostatic zinc signals regarding prolonged changes in intracellular zinc. PMID:29064429

  16. Dietary Zinc Intake and Its Association with Metabolic Syndrome Indicators among Chinese Adults: An Analysis of the China Nutritional Transition Cohort Survey 2015.

    PubMed

    Wang, Yun; Jia, Xiao-Fang; Zhang, Bing; Wang, Zhi-Hong; Zhang, Ji-Guo; Huang, Fei-Fei; Su, Chang; Ouyang, Yi-Fei; Zhao, Jian; Du, Wen-Wen; Li, Li; Jiang, Hong-Ru; Zhang, Ji; Wang, Hui-Jun

    2018-05-08

    The dietary zinc consumed in Chinese households has decreased over the past decade. However, the national dietary zinc intake in the last five years has seldom been investigated. Using data from 12,028 participants 18 to 64 years old (52.9% male) in the China Nutritional Transition Cohort Survey (CNTCS) 2015, we describe the intake of dietary zinc and the contributions of major foods and we examine the relationship between the level of dietary zinc intake and metabolic syndrome indicators, including blood pressure, fasting glucose, and triglycerides (TG), in Chinese adults. We assessed dietary zinc intake using 24 h recalls on three consecutive days. The mean daily dietary zinc intake for all participants was 10.2 milligrams per day (males 11.2 mg/day, females 9.4 mg/day, p < 0.001). The mean daily dietary zinc density for all participants was 5.2 mg/day per 1000 kilocalories. Among all participants, 31.0% were at risk of zinc deficiency, with dietary zinc intakes of less than the Estimated Average Requirement (EAR) (males 49.2%, females 14.8%, p < 0.050), and 49.9% had adequate dietary zinc intakes, equal to or greater than the recommended nutrient intake (RNI) (males 30.7%, females 67.0%, p < 0.050). We found substantial gender differences in dietary zinc intake and zinc deficiency, with nearly half of the men at risk of zinc deficiency. Males of younger age, with higher education and incomes, and who consumed higher levels of meat, had higher zinc intakes, higher zinc intake densities, and higher rates of meeting the EAR. Among all participants, grains, livestock meat, fresh vegetables, legumes, and seafood were the top five food sources of zinc, and their contributions to total dietary zinc intake were 39.5%, 17.3%, 8.9%, 6.4%, and 4.8%, respectively. The groups with relatively better dietary zinc intakes consumed lower proportions of grains and higher proportions of livestock meat. For males with adequate dietary zinc intake (≥RNI), TG levels increased by 0

  17. Zinc supplementation in children with cystic fibrosis

    USDA-ARS?s Scientific Manuscript database

    Cystic fibrosis (CF) leads to malabsorption of macro- and micronutrients. Symptomatic zinc deficiency has been reported in CF but little is known about zinc homeostasis in children with CF. Zinc supplementation (Zn suppl) is increasingly common in children with CF but it is not without theoretcial r...

  18. Zinc and Zinc Transporters: Novel Regulators of Ventricular Myocardial Development.

    PubMed

    Lin, Wen; Li, Deqiang

    2018-06-01

    Ventricular myocardial development is a well-orchestrated process involving different cardiac structures, multiple signal pathways, and myriad proteins. Dysregulation of this important developmental event can result in cardiomyopathies, such as left ventricle non-compaction, which affect the pediatric population and the adults. Human and mouse studies have shed light upon the etiology of some cardiomyopathy cases and highlighted the contribution of both genetic and environmental factors. However, the regulation of ventricular myocardial development remains incompletely understood. Zinc is an essential trace metal with structural, enzymatic, and signaling function. Perturbation of zinc homeostasis has resulted in developmental and physiological defects including cardiomyopathy. In this review, we summarize several mechanisms by which zinc and zinc transporters can impact the regulation of ventricular myocardial development. Based on our review, we propose that zinc deficiency and mutations of zinc transporters may underlie some cardiomyopathy cases especially those involving ventricular myocardial development defects.

  19. Update on zinc biology.

    PubMed

    Solomons, Noel W

    2013-01-01

    Zinc has become a prominent nutrient of clinical and public health interest in the new millennium. Functions and actions for zinc emerge as increasingly ubiquitous in mammalian anatomy, physiology and metabolism. There is undoubtedly an underpinning in fundamental biology for all of the aspects of zinc in human health (clinical and epidemiological) in pediatric and public health practice. Unfortunately, basic science research may not have achieved a full understanding as yet. As a complement to the applied themes in the companion articles, a selection of recent advances in the domains homeostatic regulation and transport of zinc is presented; they are integrated, in turn, with findings on genetic expression, intracellular signaling, immunity and host defense, and bone growth. The elements include ionic zinc, zinc transporters, metallothioneins, zinc metalloenzymes and zinc finger proteins. In emerging basic research, we find some plausible mechanistic explanations for delayed linear growth with zinc deficiency and increased infectious disease resistance with zinc supplementation. Copyright © 2013 S. Karger AG, Basel.

  20. Isoflurane anesthesia exacerbates learning and memory impairment in zinc-deficient APP/PS1 transgenic mice.

    PubMed

    Feng, Chunsheng; Liu, Ya; Yuan, Ye; Cui, Weiwei; Zheng, Feng; Ma, Yuan; Piao, Meihua

    2016-12-01

    Zinc (Zn) is known to play crucial roles in numerous brain functions including learning and memory. Zn deficiency is believed to be widespread throughout the world, particularly in patients with Alzheimer's disease (AD). A number of studies have shown that volatile anesthetics, such as isoflurane, might be potential risk factors for the development of AD. However, whether isoflurane exposure accelerates the process of AD and cognitive impairment in AD patients with Zn deficiency is yet to be documented. The aim of the present study was to explore the effects of 1.4% isoflurane exposure for 2 h on learning and memory function, and neuropathogenesis in 10-month-old Zn-adequate, Zn-deficient, and Zn-treated APP/PS1 mice with the following parameters: behavioral tests, neuronal apoptosis, Aβ, and tau pathology. The results demonstrated that isoflurane exposure showed no impact on learning and memory function, but induced transient elevation of neuroapoptosis in Zn-adequate APP/PS1 mice. Exposure of isoflurane exhibited significant neuroapoptosis, Aβ generation, tau phosphorylation, and learning and memory impairment in APP/PS1 mice in the presence of Zn deficiency. Appropriate Zn treatment improved learning and memory function, and prevented isoflurane-induced neuroapoptosis in APP/PS1 mice. Isoflurane exposure may cause potential neurotoxicity, which is tolerated to some extent in Zn-adequate APP/PS1 mice. When this tolerance is limited, like in AD with Zn deficiency, isoflurane exposure markedly exacerbated learning and memory impairment, and neuropathology, indicating that AD patients with certain conditions such as Zn deficiency may be vulnerable to volatile anesthetic isoflurane. Copyright © 2016 Elsevier Ltd. All rights reserved.

  1. Perinatal ω-3 polyunsaturated fatty acid supply modifies brain zinc homeostasis during adulthood

    PubMed Central

    Jayasooriya, Anura P.; Ackland, M. Leigh; Mathai, Michael L.; Sinclair, Andrew J.; Weisinger, Harrison S.; Weisinger, Richard S.; Halver, John E.; Kitajka, Klára; Puskás, László G.

    2005-01-01

    Dietary ω-3 polyunsaturated fatty acid (PUFA) influences the expression of a number of genes in the brain. Zinc transporter (ZnT) 3 has been identified as a putative transporter of zinc into synaptic vesicles of neurons and is found in brain areas such as hippocampus and cortex. Neuronal zinc is involved in the formation of amyloid plaques, a major characteristic of Alzheimer's disease. The present study evaluated the influence of dietary ω-3 PUFA on the expression of the ZnT3 gene in the brains of adult male Sprague-Dawley rats. The rats were raised and/or maintained on a control (CON) diet that contained ω-3 PUFA or a diet deficient (DEF) in ω-3 PUFA. ZnT3 gene expression was analyzed by using real-time PCR, free zinc in brain tissue was determined by zinquin staining, and total zinc concentrations in plasma and cerebrospinal fluid were determined by atomic absorption spectrophotometry. Compared with CON-raised animals, DEF-raised animals had increased expression of ZnT3 in the brain that was associated with an increased level of free zinc in the hippocampus. In addition, compared with CON-raised animals, DEF-raised animals had decreased plasma zinc level. No difference in cerebrospinal fluid zinc level was observed. The results suggest that overexpression of ZnT3 due to a perinatal ω-3 PUFA deficiency caused abnormal zinc metabolism in the brain. Conceivably, the influence of dietary ω-3 PUFA on brain zinc metabolism could explain the observation made in population studies that the consumption of fish is associated with a reduced risk of dementia and Alzheimer's disease. PMID:15883362

  2. Perinatal omega-3 polyunsaturated fatty acid supply modifies brain zinc homeostasis during adulthood.

    PubMed

    Jayasooriya, Anura P; Ackland, M Leigh; Mathai, Michael L; Sinclair, Andrew J; Weisinger, Harrison S; Weisinger, Richard S; Halver, John E; Kitajka, Klára; Puskás, László G

    2005-05-17

    Dietary omega-3 polyunsaturated fatty acid (PUFA) influences the expression of a number of genes in the brain. Zinc transporter (ZnT) 3 has been identified as a putative transporter of zinc into synaptic vesicles of neurons and is found in brain areas such as hippocampus and cortex. Neuronal zinc is involved in the formation of amyloid plaques, a major characteristic of Alzheimer's disease. The present study evaluated the influence of dietary omega-3 PUFA on the expression of the ZnT3 gene in the brains of adult male Sprague-Dawley rats. The rats were raised and/or maintained on a control (CON) diet that contained omega-3 PUFA or a diet deficient (DEF) in omega-3 PUFA. ZnT3 gene expression was analyzed by using real-time PCR, free zinc in brain tissue was determined by zinquin staining, and total zinc concentrations in plasma and cerebrospinal fluid were determined by atomic absorption spectrophotometry. Compared with CON-raised animals, DEF-raised animals had increased expression of ZnT3 in the brain that was associated with an increased level of free zinc in the hippocampus. In addition, compared with CON-raised animals, DEF-raised animals had decreased plasma zinc level. No difference in cerebrospinal fluid zinc level was observed. The results suggest that overexpression of ZnT3 due to a perinatal omega-3 PUFA deficiency caused abnormal zinc metabolism in the brain. Conceivably, the influence of dietary omega-3 PUFA on brain zinc metabolism could explain the observation made in population studies that the consumption of fish is associated with a reduced risk of dementia and Alzheimer's disease.

  3. New perspectives on the regulation of iron absorption via cellular zinc concentrations in humans.

    PubMed

    Knez, Marija; Graham, Robin D; Welch, Ross M; Stangoulis, James C R

    2017-07-03

    Iron deficiency is the most prevalent nutritional deficiency, affecting more than 30% of the total world's population. It is a major public health problem in many countries around the world. Over the years various methods have been used with an effort to try and control iron-deficiency anemia. However, there has only been a marginal reduction in the global prevalence of anemia. Why is this so? Iron and zinc are essential trace elements for humans. These metals influence the transport and absorption of one another across the enterocytes and hepatocytes, due to similar ionic properties. This paper describes the structure and roles of major iron and zinc transport proteins, clarifies iron-zinc interactions at these sites, and provides a model for the mechanism of these interactions both at the local and systemic level. This review provides evidence that much of the massive extent of iron deficiency anemia in the world may be due to an underlying deficiency of zinc. It explains the reasons for predominance of cellular zinc status in determination of iron/zinc interactions and for the first time thoroughly explains mechanisms by which zinc brings about these changes.

  4. Inheritance of seed iron and zinc concentrations in common bean (Phaseolus vulgaris L.)

    USDA-ARS?s Scientific Manuscript database

    Micronutrients are essential elements needed in small amounts for adequate human nutrition and include the elements iron and zinc. Both of these minerals are essential to human well-being, and an adequate supply of iron and zinc helps to prevent iron deficiency anemia and zinc deficiency, two preva...

  5. Phytotoxicity of zinc and manganese to seedlings grown in soil contaminated by zinc smelting

    USGS Publications Warehouse

    Beyer, W.N.; Green, C.E.; Beyer, M.; Chaney, R.L.

    2013-01-01

    Historic emissions from two zinc smelters have injured the forest on Blue Mountain near Palmerton, Pennsylvania, USA. Seedlings of soybeans and five tree species were grown in a greenhouse in a series of mixtures of smelter-contaminated and reference soils and then phytotoxic thresholds were calculated. As little as 10% Palmerton soil mixed with reference soil killed or greatly stunted seedlings of most species. Zinc was the principal cause of the phytotoxicity to the tree seedlings, although Mn and Cd may also have been phytotoxic in the most contaminated soil mixtures. Calcium deficiency seemed to play a role in the observed phytotoxicity. Exposed soybeans showed symptoms of Mn toxicity. A test of the effect of liming on remediation of the Zn and Mn phytotoxicity caused a striking decrease in Sr-nitrate extractable metals in soils and demonstrated that liming was critical to remediation and restoration.

  6. Repletion of Zinc and Iron Deficiencies Improves Cognition of Premenopausal Women.

    DTIC Science & Technology

    1997-10-01

    to our earlier observations in premenopausal women (1, 13) and are consistent with the fact that many premenopausal women select diets that are low...women: associations of diet with serum ferritin and plasma zinc disappearance, and of serum ferritin with plasma zinc and plasma zinc disappearance...women: Associations of diet with serum ferritin and plasma zinc disappearance and of serum ferritin with plasma zinc and plasma zinc disappearance. J

  7. Decreasing stunting, anemia, and vitamin A deficiency in Peru: results of the Good Start in Life Program.

    PubMed

    Lechtig, Aarón; Cornale, Guido; Ugaz, María Elena; Arias, Lena

    2009-03-01

    The rates of stunting, iron-deficiency anemia, and vitamin A deficiency in Peru are among the highest in South America. There is little scaled-up experience on how to solve these problems countrywide. To evaluate the Good Start in Life Program during the period from 2000 to 2004. Data on weight, height, hemoglobin, serum retinol, urinary iodine, and age were obtained from children under 3 years of age during two transverse surveys in 2000 and 2004. In 2004, the program covered 75,000 children, 35,000 mothers, and 1 million inhabitants from 223 poor communities. The rate of stunting decreased from 54.1% to 36.9%, the rate of iron-deficiency anemia decreased from 76.0% to 52.3%, and the rate of vitamin A deficiency decreased from 30.4% to 5.3% (p < .01). The annual cost per child was US$116.50. Adaptations of this participative program could contribute to decreased stunting, iron-deficiency anemia, and vitamin A deficiency at the national scale in Peru and many other countries.

  8. Critical Role of Zinc as Either an Antioxidant or a Prooxidant in Cellular Systems

    PubMed Central

    2018-01-01

    Zinc is recognized as an essential trace metal required for human health; its deficiency is strongly associated with neuronal and immune system defects. Although zinc is a redox-inert metal, it functions as an antioxidant through the catalytic action of copper/zinc-superoxide dismutase, stabilization of membrane structure, protection of the protein sulfhydryl groups, and upregulation of the expression of metallothionein, which possesses a metal-binding capacity and also exhibits antioxidant functions. In addition, zinc suppresses anti-inflammatory responses that would otherwise augment oxidative stress. The actions of zinc are not straightforward owing to its numerous roles in biological systems. It has been shown that zinc deficiency and zinc excess cause cellular oxidative stress. To gain insights into the dual action of zinc, as either an antioxidant or a prooxidant, and the conditions under which each role is performed, the oxidative stresses that occur in zinc deficiency and zinc overload in conjunction with the intracellular regulation of free zinc are summarized. Additionally, the regulatory role of zinc in mitochondrial homeostasis and its impact on oxidative stress are briefly addressed. PMID:29743987

  9. Zinc Modulates Nanosilver-Induced Toxicity in Primary Neuronal Cultures.

    PubMed

    Ziemińska, Elżbieta; Strużyńska, Lidia

    2016-02-01

    Silver nanoparticles (NAg) have recently become one of the most commonly used nanomaterials. Since the ability of nanosilver to enter the brain has been confirmed, there has been a need to investigate mechanisms of its neurotoxicity. We previously showed that primary neuronal cultures treated with nanosilver undergo destabilization of calcium homeostasis via a mechanism involving glutamatergic NMDA receptors. Considering the fact that zinc interacts with these receptors, the aim of the present study was to examine the role of zinc in mechanisms of neuronal cell death in primary cultures. In cells treated with nanosilver, we noted an imbalance between extracellular and intracellular zinc levels. Thus, the influence of zinc deficiency and supplementation on nanosilver-evoked cytotoxicity was investigated by treatment with TPEN (a chelator of zinc ions), or ZnCl(2), respectively. Elimination of zinc leads to complete death of nanosilver-treated CGCs. In contrast, supplementation with ZnCl(2) increases viability of CGCs in a dose-dependent manner. Addition of zinc provided protection against the extra/intracellular calcium imbalance in a manner similar to MK-801, an antagonist of NMDA receptors. Zinc chelation by TPEN decreases the mitochondrial potential and dramatically increases the rate of production of reactive oxygen species. Our results indicate that zinc supplementation positively influences nanosilver-evoked changes in CGCs. This is presumed to be due to an inhibitory effect on NMDA-sensitive calcium channels.

  10. Hair Zinc: an Index for Zinc Status in Under-Five Children from Low-Income Communities in Kanam Area of North-Central Nigeria.

    PubMed

    Jaryum, Kiri H; Okoye, Zebulon Sunday C; Stoecker, Barbara

    2018-06-01

    Nutritional deficiencies of trace elements are among the top ten causes of death in Sub Saharan Africa. In Kanam Local Government Area of Nigeria, the problem is compounded by high levels of poverty and illiteracy. Abnormally low hair zinc levels are important, sensitive diagnostic biochemical indices of Zinc deficiency. The purpose of this study is to assess the zinc status of children less than 5 years in Kanam local government area, north-central Nigeria, by measuring the zinc level in hair samples collected from 44 under-5 children across the area. A household survey was made to assess the pattern and frequency of consumption of zinc-rich foods which was done by means of questionnaire. Hair samples were analysed for zinc content by the inductively coupled plasma-mass spectrophotometry (ICP-MS). The data were analysed statistically using the Student's t test, z test, and Pearson correlation, while questionnaire-captured data were analysed by simple arithmetic. The results of the analyses showed that the average hair zinc level was 74.35 ± 48.05 μg/g. This was below the normal range of 130-140 μg/g, for children less than 5 years. Based on the results, 86.36% have hair zinc level below the lower limit of the normal range of 130 μg/g. Between the gender, boys have higher hair zinc content than girls. Data from the questionnaire showed that 53.45% of the population studied have poor/inadequate intake of zinc-rich foods of animal origin, a dietary behaviour reported to predispose to micronutrient deficiency, including zinc.

  11. Decreased zinc in the development and progression of malignancy: an important common relationship and potential for prevention and treatment of carcinomas

    PubMed Central

    Costello, Leslie C.; Franklin, Renty B.

    2016-01-01

    Introduction Efficacious chemotherapy does not exist for treatment or prevention of prostate, liver, and pancreatic carcinomas, and some other cancers that exhibit decreased zinc in malignancy. Zinc treatment offers a potential solution; but its support has been deterred by adverse bias. Areas covered 1. The clinical and experimental evidence for the common ZIP transporter/Zn down regulation in these cancers. 2. The evidence for a zinc approach to prevent and/or treat these carcinomas. 3. The issues that introduce bias against support for the zinc approach. Expert opinion ZIP/Zn downregulation is a clinically established common event in prostate, hepatocellular and pancreatic cancers. 2. Compelling evidence supports the plausibility that a zinc treatment regimen will prevent development of malignancy and termination of progressing malignancy in these cancers; and likely other carcinomas that exhibit decreased zinc. 3. Scientifically-unfounded issues that oppose this ZIP/Zn relationship have introduced bias against support for research and funding of a zinc treatment approach. 4. The clinically-established and supporting experimental evidence provide the scientific credibility that should dictate the support for research and funding of a zinc approach for the treatment and possible prevention of these cancers. 5. This is in the best interest of the medical community and the public-at-large. PMID:27885880

  12. [Micronutrient deficiencies and linear growth: a systematic review of observational studies].

    PubMed

    Pedraza, Dixis Figueroa; Rocha, Ana Carolina Dantas; Sales, Márcia Cristina

    2013-11-01

    This article seeks to evaluate the association of iron, vitamin A and zinc deficiencies with linear growth retardation. A systematic review of electronic databases in PubMed, LILACS and SciELO was conducted. Scientific papers published between January 1995 and March 2010 were selected, inserting the key words: (growth OR nutritional status) AND (child, preschool OR infant) AND (zinc AND iron AND vitamin A) OR (zinc AND iron) OR (zinc AND vitamin A) OR (iron AND vitamin A). Fourteen observational design studies were reviewed. In the cohort studies (two), one indicated a statistical association between iron levels and stunting; and the other revealed a statistical association between serum ferritin concentrations and an increase in height. Ten cross-sectional studies investigated the statistical association between micronutrient deficiencies and stunting, three of which resulted in an association with iron, two with vitamin A and none with zinc. Elucidation of the association between stunting and iron, vitamin A and zinc deficiencies involves difficulties of a biological nature and also related to the magnitude of these deficiencies, indicating the importance of a methodological standardization of the studies.

  13. Duration of exclusive breast-feeding and infant iron and zinc status in rural Bangladesh.

    PubMed

    Eneroth, Hanna; El Arifeen, Shams; Persson, Lars-Ake; Kabir, Iqbal; Lönnerdal, Bo; Hossain, Mohammad Bakhtiar; Ekström, Eva-Charlotte

    2009-08-01

    There is a concern that exclusive breast-feeding (EBF) for 6 mo may lead to iron and zinc deficiency in low-birth weight (LBW) infants. We assessed the association between duration of EBF and infant iron and zinc status in the Maternal and Infant Nutrition Interventions in Matlab trial, Bangladesh, stratified for normal birth weigh (NBW) and LBW. Duration of EBF was classified into EBF <4 mo and EBF 4-6 mo based on monthly recalls of foods introduced to the infant. Blood samples collected at 6 mo were analyzed for plasma zinc (n = 1032), plasma ferritin (n = 1040), and hemoglobin (Hb) (n = 791). Infants EBF 4-6 mo had a higher mean plasma zinc concentration (9.9 +/- 2.3 micromol/L) than infants EBF <4mo (9.5 +/- 2.0 micromol/L) (P < 0.01). This association was apparent in only the NBW strata and was not reflected in a lower prevalence of zinc deficiency. Duration of EBF was not associated with concentration of plasma ferritin, Hb concentration, or prevalence of iron deficiency or anemia in any strata. Regardless of EBF duration, the prevalence of zinc deficiency, iron deficiency, and anemia was high in infants in this population and strategies to prevent deficiency are needed.

  14. iTRAQ Analysis Reveals Mechanisms of Growth Defects Due to Excess Zinc in Arabidopsis1[W][OA

    PubMed Central

    Fukao, Yoichiro; Ferjani, Ali; Tomioka, Rie; Nagasaki, Nahoko; Kurata, Rie; Nishimori, Yuka; Fujiwara, Masayuki; Maeshima, Masayoshi

    2011-01-01

    The micronutrient zinc is essential for all living organisms, but it is toxic at high concentrations. Here, to understand the effects of excess zinc on plant cells, we performed an iTRAQ (for isobaric tags for relative and absolute quantification)-based quantitative proteomics approach to analyze microsomal proteins from Arabidopsis (Arabidopsis thaliana) roots. Our approach was sensitive enough to identify 521 proteins, including several membrane proteins. Among them, IRT1, an iron and zinc transporter, and FRO2, a ferric-chelate reductase, increased greatly in response to excess zinc. The expression of these two genes has been previously reported to increase under iron-deficient conditions. Indeed, the concentration of iron was significantly decreased in roots and shoots under excess zinc. Also, seven subunits of the vacuolar H+-ATPase (V-ATPase), a proton pump on the tonoplast and endosome, were identified, and three of them decreased significantly in response to excess zinc. In addition, excess zinc in the wild type decreased V-ATPase activity and length of roots and cells to levels comparable to those of the untreated de-etiolated3-1 mutant, which bears a mutation in V-ATPase subunit C. Interestingly, excess zinc led to the formation of branched and abnormally shaped root hairs, a phenotype that correlates with decreased levels of proteins of several root hair-defective mutants. Our results point out mechanisms of growth defects caused by excess zinc in which cross talk between iron and zinc homeostasis and V-ATPase activity might play a central role. PMID:21325567

  15. Zinc Levels Modulate Lifespan through Multiple Longevity Pathways in Caenorhabditis elegans

    PubMed Central

    Kumar, Jitendra; Barhydt, Tracy; Awasthi, Anjali; Lithgow, Gordon J.; Killilea, David W.; Kapahi, Pankaj

    2016-01-01

    Zinc is an essential trace metal that has integral roles in numerous biological processes, including enzymatic function, protein structure, and cell signaling pathways. Both excess and deficiency of zinc can lead to detrimental effects on development and metabolism, resulting in abnormalities and disease. We altered the zinc balance within Caenorhabditis elegans to examine how changes in zinc burden affect longevity and healthspan in an invertebrate animal model. We found that increasing zinc levels in vivo with excess dietary zinc supplementation decreased the mean and maximum lifespan, whereas reducing zinc levels in vivo with a zinc-selective chelator increased the mean and maximum lifespan in C. elegans. We determined that the lifespan shortening effects of excess zinc required expression of DAF-16, HSF-1 and SKN-1 proteins, whereas the lifespan lengthening effects of the reduced zinc may be partially dependent upon this set of proteins. Furthermore, reducing zinc levels led to greater nuclear localization of DAF-16 and enhanced dauer formation compared to controls, suggesting that the lifespan effects of zinc are mediated in part by the insulin/IGF-1 pathway. Additionally, zinc status correlated with several markers of healthspan in worms, including proteostasis, locomotion and thermotolerance, with reduced zinc levels always associated with improvements in function. Taken together, these data support a role for zinc in regulating both development and lifespan in C. elegans, and that suggest that regulation of zinc homeostasis in the worm may be an example of antagonistic pleiotropy. PMID:27078872

  16. Zinc: health effects and research priorities for the 1990s.

    PubMed Central

    Walsh, C T; Sandstead, H H; Prasad, A S; Newberne, P M; Fraker, P J

    1994-01-01

    This review critically summarizes the literature on the spectrum of health effects of zinc status, ranging from symptoms of zinc deficiency to excess exposure. Studies on zinc intake are reviewed in relation to optimum requirements as a function of age and sex. Current knowledge on the biochemical properties of zinc which are critical to the essential role of this metal in biological systems is summarized. Dietary and physiological factors influencing the bioavailability and utilization of zinc are considered with special attention to interactions with iron and copper status. The effects of zinc deficiency and toxicity are reviewed with respect to specific organs, immunological and reproductive function, and genotoxicity and carcinogenicity. Finally, key questions are identified where research is needed, such as the risks to human health of altered environmental distribution of zinc, assessment of zinc status in humans, effects of zinc status in relation to other essential metals on immune function, reproduction, neurological function, and the cardiovascular system, and mechanistic studies to further elucidate the biological effects of zinc at the molecular level. PMID:7925188

  17. Rising atmospheric CO2 lowers food zinc, iron, and protein concentrations

    USDA-ARS?s Scientific Manuscript database

    Dietary deficiencies of zinc and iron are a major global public health problem. Most people who experience these deficiencies depend on agricultural crops for zinc and iron. In this context, the influence of rising concentrations of atmospheric CO2 on the availability of these nutrients from crops i...

  18. Agronomic Approach of Zinc Biofortification Can Increase Zinc Bioavailability in Wheat Flour and thereby Reduce Zinc Deficiency in Humans

    PubMed Central

    Liu, Dunyi; Liu, Yumin; Zhang, Wei; Chen, Xinping; Zou, Chunqin

    2017-01-01

    Zinc (Zn) deficiency is a common disorder of humans in developing countries. The effect of Zn biofortification (via application of six rates of Zn fertilizer to soil) on Zn bioavailability in wheat grain and flour and its impacts on human health was evaluated. Zn bioavailability was estimated with a trivariate model that included Zn homeostasis in the human intestine. As the rate of Zn fertilization increased, the Zn concentration increased in all flour fractions, but the percentages of Zn in standard flour (25%) and bran (75%) relative to total grain Zn were constant. Phytic acid (PA) concentrations in grain and flours were unaffected by Zn biofortification. Zn bioavailability and the health impact, as indicated by disability-adjusted life years (DALYs) saved, increased with the Zn application rate and were greater in standard and refined flour than in whole grain and coarse flour. The biofortified standard and refined flour obtained with application of 50 kg/ha ZnSO4·7H2O met the health requirement (3 mg of Zn obtained from 300 g of wheat flour) and reduced DALYs by >20%. Although Zn biofortification increased Zn bioavailability in standard and refined flour, it did not reduce the bioavailability of iron, manganese, or copper in wheat flour. PMID:28481273

  19. Agronomic Approach of Zinc Biofortification Can Increase Zinc Bioavailability in Wheat Flour and thereby Reduce Zinc Deficiency in Humans.

    PubMed

    Liu, Dunyi; Liu, Yumin; Zhang, Wei; Chen, Xinping; Zou, Chunqin

    2017-05-06

    Zinc (Zn) deficiency is a common disorder of humans in developing countries. The effect of Zn biofortification (via application of six rates of Zn fertilizer to soil) on Zn bioavailability in wheat grain and flour and its impacts on human health was evaluated. Zn bioavailability was estimated with a trivariate model that included Zn homeostasis in the human intestine. As the rate of Zn fertilization increased, the Zn concentration increased in all flour fractions, but the percentages of Zn in standard flour (25%) and bran (75%) relative to total grain Zn were constant. Phytic acid (PA) concentrations in grain and flours were unaffected by Zn biofortification. Zn bioavailability and the health impact, as indicated by disability-adjusted life years (DALYs) saved, increased with the Zn application rate and were greater in standard and refined flour than in whole grain and coarse flour. The biofortified standard and refined flour obtained with application of 50 kg/ha ZnSO₄·7H₂O met the health requirement (3 mg of Zn obtained from 300 g of wheat flour) and reduced DALYs by >20%. Although Zn biofortification increased Zn bioavailability in standard and refined flour, it did not reduce the bioavailability of iron, manganese, or copper in wheat flour.

  20. Oxidative stress-induced increase of intracellular zinc in astrocytes decreases their functional expression of P2X7 receptors and engulfing activity.

    PubMed

    Furuta, Takahiro; Mukai, Ayumi; Ohishi, Akihiro; Nishida, Kentaro; Nagasawa, Kazuki

    2017-12-01

    Neuron-glia communication mediated by neuro- and glio-transmitters such as ATP and zinc is crucial for the maintenance of brain homeostasis, and its dysregulation is found under pathological conditions. It is reported that under oxidative stress-loaded conditions, astrocytes exhibit increased intra- and extra-cellular labile zinc, the latter triggering microglial M1 activation, while the pathophysiological role of the former remains unrevealed. In this study, we examined whether the oxidative stress-induced increase of intracellular labile zinc is involved in the P2X7 receptor (P2X7R)-mediated regulation of astrocytic engulfing activity. The exposure of cultured astrocytes to sub-lethal oxidative stress through their treatment with 400 μM H 2 O 2 increased intracellular labile zinc, of which the concentration reached a peak level of approximately 2 μM at 2 h after the treatment. In astrocytes under sub-lethal oxidative stress, the uptake of YO-PRO-1 and latex beads as markers for P2X7R channel/pore activity and astrocytic engulfing activity, respectively, was decreased, and these decreased activities were accompanied by decreased expression of P2X7R at the plasma membrane via intracellular labile zinc-mediated translocation of it. With the oxidative stress, the expression level of full length P2X7R relative to that of its splice variants in astrocytes was decreased, leading to a decrease of the relative expression of the trimer consisting of full length P2X7R. Collectively, sub-lethal oxidative stress induces an astrocytic modal shift from the normal resting engulfing mode to the activated astrogliosis mode via an intracellular labile zinc-mediated decrease of the functional expression of P2X7R.

  1. Acute changes in cellular zinc alters zinc uptake rates prior to zinc transporter gene expression in Jurkat cells.

    PubMed

    Holland, Tai C; Killilea, David W; Shenvi, Swapna V; King, Janet C

    2015-12-01

    A coordinated network of zinc transporters and binding proteins tightly regulate cellular zinc levels. Canonical responses to zinc availability are thought to be mediated by changes in gene expression of key zinc transporters. We investigated the temporal relationships of actual zinc uptake with patterns of gene expression in membrane-bound zinc transporters in the human immortalized T lymphocyte Jurkat cell line. Cellular zinc levels were elevated or reduced with exogenous zinc sulfate or N,N,N',N-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN), respectively. Excess zinc resulted in a rapid 44 % decrease in the rate of zinc uptake within 10 min. After 120 min, the expression of metallothionein (positive control) increased, as well as the zinc exporter, ZnT1; however, the expression of zinc importers did not change during this time period. Zinc chelation with TPEN resulted in a rapid twofold increase in the rate of zinc uptake within 10 min. After 120 min, the expression of ZnT1 decreased, while again the expression of zinc importers did not change. Overall, zinc transporter gene expression kinetics did not match actual changes in cellular zinc uptake with exogenous zinc or TPEN treatments. This suggests zinc transporter regulation may be the initial response to changes in zinc within Jurkat cells.

  2. Transcriptome sequencing and analysis of zinc-uptake-related genes in Trichophyton mentagrophytes.

    PubMed

    Zhang, Xinke; Dai, Pengxiu; Gao, Yongping; Gong, Xiaowen; Cui, Hao; Jin, Yipeng; Zhang, Yihua

    2017-11-21

    Trichophyton mentagrophytes is an important zoonotic dermatophytic (ringworm) pathogen; causing severe skin infection in humans and other animals worldwide. Fortunately, commonly used fungal skin disease prevention and treatment measures are relatively simple. However, T. mentagrophytes is primarily studied at the epidemiology and drug efficacy research levels, yet current study has been unable to meet the needs of clinical medicine. Zinc is a crucial trace element for the growth and reproduction of fungi and other microorganisms. The metal ions coordinate within a variety of proteins to form zinc finger proteins, which perform many vital biological functions. Zinc transport regulatory networks have not been resolved in T. mentagrophytes. The T. mentagrophytes transcriptome will allow us to discover new genes, particularly those genes involved in zinc uptake. We found T. mentagrophytes growth to be restricted by zinc deficiency; natural T. mentagrophytes growth requires zinc ions. T. Mentagrophytes must acquire zinc ions for growth and development. The transcriptome of T. mentagrophytes was sequenced by using Illumina HiSeq™ 2000 technology and the de novo assembly of the transcriptome was performed by using the Trinity method, and functional annotation was analyzed. We got 10,751 unigenes. The growth of T. mentagrophytes is severely inhibited and there were many genes showing significant up regulation and down regulation respectively in T. mentagrophytes when zinc deficiency. Zinc deficiency can affect the expression of multiple genes of T. mentagrophytes. The effect of the zinc deficiency could be recovered in the normal medium. And we finally found the zinc-responsive activating factor (ZafA) and speculated that 4 unigenes are zinc transporters. We knocked ZafA gene by ATMT transformation in T. mentagrophytes, the result showed that ZafA gene is very important for the growth and the generation of conidia in T. mentagrophytes. The expression of 4 zinc

  3. Recent advances in knowledge of zinc nutrition and human health.

    PubMed

    Hess, Sonja Y; Lönnerdal, Bo; Hotz, Christine; Rivera, Juan A; Brown, Kenneth H

    2009-03-01

    Zinc deficiency increases the risk and severity of a variety of infections, restricts physical growth, and affects specific outcomes of pregnancy. Global recognition of the importance of zinc nutrition in public health has expanded dramatically in recent years, and more experience has accumulated on the design and implementation of zinc intervention programs. Therefore, the Steering Committee of the International Zinc Nutrition Consultative Group (IZiNCG) completed a second IZiNCG technical document that reexamines the latest information on the intervention strategies that have been developed to enhance zinc nutrition and control zinc deficiency. In particular, the document reviews the current evidence regarding preventive zinc supplementation and the role of zinc as adjunctive therapy for selected infections, zinc fortification, and dietary diversification or modification strategies, including the promotion and protection of breastfeeding and biofortification. The purposes of this introductory paper are to summarize new guidelines on the assessment of population zinc status, as recommended by the World Health Organization (WHO), the United Nations Children's Fund (UNICEF), the International Atomic Energy Agency (IAEA), and IZiNCG, and to provide an overview on several new advances in zinc metabolism. The following papers will then review the intervention strategies individually.

  4. Soybean extracts increase cell surface ZIP4 abundance and cellular zinc levels: a potential novel strategy to enhance zinc absorption by ZIP4 targeting.

    PubMed

    Hashimoto, Ayako; Ohkura, Katsuma; Takahashi, Masakazu; Kizu, Kumiko; Narita, Hiroshi; Enomoto, Shuichi; Miyamae, Yusaku; Masuda, Seiji; Nagao, Masaya; Irie, Kazuhiro; Ohigashi, Hajime; Andrews, Glen K; Kambe, Taiho

    2015-12-01

    Dietary zinc deficiency puts human health at risk, so we explored strategies for enhancing zinc absorption. In the small intestine, the zinc transporter ZIP4 functions as an essential component of zinc absorption. Overexpression of ZIP4 protein increases zinc uptake and thereby cellular zinc levels, suggesting that food components with the ability to increase ZIP4 could potentially enhance zinc absorption via the intestine. In the present study, we used mouse Hepa cells, which regulate mouse Zip4 (mZip4) in a manner indistinguishable from that in intestinal enterocytes, to screen for suitable food components that can increase the abundance of ZIP4. Using this ZIP4-targeting strategy, two such soybean extracts were identified that were specifically able to decrease mZip4 endocytosis in response to zinc. These soybean extracts also effectively increased the abundance of apically localized mZip4 in transfected polarized Caco2 and Madin-Darby canine kidney cells and, moreover, two apically localized mZip4 acrodermatitis enteropathica mutants. Soybean components were purified from one extract and soyasaponin Bb was identified as an active component that increased both mZip4 protein abundance and zinc levels in Hepa cells. Finally, we confirmed that soyasaponin Bb is capable of enhancing cell surface endogenous human ZIP4 in human cells. Our results suggest that ZIP4 targeting may represent a new strategy to improve zinc absorption in humans. © 2015 Authors; published by Portland Press Limited.

  5. Zinc Therapy in Dermatology: A Review

    PubMed Central

    Mahajan, Vikram K.; Mehta, Karaninder S.; Chauhan, Pushpinder S.

    2014-01-01

    Zinc, both in elemental or in its salt forms, has been used as a therapeutic modality for centuries. Topical preparations like zinc oxide, calamine, or zinc pyrithione have been in use as photoprotecting, soothing agents or as active ingredient of antidandruff shampoos. Its use has expanded manifold over the years for a number of dermatological conditions including infections (leishmaniasis, warts), inflammatory dermatoses (acne vulgaris, rosacea), pigmentary disorders (melasma), and neoplasias (basal cell carcinoma). Although the role of oral zinc is well-established in human zinc deficiency syndromes including acrodermatitis enteropathica, it is only in recent years that importance of zinc as a micronutrient essential for infant growth and development has been recognized. The paper reviews various dermatological uses of zinc. PMID:25120566

  6. Marginal dietary zinc deprivation augments sepsis-induced alterations in skeletal muscle TNF-α but not protein synthesis.

    PubMed

    Crowell, Kristen T; Kelleher, Shannon L; Soybel, David I; Lang, Charles H

    2016-11-01

    Severe zinc deficiency is associated with an increased systemic inflammatory response and mortality after sepsis. However, the impact of mild zinc deficiency, which is more common in populations with chronic illnesses and sepsis, is unknown. In this study, we hypothesized that marginal dietary Zn deprivation (ZM) would amplify tissue inflammation and exacerbate the sepsis-induced decrease in muscle protein synthesis. Adult male C57BL/6 mice were fed a zinc-adequate (ZA) or ZM diet (30 or 10 mg Zn/kg, respectively) over 4 weeks, peritonitis was induced by cecal ligation and puncture (CLP), and mice were examined at either 24 h (acute) or 5 days (chronic) post-CLP Acute sepsis decreased the in vivo rate of skeletal muscle protein synthesis and the phosphorylation of the mTOR substrate 4E-BP1. Acutely, sepsis increased TNF-α and IL-6 mRNA in muscle, and the increase in TNF-α was significantly greater in ZM mice. However, muscle protein synthesis and 4E-BP1 phosphorylation returned to baseline 5 days post-CLP in both ZA and ZM mice. Protein degradation via markers of the ubiquitin proteasome pathway was increased in acute sepsis, yet only MuRF1 mRNA was increased in chronic sepsis and ZM amplified this elevation. Our data suggest that mild zinc deficiency increases TNF-α in muscle acutely after sepsis but does not significantly modulate the rate of muscle protein synthesis. © 2016 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.

  7. Systematic review of zinc fortification trials.

    PubMed

    Das, Jai K; Kumar, Rohail; Salam, Rehana A; Bhutta, Zulfiqar A

    2013-01-01

    Zinc is one of the essential trace elements required by the human body as it is present in more than a hundred specific enzymes and serves as an important structural ion in transcription factors. Around one third of the world population lives in countries with a high prevalence of zinc deficiency. Food fortification with zinc seems to be an attractive public health strategy and a number of programs have been initiated, especially in developing countries. We conducted a systematic review to assess the efficacy of zinc fortification. A total of 11 studies with 771 participants were included in our analysis. Zinc fortification was associated with significant improvements in plasma zinc concentrations [standard mean difference (SMD) 1.28, 95% CI 0.56, 2.01] which is a functional indicator of zinc status. Significant improvement was observed for height velocity (SMD 0.52, 95% CI 0.01, 1.04); however, this finding was weak and based on a restricted analysis. Further subgroup analysis showed significant improvement in height velocity among very-low-birth-weight infants (SMD 0.70, 95% CI 0.02, 1.37), while for healthy newborns, the impact was insignificant. Zinc fortification had insignificant impacts on serum alkaline levels, serum copper levels, hemoglobin and weight gain. Although the findings highlight that zinc fortification is associated with an increased serum concentration of the micronutrient, overall evidence of the effectiveness of this approach is limited. Data on pregnant and lactating women is scarce. Large-scale fortification programs with robust impact assessment should be initiated to cover larger populations in all age groups. Mass fortification of zinc may be a cost-effective strategy to overcome zinc deficiency. Copyright © 2013 S. Karger AG, Basel.

  8. Effect of supplementary zinc on body mass index, pulmonary function and hospitalization in children with cystic fibrosis.

    PubMed

    Ataee, Pedram; Najafi, Mehri; Gharagozlou, Mohammad; Aflatounian, Majid; Mahmoudi, Maryam; Khodadad, Ahmad; Farahmand, Fatemeh; Motamed, Farzaneh; Fallahi, Glolam Hossein; Kalantari, Najmoddin; Soheili, Habib; Modarresi, Vajiheh; Modarresi, Mozhgan Sabbaghian; Rezaei, Nima

    2014-01-01

    Zinc deficiency, which is common in patients with cystic fibrosis (CF), can lead to several complications that may increase the number of hospital admissions in this group of patients. As supplementary zinc can prevent such complications, this study was performed to evaluate the effect of supplementary zinc on body mass index (BMI), forced expiratory volume in one second (FEV1) and number of hospitalizations in CF patients. In this study, 30 children with CF, who were referred to the Digestive Diseases Clinic of the Children's Medical Center in Tehran, were enrolled. Supplementary zinc of 2 mg/kg per day was administered to all patients. Serum level of zinc, alkaline phosphatase, and albumin as well as BMI, FEV1, and number of hospitalizations were compared before and after zinc administration. Height (p<0.001), weight (p<0.001) and BMI (p=0.001) were significantly increased after zinc, while the number of hospitalizations was significantly decreased (p=0.023). In contrast to patients with normal pulmonary function tests who received supplement therapy, BMI was not increased in those with abnormal pulmonary function after supplementary zinc. Supplementary zinc can increase BMI in CF patients, mostly in those with normal pulmonary function. While supplementary zinc may decrease the number of hospitalizations, other factors can also influence the hospitalization number.

  9. Mena deficiency delays tumor progression and decreases metastasis in polyoma middle-T transgenic mouse mammary tumors.

    PubMed

    Roussos, Evanthia T; Wang, Yarong; Wyckoff, Jeffrey B; Sellers, Rani S; Wang, Weigang; Li, Jiufeng; Pollard, Jeffrey W; Gertler, Frank B; Condeelis, John S

    2010-01-01

    The actin binding protein Mammalian enabled (Mena), has been implicated in the metastatic progression of solid tumors in humans. Mena expression level in primary tumors is correlated with metastasis in breast, cervical, colorectal and pancreatic cancers. Cells expressing high Mena levels are part of the tumor microenvironment for metastasis (TMEM), an anatomical structure that is predictive for risk of breast cancer metastasis. Previously we have shown that forced expression of Mena adenocarcinoma cells enhances invasion and metastasis in xenograft mice. Whether Mena is required for tumor progression is still unknown. Here we report the effects of Mena deficiency on tumor progression, metastasis and on normal mammary gland development. To investigate the role of Mena in tumor progression and metastasis, Mena deficient mice were intercrossed with mice carrying a transgene expressing the polyoma middle T oncoprotein, driven by the mouse mammary tumor virus. The progeny were investigated for the effects of Mena deficiency on tumor progression via staging of primary mammary tumors and by evaluation of morbidity. Stages of metastatic progression were investigated using an in vivo invasion assay, intravital multiphoton microscopy, circulating tumor cell burden, and lung metastases. Mammary gland development was studied in whole mount mammary glands of wild type and Mena deficient mice. Mena deficiency decreased morbidity and metastatic dissemination. Loss of Mena increased mammary tumor latency but had no affect on mammary tumor burden or histologic progression to carcinoma. Elimination of Mena also significantly decreased epidermal growth factor (EGF) induced in vivo invasion, in vivo motility, intravasation and metastasis. Non-tumor bearing mice deficient for Mena also showed defects in mammary gland terminal end bud formation and branching. Deficiency of Mena decreases metastasis by slowing tumor progression and reducing tumor cell invasion and intravasation. Mena

  10. Effect of zinc intake on hepatic autophagy during acute alcohol intoxication.

    PubMed

    Liuzzi, Juan P; Narayanan, Vijaya; Doan, Huong; Yoo, Changwon

    2018-04-01

    Autophagy is a conserved mechanism that plays a housekeeping role by eliminating protein aggregates and damaged organelles. Recent studies have demonstrated that acute ethanol intoxication induces hepatic autophagy in mice. The effect of dietary zinc intake on hepatic autophagic flux during ethanol intoxication has not been evaluated using animal models. Herein, we investigated whether zinc deficiency and excess can affect autophagic flux in the liver in mice and in human hepatoma cells acutely exposed to ethanol. A mouse model of binge ethanol feeding was utilized to analyze the effect of low, adequate, and high zinc intake on hepatic autophagic flux during ethanol intoxication. Autophagic flux was inferred by analyzing LC3II/LC3I ratio, protein levels of p62/SQSTM1, Beclin1 and Atg7, and phosphorylation of 4EBP1. In addition, the degradation of the fusion protein LC3-GFP and the formation of autophagosomes and autolysosomes were evaluated in cells. Ethanol treatment stimulated autophagy in mice and cells. High zinc intake resulted in enhanced autophagy in mice exposed to ethanol. Conversely, zinc deficiency was consistently associated with impaired ethanol-induced autophagy in mice and cells. Zinc-deficient mice exhibited a high degree of ethanol-driven steatosis. Furthermore, zinc depletion increased apoptosis in cells exposed to ethanol. The results of this study suggest that adequate zinc intake is necessary for proper stimulation of autophagy by ethanol. Poor zinc status is commonly found among alcoholics and could likely contribute to faulty autophagy.

  11. Zinc Replenishment Reverses Overexpression of the Proinflammatory Mediator S100A8 and Esophageal Preneoplasia in the Rat

    PubMed Central

    Taccioli, Cristian; Wan, Shao-Gui; Liu, Chang-Gong; Alder, Hansjuerg; Volinia, Stefano; Farber, John L.; Croce, Carlo M.

    2009-01-01

    Background & Aims Zinc-deficiency is implicated in the pathogenesis of human esophageal cancer. In the rat esophagus, it induces cell proliferation, modulates genetic expression, and enhances carcinogenesis. Zinc-replenishment reverses proliferation and inhibits carcinogenesis. The zinc-deficient rat model allows the identification of biological differences affected by zinc during early esophageal carcinogenesis. Methods We evaluated gene expression profiles of esophageal epithelia from zinc-deficient and replenished rats versus sufficient rats using Affymetrix Rat Genome GeneChip. We characterized the role of the top-upregulated gene S100A8 in esophageal hyperplasia/reversal and in chemically-induced esophageal carcinogenesis in zinc-modulated animals by immunohistochemistry and real-time quantitative polymerase chain reaction. Results The hyperplastic deficient esophagus has a distinct expression signature with the proinflammation-gene S100A8 and S100A9 upregulated 57- and 5-fold. “Response to external stimulus” comprising S100A8 was the only significantly overrepresented biological pathway among the upregulated genes. Zinc-replenishment rapidly restored to control levels the expression of S100A8/A9 and 27 other genes and reversed the hyperplastic phenotype. With its receptor RAGE, co-localization and overexpression of S100A8 protein occurred in the deficient esophagus that overexpressed NF-κB p65 and COX-2 protein. Zinc-replenishment but not by a COX-2 inhibitor reduced the overexpression of these 4 proteins. Additionally, esophageal S100A8/A9 mRNA levels were directly associated with the diverse tumorigenic outcome in zinc-deficient and zinc-replenished rats. Conclusions In vivo zinc regulates S100A8 expression and modulates the link between S100A8-RAGE interaction and downstream NF-κB/COX-2 signaling. The finding that zinc regulates an inflammatory pathway in esophageal carcinogenesis may lead to prevention and therapy for this cancer. PMID:19111725

  12. Zinc oxide nanoparticles decrease the expression and activity of plasma membrane calcium ATPase, disrupt the intracellular calcium homeostasis in rat retinal ganglion cells.

    PubMed

    Guo, Dadong; Bi, Hongsheng; Wang, Daoguang; Wu, Qiuxin

    2013-08-01

    Zinc oxide nanoparticle is one of the most important materials with diverse applications. However, it has been reported that zinc oxide nanoparticles are toxic to organisms, and that oxidative stress is often hypothesized to be an important factor in cytotoxicity mediated by zinc oxide nanoparticles. Nevertheless, the mechanism of toxicity of zinc oxide nanoparticles has not been completely understood. In this study, we investigated the cytotoxic effect of zinc oxide nanoparticles and the possible molecular mechanism involved in calcium homeostasis mediated by plasma membrane calcium ATPase in rat retinal ganglion cells. Real-time cell electronic sensing assay showed that zinc oxide nanoparticles could exert cytotoxic effect on rat retinal ganglion cells in a concentration-dependent manner; flow cytometric analysis indicated that zinc oxide nanoparticles could lead to cell damage by inducing the overproduction of reactive oxygen species. Furthermore, zinc oxide nanoparticles could also apparently decrease the expression level and their activity of plasma membrane calcium ATPase, which finally disrupt the intracellular calcium homeostasis and result in cell death. Taken together, zinc oxide nanoparticles could apparently decrease the plasma membrane calcium ATPase expression, inhibit their activity, cause the elevated intracellular calcium ion level and disrupt the intracellular calcium homeostasis. Further, the disrupted calcium homeostasis will trigger mitochondrial dysfunction, generate excessive reactive oxygen species, and finally initiate cell death. Thus, the disrupted calcium homeostasis is involved in the zinc oxide nanoparticle-induced rat retinal ganglion cell death. Copyright © 2013 Elsevier Ltd. All rights reserved.

  13. Factors influencing zinc status of apparently healthy indians.

    PubMed

    Agte, Vaishali V; Chiplonkar, Shashi A; Tarwadi, Kirtan V

    2005-10-01

    To identify dietary, environmental and socio-economic factors associated with mild zinc deficiency, three zinc status indices; erythrocyte membrane zinc (RBCMZn), plasma zinc and super oxide dismutase (SOD) were assessed in free living and apparently healthy Indian population. Dietary patterns of 232 men and 223 women (20-65 yr) from rural, industrial and urban regions of Western India were evaluated by food frequency questionnaire. RBCMZn was estimated using atomic absorption spectrometry, hemoglobin and serum ceruloplasmin by spectrophotometer. On a sub sample (48 men and 51 women) plasma zinc and SOD were also assessed. Mean RBCMZn was 0.5 +/- 0.1 micromols/g protein with 46% individuals showing zinc deficiency. Mean plasma zinc was 0.98 +/- 0.12 microg/mL with 25% men and 2.5% women having values below normal range. Mean SOD was 0.97 +/- 0.1 (u/mL cells). A significant positive correlation was observed between intakes of green leafy vegetables, other vegetables and milk products with RBCMZn status (p < 0.05). But these were not correlated with plasma zinc (p > 0.2). Cereal and legume intakes were negatively correlated with RBCMZn (p < 0.05) but positively correlated with plasma zinc (p < 0.05) and not correlated with SOD (p > 0.2). Fruit and other vegetable intake were positively correlated with SOD (p < 0.05) alone. Logistic regression analyses revealed that RBCMZn was positively associated with intakes of beta-carotene, zinc and environmental conditions and negatively associated with family size (p < 0.05). Plasma zinc indicated positive association with zinc, thiamin and riboflavin intakes (p < 0.05) and SOD showed negative association with iron and family size. RBCMZn was a more sensitive indicator of long-term zinc status than plasma zinc and SOD. Prominent determinants of zinc status were intakes of beta-carotene and zinc along with environmental conditions and family size.

  14. Zinc status and cognitive function of pregnant women in Southern Ethiopia

    PubMed Central

    Stoecker, BJ; Abebe, Y; Hubbs-Tait, L; Kennedy, TS; Gibson, RS; Arbide, I; Teshome, A; Westcott, J; Krebs, NF; Hambidge, KM

    2015-01-01

    The relation between zinc status and cognitive function was examined in a cross-sectional study in the Sidama area of Southern Ethiopia. Pregnant women >24 weeks of gestation from three adjacent rural villages volunteered to participate. Mean (s.d.) plasma zinc of 99 women was 6.97 (1.07) μmol/l (below the cutoff of 7.6 μmol/l indicative of zinc deficiency at this stage of gestation). The Raven’s Coloured Progressive Matrices (CPM) test was administered individually. Scores for the Raven’s scale A, which is the simplest scale, ranged from 4 to 10 of a possible 12. Women with plasma zinc <7.6 μmol/l had significantly lower Raven’s CPM scale A scores than women with plasma zinc concentrations >7.6 μmol/l. Plasma zinc and maternal age and education predicted 17% of the variation in Raven’s CPM scale A scores. We conclude that zinc deficiency is a major factor affecting cognition in these pregnant women. PMID:19190668

  15. Interaction of zinc with dental mineral.

    PubMed

    Ingram, G S; Horay, C P; Stead, W J

    1992-01-01

    As some currently available toothpastes contain zinc compounds, the reaction of zinc with dental mineral and its effect on crystal growth rates were studied using three synthetic calcium-deficient hydroxyapatites (HAP) as being representative of dental mineral. Zinc was readily acquired by all HAP samples in the absence of added calcium, the amount adsorbed being proportional to the HAP surface area; about 9 mumol Zn/m2 was adsorbed at high zinc concentrations. As zinc was acquired, calcium was released, consistent with 1:1 Ca:Zn exchange. Soluble calcium reduced zinc uptake and similarly, calcium post-treatment released zinc. Pretreatment of HAP with 0.5 mM zinc reduced its subsequent ability to undergo seeded crystal growth, as did extracts of a toothpaste containing 0.5% zinc citrate, even in the presence of saliva. The reverse reaction, i.e. displacement of adsorbed zinc by salivary levels of calcium, however, indicates the mechanism by which zinc can reduce calculus formation in vivo by inhibiting plaque mineralisation without adversely affecting the anti-caries effects of fluoride.

  16. Rice Genotype Differences in Tolerance of Zinc-Deficient Soils: Evidence for the Importance of Root-Induced Changes in the Rhizosphere

    PubMed Central

    Mori, Asako; Kirk, Guy J. D.; Lee, Jae-Sung; Morete, Mark J.; Nanda, Amrit K.; Johnson-Beebout, Sarah E.; Wissuwa, Matthias

    2016-01-01

    Zinc (Zn) deficiency is a major constraint to rice production and Zn is also often deficient in humans with rice-based diets. Efforts to breed more Zn-efficient rice are constrained by poor understanding of the mechanisms of tolerance to deficiency. Here we assess the contributions of root growth and root Zn uptake efficiency, and we seek to explain the results in terms of specific mechanisms. We made a field experiment in a highly Zn-deficient rice soil in the Philippines with deficiency-tolerant and -sensitive genotypes, and measured growth, Zn uptake and root development. We also measured the effect of planting density. Tolerant genotypes produced more crown roots per plant and had greater uptake rates per unit root surface area; the latter was at least as important as root number to overall tolerance. Tolerant and sensitive genotypes took up more Zn per plant at greater planting densities. The greater uptake per unit root surface area, and the planting density effect can only be explained by root-induced changes in the rhizosphere, either solubilizing Zn, or neutralizing a toxin that impedes Zn uptake (possibly HCO3− or Fe2+), or both. Traits for these and crown root number are potential breeding targets. PMID:26793198

  17. Rice Genotype Differences in Tolerance of Zinc-Deficient Soils: Evidence for the Importance of Root-Induced Changes in the Rhizosphere.

    PubMed

    Mori, Asako; Kirk, Guy J D; Lee, Jae-Sung; Morete, Mark J; Nanda, Amrit K; Johnson-Beebout, Sarah E; Wissuwa, Matthias

    2015-01-01

    Zinc (Zn) deficiency is a major constraint to rice production and Zn is also often deficient in humans with rice-based diets. Efforts to breed more Zn-efficient rice are constrained by poor understanding of the mechanisms of tolerance to deficiency. Here we assess the contributions of root growth and root Zn uptake efficiency, and we seek to explain the results in terms of specific mechanisms. We made a field experiment in a highly Zn-deficient rice soil in the Philippines with deficiency-tolerant and -sensitive genotypes, and measured growth, Zn uptake and root development. We also measured the effect of planting density. Tolerant genotypes produced more crown roots per plant and had greater uptake rates per unit root surface area; the latter was at least as important as root number to overall tolerance. Tolerant and sensitive genotypes took up more Zn per plant at greater planting densities. The greater uptake per unit root surface area, and the planting density effect can only be explained by root-induced changes in the rhizosphere, either solubilizing Zn, or neutralizing a toxin that impedes Zn uptake (possibly [Formula: see text] or Fe(2+)), or both. Traits for these and crown root number are potential breeding targets.

  18. Zinc starvation induces autophagy in yeast

    PubMed Central

    Kawamata, Tomoko; Horie, Tetsuro; Matsunami, Miou; Sasaki, Michiko; Ohsumi, Yoshinori

    2017-01-01

    Zinc is an essential nutrient for all forms of life. Within cells, most zinc is bound to protein. Because zinc serves as a catalytic or structural cofactor for many proteins, cells must maintain zinc homeostasis under severely zinc-deficient conditions. In yeast, the transcription factor Zap1 controls the expression of genes required for uptake and mobilization of zinc, but to date the fate of existing zinc-binding proteins under zinc starvation remains poorly understood. Autophagy is an evolutionarily conserved cellular degradation/recycling process in which cytoplasmic proteins and organelles are sequestered for degradation in the vacuole/lysosome. In this study, we investigated how autophagy functions under zinc starvation. Zinc depletion induced non-selective autophagy, which is important for zinc-limited growth. Induction of autophagy by zinc starvation was not directly related to transcriptional activation of Zap1. Instead, TORC1 inactivation directed zinc starvation-induced autophagy. Abundant zinc proteins, such as Adh1, Fba1, and ribosomal protein Rpl37, were degraded in an autophagy-dependent manner. But the targets of autophagy were not restricted to zinc-binding proteins. When cellular zinc is severely depleted, this non-selective autophagy plays a role in releasing zinc from the degraded proteins and recycling zinc for other essential purposes. PMID:28264932

  19. Impact of glutathione metabolism on zinc homeostasis in Saccharomyces cerevisiae.

    PubMed

    Steiger, Matthias G; Patzschke, Anett; Holz, Caterina; Lang, Christine; Causon, Tim; Hann, Stephan; Mattanovich, Diethard; Sauer, Michael

    2017-06-01

    Zinc is a crucial mineral for all organisms as it is an essential cofactor for the proper function of a plethora of proteins and depletion of zinc causes oxidative stress. Glutathione is the major redox buffering agent in the cell and therefore important for mitigation of the adverse effects of oxidative stress. In mammalian cells, zinc deficiency is accompanied by a glutathione depletion. In the yeast Saccharomyces cerevisiae, the opposite effect is observed: under low zinc conditions, an elevated glutathione concentration is found. The main regulator to overcome zinc deficiency is Zap1p. However, we show that Zap1p is not involved in this glutathione accumulation phenotype. Furthermore, we found that in glutathione-accumulating strains also the metal ion-binding phytochelatin-2, which is an oligomer of glutathione, is accumulated. This increased phytochelatin concentration correlates with a lower free zinc level in the vacuole. These results suggest that phytochelatin is important for zinc buffering in S. cerevisiae and thus explains how zinc homeostasis is connected with glutathione metabolism. © FEMS 2017. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

  20. Supplementation with zinc in rats enhances memory and reverses an age-dependent increase in plasma copper.

    PubMed

    Sandusky-Beltran, Leslie A; Manchester, Bryce L; McNay, Ewan C

    2017-08-30

    Zinc and copper are essential trace elements. Dyshomeostasis in these two metals has been observed in Alzheimer's disease, which causes profound cognitive impairment. Insulin therapy has been shown to enhance cognitive performance; however, recent data suggest that this effect may be at least in part due to the inclusion of zinc in the insulin formulation used. Zinc plays a key role in regulation of neuronal glutamate signaling, suggesting a possible link between zinc and memory processes. Consistent with this, zinc deficiency causes cognitive impairments in children. The effect of zinc supplementation on short- and long-term recognition memory, and on spatial working memory, was explored in young and adult male Sprague Dawley rats. After behavioral testing, hippocampal and plasma zinc and copper were measured. Age increased hippocampal zinc and copper, as well as plasma copper, and decreased plasma zinc. An interaction between age and treatment affecting plasma copper was also found, with zinc supplementation reversing elevated plasma copper concentration in adult rats. Zinc supplementation enhanced cognitive performance across tasks. These data support zinc as a plausible therapeutic intervention to ameliorate cognitive impairment in disorders characterized by alterations in zinc and copper, such as Alzheimer's disease. Copyright © 2017 Elsevier B.V. All rights reserved.

  1. Iron and zinc bioaccessibility of fermented maize, sorghum and millets from five locations in Zimbabwe.

    PubMed

    Gabaza, Molly; Shumoy, Habtu; Muchuweti, Maud; Vandamme, Peter; Raes, Katleen

    2018-01-01

    The present study is an evaluation of iron and zinc bioaccessibility of fermented maize, sorghum, pearl millet and finger millet from five different locations in Zimbabwe. Iron and zinc contents ranged between 3.22 and 49.7 and 1.25-4.39mg/100gdm, respectively. Fermentation caused a reduction of between 20 and 88% of phytic acid (PA) while a general increase in soluble phenolic compounds (PC) and a decrease of the bound (PC) was observed. Bioaccessibility of iron and zinc ranged between 2.77 and 26.1% and 0.45-12.8%, respectively. The contribution of the fermented cereals towards iron and zinc absolute requirements ranged between 25 and 411% and 0.5-23% with higher contribution of iron coming from cereals that were contaminated with extrinsic iron. Populations subsisting on cereals could be more at risk of zinc rather than iron deficiency. Copyright © 2017 Elsevier Ltd. All rights reserved.

  2. Resistant starch does not affect zinc homeostasis in rural Malawian children

    USDA-ARS?s Scientific Manuscript database

    This study tested the hypothesis that Malawian children at risk for zinc deficiency will have reduced endogenous fecal zinc (EFZ) and increased net absorbed zinc (NAZ) following the addition of high amylose maize resistant starch (RS) to their diet. This was a small controlled clinical trial to dete...

  3. Zinc starvation induces autophagy in yeast.

    PubMed

    Kawamata, Tomoko; Horie, Tetsuro; Matsunami, Miou; Sasaki, Michiko; Ohsumi, Yoshinori

    2017-05-19

    Zinc is an essential nutrient for all forms of life. Within cells, most zinc is bound to protein. Because zinc serves as a catalytic or structural cofactor for many proteins, cells must maintain zinc homeostasis under severely zinc-deficient conditions. In yeast, the transcription factor Zap1 controls the expression of genes required for uptake and mobilization of zinc, but to date the fate of existing zinc-binding proteins under zinc starvation remains poorly understood. Autophagy is an evolutionarily conserved cellular degradation/recycling process in which cytoplasmic proteins and organelles are sequestered for degradation in the vacuole/lysosome. In this study, we investigated how autophagy functions under zinc starvation. Zinc depletion induced non-selective autophagy, which is important for zinc-limited growth. Induction of autophagy by zinc starvation was not directly related to transcriptional activation of Zap1. Instead, TORC1 inactivation directed zinc starvation-induced autophagy. Abundant zinc proteins, such as Adh1, Fba1, and ribosomal protein Rpl37, were degraded in an autophagy-dependent manner. But the targets of autophagy were not restricted to zinc-binding proteins. When cellular zinc is severely depleted, this non-selective autophagy plays a role in releasing zinc from the degraded proteins and recycling zinc for other essential purposes. © 2017 by The American Society for Biochemistry and Molecular Biology, Inc.

  4. Zinc restriction during different periods of life: influence in renal and cardiovascular diseases.

    PubMed

    Tomat, Analía Lorena; Costa, María de los Ángeles; Arranz, Cristina Teresa

    2011-04-01

    Micronutrient undernutrition during critical periods of growth has become an important health issue in developing and developed countries, particularly among pregnant women and children having an imbalanced diet. Zinc is a widely studied microelement in infant feeding because it is a component of several enzymes involved in intermediary metabolism ranging from growth to cell differentiation and metabolism of proteins, carbohydrates, and lipids. Human and experimental studies have reported an association between zinc deficiency and the etiopathogenesis of cardiovascular and renal diseases like hypertension, atherosclerosis, congestive heart failure, coronary heart disease, and diabetes. The main links between the development of these pathologies and zinc deficiency are multiple mechanisms involving oxidative stress damage, apoptosis, and inflammation. A substantial body of evidence suggests that a poor in utero environment elicited by maternal dietary or placental insufficiency may "programme" susceptibility in the fetus to later development of cardiovascular, renal, metabolic, and endocrine diseases. Zinc deficiency in rats during intrauterine and postnatal growth can also be considered a model of fetal programming of cardiovascular and renal diseases in adult life. Dietary zinc restriction during fetal life, lactation, and/or postweaning induces an increase in arterial blood pressure and impairs renal function in adult life. This review focuses on the contributions of experimental and clinical studies to current knowledge of the physiologic role of zinc in the cardiovascular and renal systems. Moreover, this review examines the relationship between zinc deficiency during different periods of life and the development of cardiovascular and renal diseases in adult life. Copyright © 2011 Elsevier Inc. All rights reserved.

  5. The Zinc Transporter Zip5 (Slc39a5) Regulates Intestinal Zinc Excretion and Protects the Pancreas against Zinc Toxicity

    PubMed Central

    Geiser, Jim; De Lisle, Robert C.; Andrews, Glen K.

    2013-01-01

    Background ZIP5 localizes to the baso-lateral membranes of intestinal enterocytes and pancreatic acinar cells and is internalized and degraded coordinately in these cell-types during periods of dietary zinc deficiency. These cell-types are thought to control zinc excretion from the body. The baso-lateral localization and zinc-regulation of ZIP5 in these cells are unique among the 14 members of the Slc39a family and suggest that ZIP5 plays a role in zinc excretion. Methods/Principal Findings We created mice with floxed Zip5 genes and deleted this gene in the entire mouse or specifically in enterocytes or acinar cells and then examined the effects on zinc homeostasis. We found that ZIP5 is not essential for growth and viability but total knockout of ZIP5 led to increased zinc in the liver in mice fed a zinc-adequate (ZnA) diet but impaired accumulation of pancreatic zinc in mice fed a zinc-excess (ZnE) diet. Loss-of-function of enterocyte ZIP5, in contrast, led to increased pancreatic zinc in mice fed a ZnA diet and increased abundance of intestinal Zip4 mRNA. Finally, loss-of-function of acinar cell ZIP5 modestly reduced pancreatic zinc in mice fed a ZnA diet but did not impair zinc uptake as measured by the rapid accumulation of 67zinc. Retention of pancreatic 67zinc was impaired in these mice but the absence of pancreatic ZIP5 sensitized them to zinc-induced pancreatitis and exacerbated the formation of large cytoplasmic vacuoles containing secretory protein in acinar cells. Conclusions These studies demonstrate that ZIP5 participates in the control of zinc excretion in mice. Specifically, they reveal a paramount function of intestinal ZIP5 in zinc excretion but suggest a role for pancreatic ZIP5 in zinc accumulation/retention in acinar cells. ZIP5 functions in acinar cells to protect against zinc-induced acute pancreatitis and attenuate the process of zymophagy. This suggests that it may play a role in autophagy. PMID:24303081

  6. Zinc in innate and adaptive tumor immunity

    PubMed Central

    2010-01-01

    Zinc is important. It is the second most abundant trace metal with 2-4 grams in humans. It is an essential trace element, critical for cell growth, development and differentiation, DNA synthesis, RNA transcription, cell division, and cell activation. Zinc deficiency has adverse consequences during embryogenesis and early childhood development, particularly on immune functioning. It is essential in members of all enzyme classes, including over 300 signaling molecules and transcription factors. Free zinc in immune and tumor cells is regulated by 14 distinct zinc importers (ZIP) and transporters (ZNT1-8). Zinc depletion induces cell death via apoptosis (or necrosis if apoptotic pathways are blocked) while sufficient zinc levels allows maintenance of autophagy. Cancer cells have upregulated zinc importers, and frequently increased zinc levels, which allow them to survive. Based on this novel synthesis, approaches which locally regulate zinc levels to promote survival of immune cells and/or induce tumor apoptosis are in order. PMID:21087493

  7. Is iron and zinc nutrition a concern for vegetarian infants and young children in industrialized countries?

    PubMed

    Gibson, Rosalind S; Heath, Anne-Louise M; Szymlek-Gay, Ewa A

    2014-07-01

    Well-planned vegetarian diets are considered adequate for all stages of the life cycle, despite limited data on the zinc status of vegetarians during early childhood. The bioavailability of iron and zinc in vegetarian diets is poor because of their higher content of absorption inhibitors such as phytate and polyphenols and the absence of flesh foods. Consequently, children as well as adult vegetarians often have lower serum ferritin concentrations than omnivores, which is indicative of reduced iron stores, despite comparable intakes of total iron; hemoglobin differences are small and rarely associated with anemia. However, data on serum zinc concentrations, the recommended biomarker for identifying population groups at elevated risk of zinc deficiency, are sparse and difficult to interpret because recommended collection and analytic procedures have not always been followed. Existing data indicate no differences in serum zinc or growth between young vegetarian and omnivorous children, although there is some evidence of low serum zinc concentrations in vegetarian adolescents. Some vegetarian immigrants from underprivileged households may be predisposed to iron and zinc deficiency because of nondietary factors such as chronic inflammation, parasitic infections, overweight, and genetic hemoglobin disorders. To reduce the risk of deficiency, the content and bioavailability of iron and zinc should be enhanced in vegetarian diets by consumption of fortified cereals and milk, by consumption of leavened whole grains, by soaking dried legumes before cooking and discarding the soaking water, and by replacing tea and coffee at meals with vitamin C-rich drinks, fruit, or vegetables. Additional recommended practices include using fermented soy foods and sprouting at least some of the legumes consumed. Fortified foods can reduce iron deficiency, but whether they can also reduce zinc deficiency is less certain. Supplements may be necessary for vegetarian children following very

  8. Adipokine zinc-α2-glycoprotein regulated by growth hormone and linked to insulin sensitivity.

    PubMed

    Balaz, Miroslav; Ukropcova, Barbara; Kurdiova, Timea; Gajdosechova, Lucia; Vlcek, Miroslav; Janakova, Zuzana; Fedeles, Jozef; Pura, Mikulas; Gasperikova, Daniela; Smith, Steven R; Tkacova, Ruzena; Klimes, Iwar; Payer, Juraj; Wolfrum, Christian; Ukropec, Jozef

    2015-02-01

    Hypertrophic obesity is associated with impaired insulin sensitivity and lipid-mobilizing activity of zinc-α2-glycoprotein. Adipose tissue (AT) of growth hormone (GH) -deficient patients is characterized by extreme adipocyte hypertrophy due to defects in AT lipid metabolism. It was hypothesized that zinc-α2-glycoprotein is regulated by GH and mediates some of its beneficial effects in AT. AT from patients with GH deficiency and individuals with obesity-related GH deficit was obtained before and after 5-year and 24-month GH supplementation therapy. GH action was tested in primary human adipocytes. Relationships of GH and zinc-α2-glycoprotein with adipocyte size and insulin sensitivity were evaluated in nondiabetic patients with noncancerous cachexia and hypertrophic obesity. AT in GH-deficient adults displayed a substantial reduction of zinc-α2-glycoprotein. GH therapy normalized AT zinc-α2-glycoprotein. Obesity-related relative GH deficit was associated with almost 80% reduction of zinc-α2-glycoprotein mRNA in AT. GH increased zinc-α2-glycoprotein mRNA in both AT of obese men and primary human adipocytes. Interdependence of GH and zinc-α2-glycoprotein in regulating AT morphology and metabolic phenotype was evident from their relationship with adipocyte size and AT-specific and whole-body insulin sensitivity. The results demonstrate that GH is involved in regulation of AT zinc-α2-glycoprotein; however, the molecular mechanism linking GH and zinc-α2-glycoprotein in AT is yet unknown. © 2014 The Obesity Society.

  9. Relationship between zinc and the growth and development of young children.

    PubMed

    Gao, S; Tu, D N; Li, H; Cao, X; Jiang, J X; Shi, Y; Zhou, X Q; You, J B

    2015-08-19

    The purpose of this study was to evaluate the relationship between zinc and the growth and development of young children. The parents of 8102 young children were surveyed in person by a trained surveyor using structured questionnaires. The hair zinc concentration of the children was determined using an atomic absorption spectrophotometer. The height, weight, sitting height, and head circumference of the children were measured at follow-up visits. There was a positive correlation between hair zinc concentration and adaptive developmental quotient (ADQ; r = 0.3164, P = 0.0272) while no correlation was found between hair zinc concentration and body measurement Z scores or intelligence quotient (IQ). There was a strong positive correlation between hair zinc concentration and weight-for-age Z scores (r = 0.3618, P = 0.0416) and ADQ (r = 0.2761, P = 0.0387) in boys; there was no correlation between hair zinc concentration and body measurement Z scores, IQ, and ADQ in girls. In boys with normal hair zinc levels, ADQ was 9.58 (P = 0.0392), higher than in boys who had zinc-deficient hair. In girls with normal hair zinc levels, ADQ was 2.52 (P = 0.0296), lower than in girls with zinc-deficient hair. In conclusion, there is no significant correlation between hair zinc levels and IQ or Z scores for all body measurements in young children.

  10. Decreased Lumbar Lordosis and Deficient Acetabular Coverage Are Risk Factors for Subchondral Insufficiency Fracture.

    PubMed

    Jo, Woo Lam; Lee, Woo Suk; Chae, Dong Sik; Yang, Ick Hwan; Lee, Kyoung Min; Koo, Kyung Hoi

    2016-10-01

    Subchondral insufficiency fracture (SIF) of the femoral head occurs in the elderly and recipients of organ transplantation. Osteoporosis and deficient lateral coverage of the acetabulum are known risk factors for SIF. There has been no study about relation between spinopelvic alignment and anterior acetabular coverage with SIF. We therefore asked whether a decrease of lumbar lordosis and a deficiency in the anterior acetabular coverage are risk factors. We investigated 37 patients with SIF. There were 33 women and 4 men, and their mean age was 71.5 years (59-85 years). These 37 patients were matched with 37 controls for gender, age, height, weight, body mass index and bone mineral density. We compared the lumbar lordosis, pelvic incidence, pelvic tilt, sacral slope, acetabular index, acetabular roof angle, acetabular head index, anterior center-edge angle and lateral center-edge angle. Lumbar lordosis, pelvic tilt, sacral slope, lateral center edge angle, anterior center edge angle, acetabular index and acetabular head index were significantly different between SIF group and control group. Lumbar lordosis (OR = 1.11), lateral center edge angle (OR = 1.30) and anterior center edge angle (OR = 1.27) had significant associations in multivariate analysis. Decreased lumbar lordosis and deficient anterior coverage of the acetabulum are risk factors for SIF as well as decreased lateral coverage of the acetabulum.

  11. Effects of rutin supplementation on antioxidant status and iron, copper, and zinc contents in mouse liver and brain.

    PubMed

    Gao, Zhonghong; Xu, Huibi; Huang, Kaixun

    2002-09-01

    The effect of rutin on total antioxidant status as well as on trace elements such as iron, copper, and zinc in mouse liver and brain were studied. Mice were administrated with 0.75 g/kg or 2.25 g/kg P. O. of rutin for 30 d consecutively. Following the treatment, the activity of total antioxidant status, catalase, Cu,Zn-superoxide dismutase, Mn-superoxide dismutase, zinc, copper, and iron were measured in mouse liver and brain. The results showed that rutin significantly increased the antioxidant status and Mn-superoxide dismutase activities in mouse liver, but it had no effect on these variables in the brain. Treatment with a higher concentration of rutin significantly decreased catalase activity and iron, zinc, and copper contents in mouse liver; it also resulted in a slower weight gain for the first 20 d. These results indicate that rutin taken in proper amount can effectively improve antioxidant status, whereas at an increased dosage, it may cause trace element (such as iron, zinc, and copper) deficiencies and a decrease in the activities of related metal-containing enzymes.

  12. A diagnostic challenge: a case of acrodermatitis enteropathica without hypozincemia and with maternal milk of low zinc level.

    PubMed

    Tatlican, Semih; Yamangokturk, Burcu; Eren, Cemile; Gulbahar, Ozlem; Eskioglu, Fatma

    2010-01-01

    Acrodermatitis enteropathica is a rare and distinct form of zinc deficiency with a requirement of life-long zinc supplementation and inherited in a recessive manner. Transient nutritional zinc deficiency is also a well known condition mimicking acrodermatitis enteropathica like skin changes in preterm and term infants who are generally breastfed with a low level of zinc containing milk. Here, a 4-month-old male, term and fully breastfed acrodermatitis enteropathica case without hypozincemia and with maternal milk of low zinc level is presented. © 2010 Wiley Periodicals, Inc.

  13. Zinc Deficiency Augments Leptin Production and Exacerbates Macrophage Infiltration into Adipose Tissue in Mice Fed a High-Fat Diet123

    PubMed Central

    Liu, Ming-Jie; Bao, Shengying; Bolin, Eric R.; Burris, Dara L.; Xu, Xiaohua; Sun, Qinghua; Killilea, David W.; Shen, Qiwen; Ziouzenkova, Ouliana; Belury, Martha A.; Failla, Mark L.; Knoell, Daren L.

    2013-01-01

    Zinc (Zn) deficiency and obesity are global public health problems. Zn deficiency is associated with obesity and comorbid conditions that include insulin resistance and type 2 diabetes. However, the function of Zn in obesity remains unclear. Using a mouse model of combined high-fat and low-Zn intake (0.5–1.5 mg/kg), we investigated whether Zn deficiency exacerbates the extent of adiposity as well as perturbations in metabolic and immune function. C57BL/6 mice were randomly assigned to receive either a high-fat diet (HFD) or a control (C) diet for 6 wk, followed by further subdivision into 2 additional groups fed Zn-deficient diets (C-Zn, HFD-Zn), along with a C diet and an HFD, for 3 wk (n = 8–9 mice/group). The extent of visceral fat, insulin resistance, or systemic inflammation was unaffected by Zn deficiency. Strikingly, Zn deficiency significantly augmented circulating leptin concentrations (HFD-Zn vs. HFD: 3.15 ± 0.16 vs. 2.59 ± 0.12 μg/L, respectively) and leptin signaling in the liver of obese mice. Furthermore, gene expression of macrophage-specific markers ADAM8 (A disintegrin and metalloproteinase domain-containing protein 8) and CD68 (cluster of differentiation 68) was significantly greater in adipose tissue in the HFD-Zn group than in the HFD group, as confirmed by CD68 protein analysis, indicative of increased macrophage infiltration. Inspection of Zn content and mRNA profiles of all Zn transporters in the adipose tissue revealed alterations of Zn metabolism to obesity and Zn deficiency. Our results demonstrate that Zn deficiency increases leptin production and exacerbates macrophage infiltration into adipose tissue in obese mice, indicating the importance of Zn in metabolic and immune dysregulation in obesity. PMID:23700340

  14. Effect of glycation on human serum albumin-zinc interaction: a biophysical study.

    PubMed

    Iqbal, Sarah; Qais, Faizan Abul; Alam, Md Maroof; Naseem, Imrana

    2018-05-01

    Zinc deficiency is common in diabetes. However, the cause of this phenomenon is largely unknown. 80% of the absorbed zinc is transported through the blood in association with human serum albumin (HSA). Under persistent hyperglycemia, HSA frequently undergoes non-enzymatic glycation which can affect its structure and metal-binding function. Hence, in this study, we have examined the interaction of zinc with native and glycated HSA. The protein samples were incubated either in the presence or in the absence of physiologically elevated glucose concentration for 21 days. The samples were then analyzed for structural changes and zinc-binding ability using various spectrometric and calorimetric approaches. The study reveals changes in the three-dimensional structure of the protein upon glycation that cause local unfolding of the molecule. Most such regions are localized in subdomain IIA of HSA which plays a key role in zinc binding. This affects zinc interaction with HSA and could in part explain the perturbed zinc distribution in patients with hyperglycemia. The varying degree of HSA glycation in blood could explain the observed heterogeneity pertaining to zinc deficiency among people suffering from diabetes.

  15. Deficiency of angiotensinogen in hepatocytes markedly decreases blood pressure in lean and obese male mice.

    PubMed

    Yiannikouris, Frederique; Wang, Yu; Shoemaker, Robin; Larian, Nika; Thompson, Joel; English, Victoria L; Charnigo, Richard; Su, Wen; Gong, Ming; Cassis, Lisa A

    2015-10-01

    We recently demonstrated that adipocyte deficiency of angiotensinogen (AGT) ablated high-fat diet-induced elevations in plasma angiotensin II (Ang II) concentrations and obesity-hypertension in male mice. Hepatocytes are the predominant source of systemic AGT. Therefore, in this study, we defined the contribution of hepatocyte-derived AGT to obesity-induced elevations in plasma AGT concentrations and hypertension. Male Agt(fl/fl) mice expressing albumin-driven Cre recombinase were bred to female Agt(fl/fl) mice to generate Agt(fl/fl) or hepatocyte AGT-deficient male mice (Agt(Alb)). Mice were fed a low-fat or high-fat diet for 16 weeks. Hepatocyte AGT deficiency had no significant effect on body weight. Plasma AGT concentrations were increased in obese Agt(fl/fl) mice. Hepatocyte AGT deficiency markedly reduced plasma AGT and Ang II concentrations in lean and obese mice. Moreover, hepatocyte AGT deficiency reduced the content and release of AGT from adipose explants. Systolic blood pressure was markedly decreased in lean (by 18 mm Hg) and obese Agt(Alb) mice (by 54 mm Hg) compared with Agt(fl/fl) controls. To define mechanisms, we quantified effects of Ang II on mRNA abundance of megalin, an AGT uptake transporter, in 3T3-L1 adipocytes. Ang II stimulated adipocyte megalin mRNA abundance and decreased media AGT concentrations. These results demonstrate that hepatocytes are the predominant source of systemic AGT in both lean and obese mice. Moreover, reductions in plasma angiotensin concentrations in obese hepatocyte AGT-deficient mice may have limited megalin-dependent uptake of AGT into adipocytes for the production of Ang II in the development of obesity-hypertension. © 2015 American Heart Association, Inc.

  16. Enhanced zinc consumption causes memory deficits and increased brain levels of zinc

    USGS Publications Warehouse

    Flinn, J.M.; Hunter, D.; Linkous, D.H.; Lanzirotti, A.; Smith, L.N.; Brightwell, J.; Jones, B.F.

    2005-01-01

    Zinc deficiency has been shown to impair cognitive functioning, but little work has been done on the effects of elevated zinc. This research examined the effect on memory of raising Sprague-Dawley rats on enhanced levels of zinc (10 ppm ZnCO3; 0.153 mM) in the drinking water for periods of 3 or 9 months, both pre- and postnatally. Controls were raised on lab water. Memory was tested in a series of Morris Water Maze (MWM) experiments, and zinc-treated rats were found to have impairments in both reference and working memory. They were significantly slower to find a stationary platform and showed greater thigmotaxicity, a measure of anxiety. On a working memory task, where the platform was moved each day, zinc-treated animals had longer latencies over both trials and days, swam further from the platform, and showed greater thigmotaxicity. On trials using an Atlantis platform, which remained in one place but was lowered on probe trials, the zinc-treated animals had significantly fewer platform crossings, spent less time in the target quadrant, and did not swim as close to the platform position. They had significantly greater latency on nonprobe trials. Microprobe synchrotron X-ray fluorescence (??SXRF) confirmed that brain zinc levels were increased by adding ZnCO 3 to the drinking water. These data show that long-term dietary administration of zinc can lead to impairments in cognitive function. ?? 2004 Elsevier Inc. All rights reserved.

  17. Does zinc moderate essential fatty acid and amphetamine treatment of attention-deficit/hyperactivity disorder?

    PubMed

    Arnold, L E; Pinkham, S M; Votolato, N

    2000-01-01

    Zinc is an important co-factor for metabolism relevant to neurotransmitters, fatty acids, prostaglandins, and melatonin, and indirectly affects dopamine metabolism, believed intimately involved in attention-deficit/hyperactivity disorder (ADHD). To explore the relationship of zinc nutrition to essential fatty acid supplement and stimulant effects in treatment of ADHD, we re-analyzed data from an 18-subject double-blind, placebo-controlled crossover treatment comparison of d-amphetamine and Efamol (evening primrose oil, rich in gamma-linolenic acid). Subjects were categorized as zinc-adequate (n = 5), borderline zinc (n = 5), and zinc-deficient (n = 8) by hair, red cell, and urine zinc levels; for each category, placebo-active difference means were calculated on teachers' ratings. Placebo-controlled d-amphetamine response appeared linear with zinc nutrition, but the relationship of Efamol response to zinc appeared U-shaped; Efamol benefit was evident only with borderline zinc. Placebo-controlled effect size (Cohen's d) for both treatments ranged up to 1.5 for borderline zinc and dropped to 0.3-0.7 with mild zinc deficiency. If upheld by prospective research, this post-hoc exploration suggests that zinc nutrition may be important for treatment of ADHD even by pharmacotherapy, and if Efamol benefits ADHD, it likely does so by improving or compensating for borderline zinc nutrition.

  18. Immune malfunction in the GPR39 zinc receptor of knockout mice: Its relationship to depressive disorder.

    PubMed

    Młyniec, Katarzyna; Trojan, Ewa; Ślusarczyk, Joanna; Głombik, Katarzyna; Basta-Kaim, Agnieszka; Budziszewska, Bogusława; Skrzeszewski, Jakub; Siwek, Agata; Holst, Birgitte; Nowak, Gabriel

    2016-02-15

    Depression is a serious psychiatric disorder affecting not only the monaminergic, glutamatergic, and GABAergic neurosystems, but also the immune system. Patients suffering from depression show disturbance in the immune parameters as well as increased susceptibility to infections. Zinc is well known as an anti-inflammatory agent, and its link with depression has been proved, zinc deficiency causing depression- and anxiety-like behavior with immune malfunction. It has been discovered that trace-element zinc acts as a neurotransmitter in the central nervous system via zinc receptor GPR39. In this study we investigated whether GPR39 knockout would cause depressive-like behavior as measured by the forced swim test, and whether these changes would coexist with immune malfunction. In GPR39 knockout mice versus a wild-type control we found: i) depressive-like behavior; ii) significantly reduced thymus weight; (iii) reduced cell viability of splenocytes; iv) reduced proliferative response of splenocytes; and v) increased IL-6 production of splenocytes after ConA stimulation and decreased IL-1b and IL-6 release after LPS stimulation. The results indicate depressive-like behavior in GPR39 KO animals with an immune response similar to that observed in depressive disorder. Here for the first time we show immunological changes under GPR39-deficient conditions. Copyright © 2015 Elsevier B.V. All rights reserved.

  19. Excessive zinc ingestion: A reversible cause of sideroblastic anemia and bone marrow depression

    SciTech Connect

    Broun, E.R.; Greist, A.; Tricot, G.

    1990-09-19

    Two patients with sideroblastic anemia secondary to zinc-induced copper deficiency absorbed excess zinc secondary to oral ingestion. The source of excess zinc was a zinc supplement in one case; in the other, ingested coins. In each case, the sideroblastic anemia was corrected promptly after removal of the source of excess zinc. These two cases emphasize the importance of recognizing this clinical entity, since the myelodysplastic features are completely reversible.

  20. Is zinc deficiency a risk factor for atherosclerosis?

    PubMed

    Beattie, John H; Kwun, In-Sook

    2004-02-01

    The development of atherosclerosis is influenced by genetic, lifestyle and nutritional risk factors. Zn and metallothionein deficiency can enhance oxidative-stress-related signalling processes in endothelial cells, and since changes in available plasma Zn may affect the Zn status of the endothelium, Zn deficiency could be a risk factor for IHD. Although the association of Zn with many proteins is essential for their function, three key signalling processes are highlighted as being principal targets for the effect of Zn deficiency: the activation of NF-kappaB, the activation of caspase enzymes and the signalling of NO. The need to develop a reliable indicator of Zn status is critical to any epidemiological approach for studying the relationship between Zn status and disease incidence. Studies using appropriate animal models and investigating how the plasma Zn pool influences endothelial intracellular labile Zn would be helpful in appreciating the importance of Zn deficiency in atherogenesis.

  1. Male infertility: decreased levels of selenium, zinc and antioxidants.

    PubMed

    Türk, Silver; Mändar, Reet; Mahlapuu, Riina; Viitak, Anu; Punab, Margus; Kullisaar, Tiiu

    2014-04-01

    In this study, we aimed to compare the level of zinc, selenium, glutathione peroxidase activity and antioxidant status in following populations of men: severe inflammation in prostate (>10(6) white blood cells in prostate secretion; n=29), severe leukocytospermia, (>10(6) white blood cells in semen; n=31), mild inflammation, (0.2-1M white blood cells in semen or prostate secretion; n=24), non-inflammatory oligozoospermia (n=32) and healthy controls (n=27). Male partners of infertile couples had reduced level of antioxidative activity, selenium and zinc in their seminal plasma. Most importantly, reduced selenium levels were evident in all patient groups regardless of inflammation status. Therefore, these patients might gain some benefit from selenium supplementation. Copyright © 2014. Published by Elsevier GmbH.

  2. Erythrocyte CuZn superoxide dismutase activity is decreased in iron-deficiency anemia.

    PubMed

    Olivares, M; Araya, M; Pizarro, F; Letelier, A

    2006-09-01

    Iron and copper are essential microminerals that are intimately related. The present study was performed to determine the effect of iron-deficiency anemia (IDA) and treatment with iron on laboratory indicators of copper status. Hemoglobin, mean corpuscular volume erythrocyte Zn protoporphyrin, serum ferritin, serum copper, serum ceruloplasmin, and erythrocyte CuZn-superoxide dismutase (SOD) activity were studied in 12 adult women with IDA before and after iron treatment for 60-90 d (100 mg/d Fe, as ferric polymaltose) and in 27 women with normal iron status. Prior to treatment with iron, serum copper and ceruloplasmin were not different between the groups and treatment with iron did not affect these measures. IDA women, before and after treatment with iron, presented a 2.9- and 2-fold decrease in erythrocyte CuZn-SOD activity compared to women with normal iron status (p < 0.001). Treatment with iron increased erythrocyte CuZn-SOD activity of the IDA group; however, this change was not statistically significant. In conclusion, CuZn-SOD activity is decreased in IDA. Measurement of this enzyme activity is not useful for evaluating copper nutrition in iron-deficient subjects.

  3. Bioavailability of Zinc in Wistar Rats Fed with Rice Fortified with Zinc Oxide

    PubMed Central

    Della Lucia, Ceres Mattos; Santos, Laura Luiza Menezes; Rodrigues, Kellen Cristina da Cruz; Rodrigues, Vivian Cristina da Cruz; Martino, Hércia Stampini Duarte; Pinheiro Sant’Ana, Helena Maria

    2014-01-01

    The study of zinc bioavailability in foods is important because this mineral intake does not meet the recommended doses for some population groups. Also, the presence of dietary factors that reduce zinc absorption contributes to its deficiency. Rice fortified with micronutrients (Ultra Rice®) is a viable alternative for fortification since this cereal is already inserted into the population habit. The aim of this study was to evaluate the bioavailability of zinc (Zn) in rice fortified with zinc oxide. During 42 days, rats were divided into four groups and fed with diets containing two different sources of Zn (test diet: UR® fortified with zinc oxide, or control diet: zinc carbonate (ZnCO3)), supplying 50% or 100%, respectively, of the recommendations of this mineral for animals. Weight gain, food intake, feed efficiency ratio, weight, thickness and length of femur; retention of zinc, calcium (Ca) and magnesium (Mg) in the femur and the concentrations of Zn in femur, plasma and erythrocytes were evaluated. Control diet showed higher weight gain, feed efficiency ratio, retention of Zn and Zn concentration in the femur (p < 0.05). However, no differences were observed (p > 0.05) for dietary intake, length and thickness of the femur, erythrocyte and plasmatic Zn between groups. Although rice fortified with zinc oxide showed a lower bioavailability compared to ZnCO3, this food can be a viable alternative to be used as a vehicle for fortification. PMID:24932657

  4. Low concentrations of zinc in gastric mucosa are associated with increased severity of Helicobacter pylori-induced inflammation.

    PubMed

    Sempértegui, Fernando; Díaz, Myriam; Mejía, Ricardo; Rodríguez-Mora, Oswaldo G; Rentería, Edgar; Guarderas, Carlos; Estrella, Bertha; Recalde, Ramiro; Hamer, Davidson H; Reeves, Philip G

    2007-02-01

    Chronic Helicobacter pylori infection is the most common cause of gastric cancer. H. pylori induces oxidative stress while zinc deficiency results in increased sensitivity to it. In Ecuador, the prevalence of gastric cancer and zinc deficiency are high. We hypothesized that zinc deficiency in Ecuadorian people would cause increased H. pylori-induced inflammation in the gastric mucosa associated with lower tissue zinc concentrations. Three hundred and fifty-two patients with dyspepsia underwent endoscopy to obtain gastric mucosa biopsies. Diagnosis of H. pylori infection and its severity, histopathology, mucosal zinc concentration, and inflammation intensity were determined. H. pylori-infected patients with non-atrophic chronic gastritis had lower concentrations of zinc in gastric mucosa than uninfected patients with the same type of gastritis (251.3 +/- 225.3 vs. 426.2 +/- 279.9 ng/mg of protein; p = .016). Considering all patients, the more severe the H. pylori infection, the higher the percentage of subjects with infiltration by polymorphonuclear (PMN) cells (p = .0001). Patients with high PMN infiltration had lower mucosal zinc concentrations than patients with low PMN infiltration (35.2 +/- 20.7 vs. 242.9 +/- 191.8 ng/mg of protein; p = .021). The degree of inflammation in H. pylori-induced gastritis appears to be modulated by gastric tissue zinc concentrations.

  5. DOSE-DEPENDENT TRANSITIONS IN MECHANISMS OF TOXICITY: ZINC CASE EXAMPLE

    EPA Science Inventory

    Zinc (Zn) is an essential trace element. Maternal Zn deficiency can result in complications of pregnancy and inadequate supply of Zn to the conceptus can interfere with the development of numerous organ systems. Maternal dietary Zn deficiency has been shown to be teratogenic in a...

  6. Induction of regulatory T cells in Th1-/Th17-driven experimental autoimmune encephalomyelitis by zinc administration.

    PubMed

    Rosenkranz, Eva; Maywald, Martina; Hilgers, Ralf-Dieter; Brieger, Anne; Clarner, Tim; Kipp, Markus; Plümäkers, Birgit; Meyer, Sören; Schwerdtle, Tanja; Rink, Lothar

    2016-03-01

    The essential trace element zinc is indispensable for proper immune function as zinc deficiency accompanies immune defects and dysregulations like allergies, autoimmunity and an increased presence of transplant rejection. This point to the importance of the physiological and dietary control of zinc levels for a functioning immune system. This study investigates the capacity of zinc to induce immune tolerance. The beneficial impact of physiological zinc supplementation of 6 μg/day (0.3mg/kg body weight) or 30 μg/day (1.5mg/kg body weight) on murine experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis with a Th1/Th17 (Th, T helper) cell-dominated immunopathogenesis, was analyzed. Zinc administration diminished EAE scores in C57BL/6 mice in vivo (P<.05), reduced Th17 RORγT(+) cells (P<.05) and significantly increased inducible iTreg cells (P<.05). While Th17 cells decreased systemically, iTreg cells accumulated in the central nervous system. Cumulatively, zinc supplementation seems to be capable to induce tolerance in unwanted immune reactions by increasing iTreg cells. This makes zinc a promising future tool for treating autoimmune diseases without suppressing the immune system. Copyright © 2015 Elsevier Inc. All rights reserved.

  7. Mercury exposure, nutritional deficiencies and metabolic disruptions may affect learning in children

    PubMed Central

    Dufault, Renee; Schnoll, Roseanne; Lukiw, Walter J; LeBlanc, Blaise; Cornett, Charles; Patrick, Lyn; Wallinga, David; Gilbert, Steven G; Crider, Raquel

    2009-01-01

    Among dietary factors, learning and behavior are influenced not only by nutrients, but also by exposure to toxic food contaminants such as mercury that can disrupt metabolic processes and alter neuronal plasticity. Neurons lacking in plasticity are a factor in neurodevelopmental disorders such as autism and mental retardation. Essential nutrients help maintain normal neuronal plasticity. Nutritional deficiencies, including deficiencies in the long chain polyunsaturated fatty acids eicosapentaenoic acid and docosahexaenoic acid, the amino acid methionine, and the trace minerals zinc and selenium, have been shown to influence neuronal function and produce defects in neuronal plasticity, as well as impact behavior in children with attention deficit hyperactivity disorder. Nutritional deficiencies and mercury exposure have been shown to alter neuronal function and increase oxidative stress among children with autism. These dietary factors may be directly related to the development of behavior disorders and learning disabilities. Mercury, either individually or in concert with other factors, may be harmful if ingested in above average amounts or by sensitive individuals. High fructose corn syrup has been shown to contain trace amounts of mercury as a result of some manufacturing processes, and its consumption can also lead to zinc loss. Consumption of certain artificial food color additives has also been shown to lead to zinc deficiency. Dietary zinc is essential for maintaining the metabolic processes required for mercury elimination. Since high fructose corn syrup and artificial food color additives are common ingredients in many foodstuffs, their consumption should be considered in those individuals with nutritional deficits such as zinc deficiency or who are allergic or sensitive to the effects of mercury or unable to effectively metabolize and eliminate it from the body. PMID:19860886

  8. Decreased Glutathione S-transferase Level and Neonatal Hyperbilirubinemia Associated with Glucose-6-phosphate Dehydrogenase Deficiency: A Perspective Review.

    PubMed

    Al-Abdi, Sameer Yaseen

    2017-02-01

    Classically, genetically decreased bilirubin conjugation and/or hemolysis account for the mechanisms contributing to neonatal hyperbilirubinemia associated with glucose-6-phosphate dehydrogenase (G6PD) deficiency. However, these mechanisms are not involved in most cases of this hyperbilirubinemia. Additional plausible mechanisms for G6PD deficiency-associated hyperbilirubinemia need to be considered. Glutathione S-transferases (GST) activity depends on a steady quantity of reduced form of glutathione (GSH). If GSH is oxidized, it is reduced back by glutathione reductase, which requires the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH). The main source of NADPH is the pentose phosphate pathway, in which G6PD is the first enzyme. Rat kidney GSH, rat liver GST, and human red blood cell GST levels have been found to positively correlate with G6PD levels in their respective tissues. As G6PD is expressed in hepatocytes, it is expected that GST levels would be significantly decreased in hepatocytes of G6PD-deficient neonates. As hepatic GST binds bilirubin and prevents their reflux into circulation, hypothesis that decreased GST levels in hepatocytes is an additional mechanism contributing to G6PD deficiency-associated hyperbilirubinemia seems plausible. Evidence for and against this hypothesis are discussed in this article hoping to stimulate further research on the role of GST in G6PD deficiency-associated hyperbilirubinemia. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

  9. Possible role of zinc in diminishing lead-related occupational stress-a zinc nutrition concern.

    PubMed

    Wani, Ab Latif; Ahmad, Ajaz; Shadab, G G H A; Usmani, Jawed Ahmad

    2017-03-01

    Lead and zinc are mostly present at the same occupational source and usually found as co-contaminants. Lead is known to associate with detrimental effects to humans. Zinc however is an essential nutrient and its deficiency causes debilitating effects on growth and development. Besides, it acts as core ion of important enzymes and proteins. The purpose of this study was to examine if zinc concentrations are associated with blood lead levels and if zinc may prevent lead-induced DNA damage. Blood samples were collected from 92 workers as participants occupationally exposed to lead or lead and zinc and 38 comparison participants having no history of such exposure. Lead and zinc levels were determined from blood by atomic absorption spectrophotometry and genetic damage was assessed by comet assay. Correlation was calculated by Spearman's rho. Lead concentrations were observed to increase among workers with increase in years of exposure. There was a significant difference (p < 0.001) in blood lead levels between workers and controls. In addition, significant difference (p < 0.001) in the genetic damage was observed among workers and controls. A clear effect of increased occupational exposure was visible among workers. Multiple regression analysis further reveals the positive effect of lead, while as the inverse effect of zinc on DNA damage. The results suggest that zinc may influence body lead absorption and may have a role in preventing the genetic damage caused by lead.

  10. Oral zinc for treating diarrhoea in children

    PubMed Central

    Lazzerini, Marzia; Wanzira, Humphrey

    2016-01-01

    Background In developing countries, diarrhoea causes around 500,000 child deaths annually. Zinc supplementation during acute diarrhoea is currently recommended by the World Health Organization (WHO) and the United Nations Children's Fund (UNICEF). Objectives To evaluate oral zinc supplementation for treating children with acute or persistent diarrhoea. Search methods We searched the Cochrane Infectious Diseases Group Specialized Register, CENTRAL (the Cochrane Library 2016, Issue 5), MEDLINE, Embase, LILACS, CINAHL, mRCT, and reference lists up to 30 September 2016. We also contacted researchers. Selection criteria Randomized controlled trials (RCTs) that compared oral zinc supplementation with placebo in children aged one month to five years with acute or persistent diarrhoea, including dysentery. Data collection and analysis Both review authors assessed trial eligibility and risk of bias, extracted and analysed data, and drafted the review. The primary outcomes were diarrhoea duration and severity. We summarized dichotomous outcomes using risk ratios (RR) and continuous outcomes using mean differences (MD) with 95% confidence intervals (CI). Where appropriate, we combined data in meta-analyses (using either a fixed-effect or random-effects model) and assessed heterogeneity. We assessed the certainty of the evidence using the GRADE approach. Main results Thirty-three trials that included 10,841 children met our inclusion criteria. Most included trials were conducted in Asian countries that were at high risk of zinc deficiency. Acute diarrhoea There is currently not enough evidence from well-conducted RCTs to be able to say whether zinc supplementation during acute diarrhoea reduces death or number of children hospitalized (very low certainty evidence). In children older than six months of age, zinc supplementation may shorten the average duration of diarrhoea by around half a day (MD −11.46 hours, 95% CI −19.72 to −3.19; 2581 children, 9 trials, low

  11. Hematopoietic G-protein-coupled receptor kinase 2 deficiency decreases atherosclerotic lesion formation in LDL receptor-knockout mice

    PubMed Central

    Otten, Jeroen J. T.; de Jager, Saskia C. A.; Kavelaars, Annemieke; Seijkens, Tom; Bot, Ilze; Wijnands, Erwin; Beckers, Linda; Westra, Marijke M.; Bot, Martine; Busch, Matthias; Bermudez, Beatriz; van Berkel, Theo J. C.; Heijnen, Cobi J.; Biessen, Erik A. L.

    2013-01-01

    Leukocyte chemotaxis is deemed instrumental in initiation and progression of atherosclerosis. It is mediated by G-protein-coupled receptors (e.g., CCR2 and CCR5), the activity of which is controlled by G-protein-coupled receptor kinases (GRKs). In this study, we analyzed the effect of hematopoietic deficiency of a potent regulator kinase of chemotaxis (GRK2) on atherogenesis. LDL receptor-deficient (LDLr−/−) mice with heterozygous hematopoietic GRK2 deficiency, generated by bone marrow transplantation (n=15), displayed a dramatic attenuation of plaque development, with 79% reduction in necrotic core and increased macrophage content. Circulating monocytes decreased and granulocytes increased in GRK2+/− chimeras, which could be attributed to diminished granulocyte colony-forming units in bone marrow. Collectively, these data pointed to myeloid cells as major mediators of the impaired atherogenic response in GRK2+/− chimeras. LDLr−/− mice with macrophage/granulocyte-specific GRK2 deficiency (LysM-Cre GRK2flox/flox; n=8) failed to mimic the aforementioned phenotype, acquitting these cells as major responsible subsets for GRK2 deficiency-associated atheroprotection. To conclude, even partial hematopoietic GRK2 deficiency prevents atherosclerotic lesion progression beyond the fatty streak stage, identifying hematopoietic GRK2 as a potential target for intervention in atherosclerosis.—Otten, J. J. T., de Jager, S. C. A., Kavelaars, A., Seijkens, T., Bot, I., Wijnands, E., Beckers, L., Westra, M. M., Bot, M., Busch, M., Bermudez, B., van Berkel, T. J. C., Heijnen, C. J., Biessen, E. A. L. Hematopoietic G-protein-coupled receptor kinase 2 deficiency decreases atherosclerotic lesion formation in LDL receptor-knockout mice. PMID:23047899

  12. Prevalence of anemia and micronutrient deficiencies in early pregnancy in rural Bangladesh, the MINIMat trial.

    PubMed

    Lindström, Emma; Hossain, Mohammad B; Lönnerdal, Bo; Raqib, Rubhana; El Arifeen, Shams; Ekström, Eva-Charlotte

    2011-01-01

    To describe the prevalence of anemia and micronutrient deficiencies as well as their determinants in early pregnancy. Baseline data from a population-based randomized intervention trial. The study was conducted in Matlab, a sub-district in rural Bangladesh from 1 January to 31 December 2002. Pregnant women (n= 740) were enrolled in approximately week 14 in pregnancy. Data were collected using questionnaires, physical examinations and laboratory analyses of blood samples for concentrations of hemoglobin, ferritin, zinc, folate and vitamin B-12. Covariates associated with anemia and micronutrient deficiencies in bivariate analyses were evaluated in multivariate logistic regression models adjusting for potential confounders. Anemia was present in 28% of the women, 55% were zinc deficient, 46% were vitamin B-12 deficient and 18% were folate deficient. Anemia was not associated with iron deficiency but rather with vitamin B-12 deficiency. Infestation with Ascaris was highly prevalent (67%) and associated with both folate and vitamin B-12 deficiency. Anemia and micronutrient deficiencies all varied significantly with season. The high prevalences of zinc and vitamin B-12 deficiencies in early pregnancy are a concern, as it could lead to adverse pregnancy outcomes and increased health risks for both mother and child. The prevalence of iron deficiency was low, but as this was during early pregnancy, the women might develop iron deficiency and consequently iron deficiency anemia as the pregnancy progresses. © 2010 The Authors Acta Obstetricia et Gynecologica Scandinavica© 2010 Nordic Federation of Societies of Obstetrics and Gynecology.

  13. A comprehensive review of the role of zinc in normal prostate function and metabolism; and its implications in prostate cancer☆

    PubMed Central

    Costello, Leslie C.; Franklin, Renty B.

    2016-01-01

    The human prostate gland contains extremely high zinc levels; which is due to the specialized zinc-accumulating acinar epithelial of the peripheral zone. These cells evolved for their unique capability to produce and secrete extremely levels of citrate, which is achieved by the high cellular zinc level effects on the cell metabolism. This review highlights the specific functional and metabolic alterations that result from the accumulation of the high zinc levels, especially its effects on mitochondrial citrate metabolism and terminal oxidation. The implications of zinc in the development and progression of prostate cancer are described, which is the most consistent hallmark characteristic of prostate cancer. The requirement for decreased zinc resulting from down regulation of ZIP1 to prevent zinc cytotoxicity in the malignant cells is described as an essential early event in prostate oncogenesis. This provides the basis for the concept that an agent (such as the zinc ionophore, clioquinol) that facilitates zinc uptake and accumulation in ZIP1-deficient prostate tumors cells will markedly inhibit tumor growth. In the current absence of an efficacious chemotherapy for advanced prostate cancer, and for prevention of early development of malignancy; a zinc treatment regimen is a plausible approach that should be pursued. PMID:27132038

  14. Zinc status in chronic pancreatitis and its relationship with exocrine and endocrine insufficiency.

    PubMed

    Girish, Banavara Narasimhamurthy; Rajesh, Gopalakrishna; Vaidyanathan, Kannan; Balakrishnan, Vallath

    2009-11-05

    A major role of the pancreas in zinc homeostasis has been suggested. To assess erythrocyte zinc status in chronic pancreatitis and to correlate it with pancreatic exocrine and endocrine insufficiency. One hundred and one patients with chronic pancreatitis (34 alcoholic chronic pancreatitis, 67 tropical chronic pancreatitis) were prospectively studied. Disease characteristics and imaging features were recorded. Erythrocyte zinc was estimated by flame atomic absorption spectrophotometry. Exocrine insufficiency was assessed using polyclonal antibody ELISA for pancreatic stool elastase1. Endocrine insufficiency was assessed by serum glucose levels and insulin requirement. Erythrocyte zinc was significantly lower in chronic pancreatitis patients than in the controls (26.5+/-9.5 microg/g Hb vs. 38.0+/-6.6 microg/g Hb; P<0.001), and in tropical chronic pancreatitis than in alcoholic chronic pancreatitis (25.0+/-10.4 microg/g Hb vs. 29.6+/-6.5 microg/g Hb, P=0.001). In chronic pancreatitis patients who had exocrine insufficiency, erythrocyte zinc positively correlated with stool elastase1 (r=0.587, P<0.001). Erythrocyte zinc levels were significantly lower in diabetic patients as compared to non-diabetics (P=0.036). This study demonstrates zinc deficiency in chronic pancreatitis patients, and that zinc deficiency correlates with exocrine and endocrine insufficiency. Further studies may clarify the possible benefits of zinc supplementation in chronic pancreatitis.

  15. [Association between serum zinc level and hypercholesterolemia and insulin resistance in Brazilian children].

    PubMed

    Albuquerque, Fernanda Martins de; Filgueiras, Mariana De Santis; Rocha, Naruna Pereira; Castro, Ana Paula Pereira; Milagres, Luana Cupertino; Pessoa, Milene Cristine; Fransceschini, Sylvia do Carmo Castro; Novaes, Juliana Farias de

    2018-02-05

    The objective of the study was to assess the association between serum zinc level and cardiometabolic factors in prepubertal Brazilian children. This was a cross-sectional study in a representative sample of schoolchildren 8 to 9 years of age in public and private urban schools in Viçosa, Minas Gerais State, Brazil. Body composition was assessed with dual-energy x-ray absorptiometry. The study measured serum glucose, insulin, total cholesterol, high and low density lipoprotein cholesterol, triglycerides, apolipoproteins A (Apo A) and B, uric acid, leptin, homocysteine, ultrasenstive C-reactive protein, and serum zinc. Arterial pressure was measured with automatic inflation equipment. Zinc deficiency was observed in 1.3% of the children. Girls showed the worst cardiometabolic profile, with higher prevalence of increased android fat, triglycerides, insulin resistance, leptin, zinc, and Apo A. In the first tertile of serum zinc concentration, prevalence of insulin resistance was 96% higher (PR = 1.96; 95%CI: 1.04-3.66) and hypercholesterolemia was 23% lower (PR = 0.77; 95%CI: 0.61-0.96) than in the reference category (grouped 2nd and 3rd tertiles of serum zinc concentration). Despite the low prevalence of zinc deficiency, insulin resistance was more prevalent in children in the lowest third of serum zinc concentration. It is important to prevent cardiometabolic alterations in childhood, especially insulin resistance, with an emphasis on serum zinc level.

  16. Preparation, characterization and bioactivities of Athelia rolfsii exopolysaccharide-zinc complex (AEPS-zinc).

    PubMed

    Dong, Jinman; Li, Hongmei; Min, Weihong

    2018-07-01

    A new Athelia rolfsii exopolysaccharides (AEPS) were purified by Sephacryl S-300 and S-200. The physicochemical characteristics of AEPS fractions were assayed by HPGPC and GC methods. The structures of AEPS and AEPS‑zinc complex were characterized by SEM, FTIR and NMR. Moreover, the bioactivities of complex were also evaluated by experiments in vitro and in vivo. AEPSI consisted of glucose, galacturonic acid, talose, galactose, mannose and xylose, the relative contents of them were 24.74, 19.60, 33.65, 8.77, 7.97 and 5.28%, respectively. AEPSII consisted of glucose, inositol, galacturonic acid, ribitol, gluconic acid, talose and xylose, whose relative contents were 36.06, 21.21, 12.78, 11.07, 6.58, 5.45 and 6.82%, respectively. The Mw and Mn of AEPSI were 6.1324×10 4 and 1.4218×10 4 Da, those of AEPSII were 517 and 248Da. SEM observations showed that microstructures of AEPS and AEPS‑zinc complex were obviously different both in size and shape. FTIR and NMR analysis indicated that AEPS might chelate with zinc ion through hydroxy and carboxy group. In vitro experiments showed that AEPS‑zinc complex had a good bioavailability, in vivo experiments showed that it had good effect on improving zinc deficiency and antioxidant activities, which suggested that it could be used as zinc supplementation with high antioxidant activities. Copyright © 2018 Elsevier B.V. All rights reserved.

  17. The beneficial effects of zinc on diabetes-induced kidney damage in murine rodent model of type 1 diabetes mellitus.

    PubMed

    Yang, Fan; Li, Bing; Dong, Xiaoming; Cui, Wenpeng; Luo, Ping

    2017-07-01

    Diabetes mellitus is a chronic multi-factorial metabolic disorder resulting from impaired glucose homeostasis. Zinc is a key co-factor for the correct functioning of anti-oxidant enzymes. Zinc deficiency therefore, impairs their synthesis, leading to increased oxidative stress within cells. Zinc deficiency occurs commonly in diabetic patients. The aim of this study is to investigate the effects of varying concentrations of zinc on diabetic nephropathy (DN) and the underlying mechanisms involved. FVB male mice aged 8 weeks were injected intraperitoneally with multiple low-dose streptozotocin at a concentration of 50mg/kg body weight daily for 5 days. Diabetic and age-matched control mice were treated with special diets supplemented with zinc at varying concentrations (0.85mg/kg, 30mg/kg, 150mg/kg) for 3 months. The mice were fed with zinc diets to mimic the process of oral administration of zinc in human. Zinc deficiency to some extent aggravated the damage of diabetic kidney. Feeding with normal (30mg/kg zinc/kg diet) and especially high (150mg/kg zinc/kg diet) concentration zinc could protect the kidney against diabetes-induced damage. The beneficial effects of zinc on DN are achieved most likely due to the upregulation of Nrf2 and its downstream factors NQO1, SOD1, SOD2. Zinc upregulated the expression of Akt phosphorylation and GSK-3β phosphorylation, resulting in a reduction in Fyn nuclear translocation and export of Nrf2 to the cytosol. Thus, regular monitoring and maintaining of adequate levels of zinc are recommended in diabetic individuals in order to delay the development of DN. Copyright © 2017 Elsevier GmbH. All rights reserved.

  18. Efficacy of highly bioavailable zinc from fortified water: a randomized controlled trial in rural Beninese children.

    PubMed

    Galetti, Valeria; Kujinga, Prosper; Mitchikpè, Comlan Evariste S; Zeder, Christophe; Tay, Fabian; Tossou, Félicien; Hounhouigan, Joseph D; Zimmermann, Michael B; Moretti, Diego

    2015-11-01

    Zinc deficiency and contaminated water are major contributors to diarrhea in developing countries. Food fortification with zinc has not shown clear benefits, possibly because of low zinc absorption from inhibitory food matrices. We used a novel point-of-use water ultrafiltration device configured with glass zinc plates to produce zinc-fortified, potable water. The objective was to determine zinc bioavailability from filtered water and the efficacy of zinc-fortified water in improving zinc status. In a crossover balanced study, we measured fractional zinc absorption (FAZ) from the zinc-fortified water in 18 healthy Swiss adults using zinc stable isotopes and compared it with zinc-fortified maize porridge. We conducted a 20-wk double-blind randomized controlled trial (RCT) in 277 Beninese school children from rural settings who were randomly assigned to receive a daily portion of zinc-fortified filtered water delivering 2.8 mg Zn (Zn+filter), nonfortified filtered water (Filter), or nonfortified nonfiltered water (Pump) from the local improved supply, acting as the control group. The main outcome was plasma zinc concentration (PZn), and the 3 groups were compared by using mixed-effects models. Secondary outcomes were prevalence of zinc deficiency, diarrhea prevalence, and growth. Geometric mean (-SD, +SD) FAZ was 7-fold higher from fortified water (65.9%; 42.2, 102.4) than from fortified maize (9.1%; 6.0, 13.7; P < 0.001). In the RCT, a significant time-by-treatment effect on PZn (P = 0.026) and on zinc deficiency (P = 0.032) was found; PZn in the Zn+filter group was significantly higher than in the Filter (P = 0.006) and Pump (P = 0.025) groups. We detected no effect on diarrhea or growth, but our study did not have the duration and power to detect such effects. Consumption of filtered water fortified with a low dose of highly bioavailable zinc is an effective intervention in children from rural African settings. Large community-based trials are needed to assess the

  19. Zinc and the modulation of redox homeostasis

    PubMed Central

    Oteiza, Patricia I.

    2012-01-01

    Zinc, a redox inactive metal, has been long viewed as a component of the antioxidant network, and growing evidence points to its involvement in redox-regulated signaling. These actions are exerted through several mechanisms based on the unique chemical and functional properties of zinc. Overall, zinc contributes to maintain the cell redox balance through different mechanisms including: i) the regulation of oxidant production and metal-induced oxidative damage; ii) the dynamic association of zinc with sulfur in protein cysteine clusters, from which the metal can be released by nitric oxide, peroxides, oxidized glutathione and other thiol oxidant species; iii) zinc-mediated induction of the zinc-binding protein metallothionein, which releases the metal under oxidative conditions and act per se scavenging oxidants; iv) the involvement of zinc in the regulation of glutathione metabolism and of the overall protein thiol redox status; and v) a direct or indirect regulation of redox signaling. Findings of oxidative stress, altered redox signaling, and associated cell/tissue disfunction in cell and animal models of zinc deficiency, stress the relevant role of zinc in the preservation of cell redox homeostasis. However, while the participation of zinc in antioxidant protection, redox sensing, and redox-regulated signaling is accepted, the involved molecules, targets and mechanisms are still partially known and the subject of active research. PMID:22960578

  20. Elevation of NO production increases Fe immobilization in the Fe-deficiency roots apoplast by decreasing pectin methylation of cell wall

    PubMed Central

    Ye, Yi Quan; Jin, Chong Wei; Fan, Shi Kai; Mao, Qian Qian; Sun, Cheng Liang; Yu, Yan; Lin, Xian Yong

    2015-01-01

    Cell wall is the major component of root apoplast which is the main reservoir for iron in roots, while nitric oxide (NO) is involved in regulating the synthesis of cell wall. However, whether such regulation could influence the reutilization of iron stored in root apoplast remains unclear. In this study, we observed that iron deficiency elevated NO level in tomato (Solanum lycopersicum) roots. However, application of S-nitrosoglutathione, a NO donor, significantly enhanced iron retention in root apoplast of iron-deficient plants, accompanied with a decrease of iron level in xylem sap. Consequently, S-nitrosoglutathione treatment increased iron concentration in roots, but decreased it in shoots. The opposite was true for the NO scavenging treatment with 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO). Interestingly, S-nitrosoglutathione treatment increased pectin methylesterase activity and decreased degree of pectin methylation in root cell wall of both iron-deficient and iron-sufficient plants, which led to an increased iron retention in pectin fraction, thus increasing the binding capacity of iron to the extracted cell wall. Altogether, these results suggested that iron-deficiency-induced elevation of NO increases iron immobilization in root apoplast by decreasing pectin methylation in cell wall. PMID:26073914

  1. Decreased erythrocyte nucleoside transport and hENT1 transporter expression in glucose 6-phosphate dehydrogenase deficiency.

    PubMed

    Al-Ansari, Mohammad; Craik, James D

    2015-01-01

    Glucose-6-phosphate dehydrogenase (G6PD) deficiency is associated with erythrocyte sensitivity to oxidative damage and hemolytic crises. In β-thalassemia major, where hemoglobin instability imposes oxidative stress, erythrocytes show reduced hENT1 nucleoside transporter expression and decreased nucleoside uptake. This study investigated hENT1 expression and nucleoside transport in G6PD-deficient erythrocytes to determine if decreased hENT1 activity might be a contributory feature in the variable pathology of this enzymopathy. Uptake of (3)H-uridine was measured at room temperature using an inhibitor-oil stop protocol and 5-s incubations. Erythrocyte membranes were analyzed by SDS-PAGE and nucleoside (hENT1), glucose (GLUT-1), and anion exchange (Band 3) transporter polypeptides quantitated on immunoblots. In G6PD-deficient cells, uridine uptake (mean 8.18, 95 % CI 5.6-10.7 vs controls mean 12.35, 95 % CI 9.2-15.5, pmol uridine/gHb/min; P = 0.031) and expression of hENT1 (mean 50.4 %, 95 % CI 38.1-62.7 %, arbitrary units n = 11 vs controls mean 95.23 %, 95 % CI 88.38-102.1 % arbitrary units, n = 8; P < 0.001) were significantly lower; expression of GLUT-1 (mean 106.9 %, vs control mean 99.75 %; P = 0.308) and Band 3 polypeptides (mean 100.1 %, vs control mean 102.84 %; P = 0.329) were unchanged. Nucleoside transporter activity in human erythrocytes sustains intracellular purine nucleotide levels and assists in control of plasma adenosine levels; decreased hENT1 expression and activity in G6PD-deficiency could affect red metabolism and influence a wide spectrum of responses mediated by adenosine receptors.

  2. [Vitamin A and zinc levels in gastroenterological surgical patients: Relation with inflammation and postoperative complications].

    PubMed

    Zago, L B; Danguise, E; González Infantino, C A; Río, M E; Callegari, M

    2011-01-01

    It is accepted that even mild nutrient depletion may affect the evolution of the surgical patient. To evaluate the influence of preoperative levels of plasma retinol and zinc on postoperative evolution of surgical patients; to evaluate the influence of inflammation on both level markers. Plasma retinol and zinc were determined in 50 patients before programmed gastroenterological surgeries. To detect global malnutrition BMI and weight loss percentage (WL%) were included. C-reactive protein (CRP) was included as inflammation marker. During follow up postoperative complications were recorded. The present analysis was carried out in 43 patients with complete information. Low retinol values (< 20 μg/dl) were founded in 3 cases and low Zn values (< 85 μg/dl) in 20 cases, being 9 of them indicative of severe deficiency (< 70 μg/dl). Postoperative complications were recorded in 17 patients; patients with complications presented lower values of plasma Zn (78.4 ± 25.8 vs. 87.8 ± 25.7 μg/dl) and retinol (36.9 ± 14.5 vs. 49.7 ± 20.6; P = 0.0318) than those with no complications; the number of patients with complications decreased when retinol and Zn ranges increased. No relation between BMI or WL% and appearance of complications was founded; patients with higher WL% were those with higher usual weight. Inflammation affected both markers: retinol dropped from 50.1 ± 17.2 to 44.0 ±20.8 and to 23.7 ± 4.0 μg/dl for CRP ranges of < 0.5, 0.5-3.9 and ≥ 4 mg/dl, respectively (p = 0.0193); levels of zinc fell from 90.1 ± 17.8 to 85.2 ± 29.9 and to 55.0 ± 25.9 μg/dl for the same CRP ranges (P = 0.0195). Zn level influenced retinol level, dropping to 33.1 ± 11.7 μg/dl of retinol in the Zn severe deficiency group (P = 0.0386). The obtained results confirm the influence of vitamin A and zinc on postoperative evolution of the surgical patient, while alert about the interrelationships among vitamin A, zinc and inflammation, which lead to difficulty to establish the real

  3. Serum Zinc and β D Glucuronidase Enzyme Level in Type 2 Diabetes Mellitus with Periodontitis.

    PubMed

    Pushparani, D S

    2016-01-01

    The exact mechanism by which nutritional deficiency and lysosomal enzyme change, modify periodontal destruction has not yet been precisely defined. The study aimed to determine the serum zinc and β D glucuronidase enzyme level in the selected groups and how its increase or decrease levels are related to type 2 diabetes mellitus (T2DM) with periodontitis when compared to other groups. Six hundred subjects were selected and are categorized into four groups as Group I (control healthy subjects, n=150), Group II (T2DM with periodontitis, n=150), Group III (T2DM without periodontitis, n=150) and Group IV (Non-DM with periodontitis, n=150). The lab investigations included measuring fasting blood glucose, serum zinc and β D- glucuronidase levels. In the results, the level of serum zinc was found to be lesser in group III subjects and the activity of serum β D glucuronidase was found to be elevated nine times in group III (T2DM with periodontitis) and two times elevated in group II (T2DM without periodontitis) and group IV (Non-DM with periodontitis), when compared to control. Zinc has been reported to reduce the stabilization of lysosomal membranes. Periodontitis has been taken as the prime condition in this study and categorized as experimental groups. Perturbations in mineral metabolism are more pronounced in diabetic populations. When the level of zinc is decreased, the structural integrity of lysosomal membrane has been lost and it would have caused for the increased release of β D glucuronidase in T2DM with periodontitis.

  4. Nutrition and hair: deficiencies and supplements.

    PubMed

    Finner, Andreas M

    2013-01-01

    Hair follicle cells have a high turnover. A caloric deprivation or deficiency of several components, such as proteins, minerals, essential fatty acids, and vitamins, caused by inborn errors or reduced uptake, can lead to structural abnormalities, pigmentation changes, or hair loss, although exact data are often lacking. The diagnosis is established through a careful history, clinical examination of hair loss activity, and hair quality and confirmed through targeted laboratory tests. Examples of genetic hair disorders caused by reduced nutritional components are zinc deficiency in acrodermatitis enteropathica and copper deficiency in Menkes kinky hair syndrome. Copyright © 2013 Elsevier Inc. All rights reserved.

  5. Effect of nutrient deficiencies on in vitro Th1 and Th2 cytokine response of peripheral blood mononuclear cells to Plasmodium falciparum infection

    PubMed Central

    2010-01-01

    Background An appropriate balance between pro-inflammatory and anti-inflammatory cytokines that mediate innate and adaptive immune responses is required for effective protection against human malaria and to avoid immunopathology. In malaria endemic countries, this immunological balance may be influenced by micronutrient deficiencies. Methods Peripheral blood mononuclear cells from Tanzanian preschool children were stimulated in vitro with Plasmodium falciparum-parasitized red blood cells to determine T-cell responses to malaria under different conditions of nutrient deficiencies and malaria status. Results The data obtained indicate that zinc deficiency is associated with an increase in TNF response by 37%; 95% CI: 14% to 118% and IFN-γ response by 74%; 95% CI: 24% to 297%. Magnesium deficiency, on the other hand, was associated with an increase in production of IL-13 by 80%; 95% CI: 31% to 371% and a reduction in IFN-γ production. These results reflect a shift in cytokine profile to a more type I cytokine profile and cell-cell mediated responses in zinc deficiency and a type II response in magnesium deficiency. The data also reveal a non-specific decrease in cytokine production in children due to iron deficiency anaemia that is largely associated with malaria infection status. Conclusions The pathological sequels of malaria potentially depend more on the balance between type I and type II cytokine responses than on absolute suppression of these cytokines and this balance may be influenced by a combination of micronutrient deficiencies and malaria status. PMID:20546583

  6. Randomized trial of the effect of zinc supplementation on the mental health of school-age children in Guatemala123

    PubMed Central

    DiGirolamo, Ann M; Ramirez-Zea, Manuel; Wang, Meng; Flores-Ayala, Rafael; Martorell, Reynaldo; Neufeld, Lynnette M; Ramakrishnan, Usha; Sellen, Daniel; Black, Maureen M; Stein, Aryeh D

    2010-01-01

    Background: Rates of mental illness in children are increasing throughout the world. Observational studies of depression, anxiety, and attention-deficit hyperactivity disorder suggest that zinc is an alternative treatment. Objective: We examined the effect of zinc supplementation on the mental health of school-age children in Guatemala. Design: From January to October 2006, we conducted a 6-mo randomized, double-blind, controlled trial comparing zinc supplementation (10 mg ZnO/d for 5 d/wk) with a placebo (10 mg glucose) in 674 Guatemalan children in grades 1–4. Outcome measures included internalizing (ie, depression and anxiety) and externalizing (ie, hyperactivity and conduct disorder) problem behaviors, positive behaviors (ie, socialization and leadership), and serum zinc concentrations. Results: Zinc and placebo groups did not differ significantly in any behavioral measures at baseline or at follow-up. At baseline, 21.4% of children had serum zinc concentrations <65 μg/dL. At follow-up, both groups improved significantly, and zinc concentrations were higher in the zinc group. Increases in serum zinc concentrations were inversely associated with decreases in depressive symptoms (estimate: −0.01 points per μg Zn/dL; P = 0.01), anxiety (estimate: −0.012 points per μg Zn/dL; P = 0.02), internalizing symptoms (estimate: −0.021 points per μg Zn/dL; P = 0.02), and social skills (estimate: −0.019 points per μg Zn/dL; P = 0.01) in adjusted models that were controlled for child age, sex, socioeconomic status, household, and treatment group. Conclusions: Six months of zinc supplementation did not induce differences in mental health outcomes between zinc and placebo groups. However, increases in serum zinc concentrations were associated with decreases in internalizing symptoms (ie, depression and anxiety) in a community-based sample of children at risk of zinc deficiency. This trial was registered at clinicaltrials.gov as NCT00283660. PMID:20881069

  7. The effects of zinc status on early growth in infants with sickle cell disease

    USDA-ARS?s Scientific Manuscript database

    Growth failure, maturational delay, and alterations in body composition occur in older children and adults with Sickle Cell Disease (SCD). Poor nutritional status, specifically zinc deficiency, has been widely implicated, although infants with SCD have not been studied. We determined zinc status in ...

  8. LiZIP3 is a cellular zinc transporter that mediates the tightly regulated import of zinc in Leishmania infantum parasites

    PubMed Central

    Carvalho, Sandra; da Silva, Rosa Barreira; Shawki, Ali; Castro, Helena; Lamy, Márcia; Eide, David; Costa, Vítor; Mackenzie, Bryan; Tomás, Ana M.

    2016-01-01

    Summary Cellular zinc homeostasis ensures that the intracellular concentration of this element is kept within limits that enable its participation in critical physiological processes without exerting toxic effects. We report here the identification and characterization of the first mediator of zinc homeostasis in Leishmania infantum, LiZIP3, a member of the ZIP family of divalent metal-ion transporters. The zinc transporter activity of LiZIP3 was first disclosed by its capacity to rescue the growth of Saccharomyces cerevisiae strains deficient in zinc acquisition. Subsequent expression of LiZIP3 in Xenopus laevis oocytes was shown to stimulate the uptake of a broad range of metal ions, among which Zn2+ was the preferred LiZIP3 substrate (K0.5 ≈ 0.1 μM). Evidence that LiZIP3 functions as a zinc importer in L. infantum came from the observations that the protein locates to the cell membrane and that its overexpression leads to augmented zinc internalization. Importantly, expression and cell-surface location of LiZIP3 are lost when parasites face high zinc bioavailability. LiZIP3 decline in response to zinc is regulated at the mRNA level in a process involving (a) short-lived protein(s). Collectively, our data reveal that LiZIP3 enables L. infantum to acquire zinc in a highly regulated manner, hence contributing to zinc homeostasis. PMID:25644708

  9. Zinc in the Monoaminergic Theory of Depression: Its Relationship to Neural Plasticity

    PubMed Central

    Doboszewska, Urszula; Wlaź, Piotr; Nowak, Gabriel; Radziwoń-Zaleska, Maria

    2017-01-01

    Preclinical and clinical studies have demonstrated that zinc possesses antidepressant properties and that it may augment the therapy with conventional, that is, monoamine-based, antidepressants. In this review we aim to discuss the role of zinc in the pathophysiology and treatment of depression with regard to the monoamine hypothesis of the disease. Particular attention will be paid to the recently described zinc-sensing GPR39 receptor as well as aspects of zinc deficiency. Furthermore, an attempt will be made to give a possible explanation of the mechanisms by which zinc interacts with the monoamine system in the context of depression and neural plasticity. PMID:28299207

  10. Height, Zinc and Soil-Transmitted Helminth Infections in Schoolchildren: A Study in Cuba and Cambodia

    PubMed Central

    de Gier, Brechje; Mpabanzi, Liliane; Vereecken, Kim; van der Werff, Suzanne D.; D’Haese, Patrick C.; Fiorentino, Marion; Khov, Kuong; Perignon, Marlene; Chamnan, Chhoun; Berger, Jacques; Parker, Megan E.; Junco Díaz, Raquel; Angel Núñez, Fidel; Rojas Rivero, Lázara; Bonet Gorbea, Mariano; Doak, Colleen M.; Campos Ponce, Maiza; Wieringa, Frank T.; Polman, Katja

    2015-01-01

    Soil-transmitted helminth (STH) infections and zinc deficiency are often found in low- and middle-income countries and are both known to affect child growth. However, studies combining data on zinc and STH are lacking. In two studies in schoolchildren in Cuba and Cambodia, we collected data on height, STH infection and zinc concentration in either plasma (Cambodia) or hair (Cuba). We analyzed whether STH and/or zinc were associated with height for age z-scores and whether STH and zinc were associated. In Cuba, STH prevalence was 8.4%; these were mainly Ascaris lumbricoides and Trichuris trichiura infections. In Cambodia, STH prevalence was 16.8%, mostly caused by hookworm. In Cuban children, STH infection had a strong association with height for age (aB-0.438, p = 0.001), while hair zinc was significantly associated with height for age only in STH uninfected children. In Cambodian children, plasma zinc was associated with height for age (aB-0.033, p = 0.029), but STH infection was not. Only in Cambodia, STH infection showed an association with zinc concentration (aB-0.233, p = 0.051). Factors influencing child growth differ between populations and may depend on prevalences of STH species and zinc deficiency. Further research is needed to elucidate these relationships and their underlying mechanisms. PMID:25903454

  11. Height, zinc and soil-transmitted helminth infections in schoolchildren: a study in Cuba and Cambodia.

    PubMed

    de Gier, Brechje; Mpabanzi, Liliane; Vereecken, Kim; van der Werff, Suzanne D; D'Haese, Patrick C; Fiorentino, Marion; Khov, Kuong; Perignon, Marlene; Chamnan, Chhoun; Berger, Jacques; Parker, Megan E; Díaz, Raquel Junco; Núñez, Fidel Angel; Rivero, Lázara Rojas; Gorbea, Mariano Bonet; Doak, Colleen M; Ponce, Maiza Campos; Wieringa, Frank T; Polman, Katja

    2015-04-20

    Soil-transmitted helminth (STH) infections and zinc deficiency are often found in low- and middle-income countries and are both known to affect child growth. However, studies combining data on zinc and STH are lacking. In two studies in schoolchildren in Cuba and Cambodia, we collected data on height, STH infection and zinc concentration in either plasma (Cambodia) or hair (Cuba). We analyzed whether STH and/or zinc were associated with height for age z-scores and whether STH and zinc were associated. In Cuba, STH prevalence was 8.4%; these were mainly Ascaris lumbricoides and Trichuris trichiura infections. In Cambodia, STH prevalence was 16.8%, mostly caused by hookworm. In Cuban children, STH infection had a strong association with height for age (aB-0.438, p = 0.001), while hair zinc was significantly associated with height for age only in STH uninfected children. In Cambodian children, plasma zinc was associated with height for age (aB-0.033, p = 0.029), but STH infection was not. Only in Cambodia, STH infection showed an association with zinc concentration (aB-0.233, p = 0.051). Factors influencing child growth differ between populations and may depend on prevalences of STH species and zinc deficiency. Further research is needed to elucidate these relationships and their underlying mechanisms.

  12. Influence of DNA-methylation on zinc homeostasis in myeloid cells: Regulation of zinc transporters and zinc binding proteins.

    PubMed

    Kessels, Jana Elena; Wessels, Inga; Haase, Hajo; Rink, Lothar; Uciechowski, Peter

    2016-09-01

    The distribution of intracellular zinc, predominantly regulated through zinc transporters and zinc binding proteins, is required to support an efficient immune response. Epigenetic mechanisms such as DNA methylation are involved in the expression of these genes. In demethylation experiments using 5-Aza-2'-deoxycytidine (AZA) increased intracellular (after 24 and 48h) and total cellular zinc levels (after 48h) were observed in the myeloid cell line HL-60. To uncover the mechanisms that cause the disturbed zinc homeostasis after DNA demethylation, the expression of human zinc transporters and zinc binding proteins were investigated. Real time PCR analyses of 14 ZIP (solute-linked carrier (SLC) SLC39A; Zrt/IRT-like protein), and 9 ZnT (SLC30A) zinc transporters revealed significantly enhanced mRNA expression of the zinc importer ZIP1 after AZA treatment. Because ZIP1 protein was also enhanced after AZA treatment, ZIP1 up-regulation might be the mediator of enhanced intracellular zinc levels. The mRNA expression of ZIP14 was decreased, whereas zinc exporter ZnT3 mRNA was also significantly increased; which might be a cellular reaction to compensate elevated zinc levels. An enhanced but not significant chromatin accessibility of ZIP1 promoter region I was detected by chromatin accessibility by real-time PCR (CHART) assays after demethylation. Additionally, DNA demethylation resulted in increased mRNA accumulation of zinc binding proteins metallothionein (MT) and S100A8/S100A9 after 48h. MT mRNA was significantly enhanced after 24h of AZA treatment also suggesting a reaction of the cell to restore zinc homeostasis. These data indicate that DNA methylation is an important epigenetic mechanism affecting zinc binding proteins and transporters, and, therefore, regulating zinc homeostasis in myeloid cells. Copyright © 2016 Elsevier GmbH. All rights reserved.

  13. Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging

    PubMed Central

    Atamna, Hani; Killilea, David W.; Killilea, Alison Nisbet; Ames, Bruce N.

    2002-01-01

    Heme, a major functional form of iron in the cell, is synthesized in the mitochondria by ferrochelatase inserting ferrous iron into protoporphyrin IX. Heme deficiency was induced with N-methylprotoporphyrin IX, a selective inhibitor of ferrochelatase, in two human brain cell lines, SHSY5Y (neuroblastoma) and U373 (astrocytoma), as well as in rat primary hippocampal neurons. Heme deficiency in brain cells decreases mitochondrial complex IV, activates nitric oxide synthase, alters amyloid precursor protein, and corrupts iron and zinc homeostasis. The metabolic consequences resulting from heme deficiency seem similar to dysfunctional neurons in patients with Alzheimer's disease. Heme-deficient SHSY5Y or U373 cells die when induced to differentiate or to proliferate, respectively. The role of heme in these observations could result from its interaction with heme regulatory motifs in specific proteins or secondary to the compromised mitochondria. Common causes of heme deficiency include aging, deficiency of iron and vitamin B6, and exposure to toxic metals such as aluminum. Iron and B6 deficiencies are especially important because they are widespread, but they are also preventable with supplementation. Thus, heme deficiency or dysregulation may be an important and preventable component of the neurodegenerative process. PMID:12417755

  14. Burning mouth syndrome: results of screening tests for vitamin and mineral deficiencies, thyroid hormone, and glucose levels-experience at Mayo Clinic over a decade.

    PubMed

    Morr Verenzuela, Claudia S; Davis, Mark D P; Bruce, Alison J; Torgerson, Rochelle R

    2017-09-01

    Burning mouth syndrome (BMS) is a disorder characterized by chronic mouth pain in the absence of objective clinical abnormalities. Vitamin or mineral deficiencies may have a role in BMS, but data regarding the prevalence and relevance of hematinic deficiencies are conflicting. We aimed to determine the frequency of specific laboratory abnormalities in patients with BMS. We retrospectively reviewed the results of screening blood tests in patients with BMS at our institution between January 2003 and December 2013. Among 659 patients with BMS, the most common decreased values or deficiencies were vitamin D 3 (15%), vitamin B 2 (15%), vitamin B 6 (5.7%), zinc (5.7%), vitamin B 1 (5.3%), thyrotropin (TSH) (3.2%), vitamin B 12 (0.8%), and folic acid (0.7%). Laboratory values for fasting blood glucose and TSH were increased in 23.7% and 5.2%, respectively. In patients with symptoms of BMS, our results suggest it is reasonable to screen for fasting blood glucose, vitamin D (D 2 and D 3 ), vitamin B 6 , zinc, vitamin B 1 , and TSH. Deficiencies of vitamin B 12 and folic acid were rare (<1% abnormal). © 2017 The International Society of Dermatology.

  15. Low Plasma Zinc Is Associated with Higher Mitochondrial Oxidative Stress and Faster Liver Fibrosis Development in the Miami Adult Studies in HIV Cohort.

    PubMed

    Martinez, Sabrina S; Campa, Adriana; Li, Yinghui; Fleetwood, Christina; Stewart, Tiffanie; Ramamoorthy, Venkataraghavan; Baum, Marianna K

    2017-04-01

    Background: Oxidative stress and reduced antioxidants may be a trigger for liver fibrogenesis. Reducing oxidative stress through higher antioxidant concentration may be a potential antifibrotic target. Objective: We aimed to investigate longitudinally whether plasma zinc, an antioxidant, is related to mitochondrial oxidative stress and the progression of liver fibrosis in the Miami Adult Studies in HIV (MASH) cohort. Methods: A prospective observational cohort study was conducted in 487 predominantly African American HIV-monoinfected and HIV/hepatitis C virus (HCV)-coinfected adults with a mean ± SD age of 47.08 ± 7.67 y from the MASH cohort and followed for a median of 34 mo. Blood was collected for plasma zinc and measures were used to calculate the fibrosis-4 (FIB-4) score (aspartate amino transferase, alanine aminotransferase, and platelets). Plasma zinc deficiency was defined as <0.75 mg/L. Total DNA was extracted from peripheral blood mononuclear cells and mitochondrial DNA (mtDNA) 8-hydroxyguanosine (8-oxo-dG) was determined. Adjusted mixed models were used to assess the relations between zinc, stage of liver disease, and oxidative stress over time and compared between HIV and HIV/HCV groups. Results: Zinc concentrations (β: -0.368, SE = 0.172; P = 0.033) and deficiency were associated with lower FIB-4 scores over time (β: 0.381, SE = 0.118; P = 0.001). Compared with those who were not zinc deficient, zinc-deficient participants had an increased risk of having more-progressed liver disease (OR: 1.91; 95% CI: 1.15, 3.16; P = 0.012). Higher mtDNA 8-oxo-dG was associated with zinc deficiency (β: 0.049, SE = 0.024; P = 0.044) and higher FIB-4 scores over time (β: 0.597, SE = 0.168, P < 0.001). Conclusions: Lower plasma zinc concentrations were associated with liver fibrosis progression and mitochondrial oxidative stress in the HIV and HIV/HCV groups. Zinc may play a role in the impact of liver disease outcomes. © 2017 American Society for Nutrition.

  16. Zinc and Chlamydia trachomatis

    SciTech Connect

    Sugarman, B.; Epps, L.R.

    1985-07-01

    Zinc was noted to have significant effects upon the infection of McCoy cells by each of two strains of Chlamydia trachomatis. With a high or low Chlamydia inoculant, the number of infected cells increased up to 200% utilizing supplemental zinc (up to 1 x 10/sup -4/ M) in the inoculation media compared with standard Chlamydia cultivation media (8 x 10/sup -6/ M zinc). Ferric chloride and calcium chloride did not effect any such changes. Higher concentrations of zinc, after 2 hr of incubation with Chlamydia, significantly decreased the number of inclusions. This direct effect of zinc on the Chlamydia remainedmore » constant after further repassage of the Chlamydia without supplemental zinc, suggesting a lethal effect of the zinc. Supplemental zinc (up to 10/sup -4/ M) may prove to be a useful addition to inoculation media to increase the yield of culturing for Chlamydia trachomatis. Similarly, topical or oral zinc preparations used by people may alter their susceptibility to Chamydia trachomatis infections.« less

  17. Dysregulation of hepatic zinc transporters in a mouse model of alcoholic liver disease

    PubMed Central

    Sun, Qian; Li, Qiong; Zhong, Wei; Zhang, Jiayang; Sun, Xiuhua; Tan, Xiaobing; Yin, Xinmin; Sun, Xinguo; Zhang, Xiang

    2014-01-01

    Zinc deficiency is a consistent phenomenon observed in patients with alcoholic liver disease, but the mechanisms have not been well defined. The objective of this study was to determine if alcohol alters hepatic zinc transporters in association with reduction of hepatic zinc levels and if oxidative stress mediates the alterations of zinc transporters. C57BL/6 mice were pair-fed with the Lieber-DeCarli control or ethanol diets for 2, 4, or 8 wk. Chronic alcohol exposure reduced hepatic zinc levels, but increased plasma and urine zinc levels, at all time points. Hepatic zinc finger proteins, peroxisome proliferator-activated receptor-α (PPAR-α) and hepatocyte nuclear factor 4α (HNF-4α), were downregulated in ethanol-fed mice. Four hepatic zinc transporter proteins showed significant alterations in ethanol-fed mice compared with the controls. ZIP5 and ZIP14 proteins were downregulated, while ZIP7 and ZnT7 proteins were upregulated, by ethanol exposure at all time points. Immunohistochemical staining demonstrated that chronic ethanol exposure upregulated cytochrome P-450 2E1 and caused 4-hydroxynonenal accumulation in the liver. For the in vitro study, murine FL-83B hepatocytes were treated with 5 μM 4-hydroxynonenal or 100 μM hydrogen peroxide for 72 h. The results from in vitro studies demonstrated that 4-hydroxynonenal treatment altered ZIP5 and ZIP7 protein abundance, and hydrogen peroxide treatment changed ZIP7, ZIP14, and ZnT7 protein abundance. These results suggest that chronic ethanol exposure alters hepatic zinc transporters via oxidative stress, which might account for ethanol-induced hepatic zinc deficiency. PMID:24924749

  18. Crosstalk between Zinc Status and Giardia Infection: A New Approach

    PubMed Central

    Astiazarán-García, Humberto; Iñigo-Figueroa, Gemma; Quihui-Cota, Luis; Anduro-Corona, Iván

    2015-01-01

    Zinc supplementation has been shown to reduce the incidence and prevalence of diarrhea; however, its anti-diarrheal effect remains only partially understood. There is now growing evidence that zinc can have pathogen-specific protective effects. Giardiasis is a common yet neglected cause of acute-chronic diarrheal illness worldwide which causes disturbances in zinc metabolism of infected children, representing a risk factor for zinc deficiency. How zinc metabolism is compromised by Giardia is not well understood; zinc status could be altered by intestinal malabsorption, organ redistribution or host-pathogen competition. The potential metal-binding properties of Giardia suggest unusual ways that the parasite may interact with its host. Zinc supplementation was recently found to reduce the rate of diarrhea caused by Giardia in children and to upregulate humoral immune response in Giardia-infected mice; in vitro and in vivo, zinc-salts enhanced the activity of bacitracin in a zinc-dose-dependent way, and this was not due to zinc toxicity. These findings reflect biological effect of zinc that may impact significantly public health in endemic areas of infection. In this paper, we shall explore one direction of this complex interaction, discussing recent information regarding zinc status and its possible contribution to the outcome of the encounter between the host and Giardia. PMID:26046395

  19. Modeling the temporal variability of zinc concentrations in zinc roof runoff-experimental study and uncertainty analysis.

    PubMed

    Sage, Jérémie; El Oreibi, Elissar; Saad, Mohamed; Gromaire, Marie-Christine

    2016-08-01

    This study investigates the temporal variability of zinc concentrations from zinc roof runoff. The influence of rainfall characteristics and dry period duration is evaluated by combining laboratory experiment on small zinc sheets and in situ measurements under real weather conditions from a 1.6-m(2) zinc panel. A reformulation of a commonly used conceptual runoff quality model is introduced and its ability to simulate the evolution of zinc concentrations is evaluated. A systematic and sharp decrease from initially high to relatively low and stable zinc concentrations after 0.5 to 2 mm of rainfall is observed for both experiments, suggesting that highly soluble corrosion products are removed at early stages of runoff. A moderate dependence between antecedent dry period duration and the magnitude of zinc concentrations at the beginning of a rain event is evidenced. Contrariwise, results indicate that concentrations are not significantly influenced by rainfall intensities. Simulated rainfall experiment nonetheless suggests that a slight effect of rainfall intensities may be expected after the initial decrease of concentrations. Finally, this study shows that relatively simple conceptual runoff quality models may be adopted to simulate the variability of zinc concentrations during a rain event and from a rain event to another.

  20. [Impact of fortified milk on the iron and zinc levels in Mexican preschool children].

    PubMed

    Grijalva-Haro, María Isabel; Chavarria, Elsa Yolanda; Artalejo, Elizabeth; Nieblas, Amparo; Ponce, José Antonio; Robles-Sardin, Alma E

    2014-02-01

    The aim of this study was to assess the efficacy of a national program of consumption of fortified milk "Liconsa" on the nutritional status of iron and zinc in pre-school children (3-5 y). The study was conducted in 77 healthy children of both genders. 54 of them consumed Liconsa fortified milk (GCLFL) and 23 consumed no fortified milk (GR). Iron status was determined by measuring hemoglobin and ferritin and zinc status by serum zinc. The consumption of milk was on free demand and it was estimated at baseline and 6 mo after. Through 24-h recall of measured consumption of iron and zinc in the total diet. Descriptive statistics, Student's t test for independent samples and chi-square test for differences in proportions. Children who consumed fortified milk showed an increase of hemoglobin and ferritin levels [1.13 g/dL (p < 0.05) and 5.83 μg/L (p < 0.05) respectively]. Additionally, a decrease was found of the prevalence of low iron stores from 20.4 to 4.1% (p < 0.05). The serum zinc level showed an increase of 45.2 μg/dL (p < 0.05). At the end of the study no child showed a micronutrient deficiency. Children who did not consume fortified milk Liconsa showed no significant change in their serum iron and zinc values. The average consumption of milk powder Liconsa was 22.7 ± 14.5 g, providing 2.5 mg of daily iron and zinc. Supplied diet 9.2 ± 3.4 mg of iron and 6.9 ± 3 mg of zinc. The consumption of fortified milk had a beneficial effect on the serum levels of iron and zinc in children's social welfare program Liconsa. Copyright AULA MEDICA EDICIONES 2014. Published by AULA MEDICA. All rights reserved.

  1. Low Plasma Zinc Is Associated with Higher Mitochondrial Oxidative Stress and Faster Liver Fibrosis Development in the Miami Adult Studies in HIV Cohort1234

    PubMed Central

    Martinez, Sabrina S; Campa, Adriana; Li, Yinghui; Fleetwood, Christina; Stewart, Tiffanie; Ramamoorthy, Venkataraghavan; Baum, Marianna K

    2017-01-01

    Background: Oxidative stress and reduced antioxidants may be a trigger for liver fibrogenesis. Reducing oxidative stress through higher antioxidant concentration may be a potential antifibrotic target. Objective: We aimed to investigate longitudinally whether plasma zinc, an antioxidant, is related to mitochondrial oxidative stress and the progression of liver fibrosis in the Miami Adult Studies in HIV (MASH) cohort. Methods: A prospective observational cohort study was conducted in 487 predominantly African American HIV-monoinfected and HIV/hepatitis C virus (HCV)–coinfected adults with a mean ± SD age of 47.08 ± 7.67 y from the MASH cohort and followed for a median of 34 mo. Blood was collected for plasma zinc and measures were used to calculate the fibrosis-4 (FIB-4) score (aspartate amino transferase, alanine aminotransferase, and platelets). Plasma zinc deficiency was defined as <0.75 mg/L. Total DNA was extracted from peripheral blood mononuclear cells and mitochondrial DNA (mtDNA) 8-hydroxyguanosine (8-oxo-dG) was determined. Adjusted mixed models were used to assess the relations between zinc, stage of liver disease, and oxidative stress over time and compared between HIV and HIV/HCV groups. Results: Zinc concentrations (β: −0.368, SE = 0.172; P = 0.033) and deficiency were associated with lower FIB-4 scores over time (β: 0.381, SE = 0.118; P = 0.001). Compared with those who were not zinc deficient, zinc-deficient participants had an increased risk of having more-progressed liver disease (OR: 1.91; 95% CI: 1.15, 3.16; P = 0.012). Higher mtDNA 8-oxo-dG was associated with zinc deficiency (β: 0.049, SE = 0.024; P = 0.044) and higher FIB-4 scores over time (β: 0.597, SE = 0.168, P < 0.001). Conclusions: Lower plasma zinc concentrations were associated with liver fibrosis progression and mitochondrial oxidative stress in the HIV and HIV/HCV groups. Zinc may play a role in the impact of liver disease outcomes. PMID:28228506

  2. Could giardiasis be a risk factor for low zinc status in schoolchildren from northwestern Mexico? A cross-sectional study with longitudinal follow-up

    PubMed Central

    2010-01-01

    Background Both giardiasis and zinc deficiency are serious health problems worldwide. In Mexico, the prevalence of G. intestinalis was estimated at 32% in 1994. It remains a health problem in northwestern Mexico. Recent surveys (1987, 1995, and 1999) reported zinc deficiency in the Mexican population. The association of giardiasis and malabsorption of micronutrients has been well documented, although the association with zinc remains controversial. This study investigated the association between giardiasis and zinc deficiency in schoolchildren from northwestern Mexico. Methods We combined a cross-sectional design with a longitudinal follow-up six months after parasite treatment. The baseline sample consisted of 114 schoolchildren (mean age 8.8 yr) from seven suburban public schools, grouped as Giardia-free (n = 65, 57%) and Giardia-infected (n = 49, 43%). Three stool analyses per child were done using Faust's method. Children with giardiasis received secnidazole. Serum zinc was determined by atomic absorption spectrophotometry. Height and weight were measured. Socioeconomic information was obtained in an oral questionnaire, and daily zinc intake was assessed using 24 hour-recalls. Pearson's correlation and ANCOVA and paired t-test analyses were used to determine the association between giardiasis and zinc status. Results Longitudinal analysis demonstrated a significant increase of the mean serum zinc levels in the Giardia-infected group six months after treatment (13.78 vs. 19.24 μmol/L μmol/L; p = 0.001), although no difference was found between the Giardia-free and the Giardia-infected groups (p = 0.86) in the baseline analysis. Z scores for W/A and H/A were lower in the Giardia-infected than in the Giardia-free group (p < 0.05). No difference was observed in the socioeconomic characteristics and mean daily intakes of zinc between the groups (p > 0.05). Conclusions Giardiasis may be a risk factor for zinc deficiency in schoolchildren from northwestern Mexico

  3. [Distribution iodine deficiency diseases in coastal areas depending on geochemical conditions].

    PubMed

    Kiku, P F; Andryukov, B G

    2014-01-01

    In the Primorsky Krai there was performed a population ecological and hygienic analysis of the relationship between the content of chemical elements in the soil and thyroid morbidity in the population of the region. The assessment of the prevalence of iodine deficiency and iodine deficiency diseases was carried out on the basis of the impact of the priority environmental toxic (strontium, nickel, cadmium, lead, arsenic, tin) and essential (nickel, iron, germanium, molybdenum, zinc, selenium) trace elements on the level of iodine deficiency diseases. The level of thyroid pathology in the territory of Primorye was established to be the highest one in areas characterized by the severe iodine deficiency (Northwest geochemical zones), where the structure of thyroid diseases is presented mainly by diffuse nontoxic goiter. Thyroid diseases associated with iodine deficiency in the population of different age groups are the result of multiple and combined imbalance of trace elements, which causes a relative (secondary) iodine deficiency. Thyroid disease in Primorye are environmentally caused diseases of technogenic origin, they are a consequence of the relative iodine deficiency, when on the background of normal iodine supply an imbalance of zinc, iron, cobalt, manganese with excess of such toxic trace elements as lead, strontium, nickel and chromium takes place. Thyroid pathology associated with iodine deficiency, along with other environmentally dependent diseases can be considered as a marker of ecological environment trouble.

  4. The effect of zinc on cellular immunity in chronic uremia.

    PubMed

    Antoniou, L D; Shalhoub, R J; Schechter, G P

    1981-09-01

    Delayed hypersensitivity to mumps was examined in 25 apparently well-nourished men receiving regular hemodialysis, each of whom had a history of mumps. A positive reaction was observed in eight of nine patients already under therapy with zinc added to the dialysis bath. In contrast, 11 of 16 untreated patients were anergic. Four of the anergic patients were subsequently treated with zinc resulting in restoration of sensitivity in three patients. There were no significant differences in lymphocyte, monocyte, or T-cell counts between the two groups of patients. Consequently, zinc probably acts by improving the function of one or more of these cell types. Protracted zinc deficiency may be a major cause of impaired cellular immunity in chronic renal failure.

  5. Mutations in a CCHC zinc-binding motif of the reovirus sigma 3 protein decrease its intracellular stability.

    PubMed Central

    Mabrouk, T; Lemay, G

    1994-01-01

    It has been demonstrated that the sigma 3 protein of reovirus harbors a zinc-binding domain in its amino-terminal portion. A putative zinc finger in the CCHH form is located in this domain and was considered to be a good candidate for the zinc-binding motif. We performed site-directed mutagenesis to substitute amino acids in this region and demonstrated that many of these mutants, although expressed in COS cells, were unstable compared with the wild-type protein. Further analysis revealed that zinc-binding capability, as measured by retention on a zinc chelate affinity adsorbent, correlates with stability. These studies also allowed us to identify a CCHC box as the most probable zinc-binding motif. Images PMID:8035527

  6. Zinc rescues obesity-induced cardiac hypertrophy via stimulating metallothionein to suppress oxidative stress-activated BCL10/CARD9/p38 MAPK pathway.

    PubMed

    Wang, Shudong; Gu, Junlian; Xu, Zheng; Zhang, Zhiguo; Bai, Tao; Xu, Jianxiang; Cai, Jun; Barnes, Gregory; Liu, Qiu-Ju; Freedman, Jonathan H; Wang, Yonggang; Liu, Quan; Zheng, Yang; Cai, Lu

    2017-06-01

    Obesity often leads to obesity-related cardiac hypertrophy (ORCH), which is suppressed by zinc-induced inactivation of p38 mitogen-activated protein kinase (p38 MAPK). In this study, we investigated the mechanisms by which zinc inactivates p38 MAPK to prevent ORCH. Mice (4-week old) were fed either high fat diet (HFD, 60% kcal fat) or normal diet (ND, 10% kcal fat) containing variable amounts of zinc (deficiency, normal and supplement) for 3 and 6 months. P38 MAPK siRNA and the p38 MAPK inhibitor SB203580 were used to suppress p38 MAPK activity in vitro and in vivo, respectively. HFD activated p38 MAPK and increased expression of B-cell lymphoma/CLL 10 (BCL10) and caspase recruitment domain family member 9 (CARD9). These responses were enhanced by zinc deficiency and attenuated by zinc supplement. Administration of SB203580 to HFD mice or specific siRNA in palmitate-treated cardiomyocytes eliminated the HFD and zinc deficiency activation of p38 MAPK, but did not significantly impact the expression of BCL10 and CARD9. In cultured cardiomyocytes, inhibition of BCL10 expression by siRNA prevented palmitate-induced increased p38 MAPK activation and atrial natriuretic peptide (ANP) expression. In contrast, inhibition of p38 MAPK prevented ANP expression, but did not affect BCL10 expression. Deletion of metallothionein abolished the protective effect of zinc on palmitate-induced up-regulation of BCL10 and phospho-p38 MAPK. HFD and zinc deficiency synergistically induce ORCH by increasing oxidative stress-mediated activation of BCL10/CARD9/p38 MAPK signalling. Zinc supplement ameliorates ORCH through activation of metallothionein to repress oxidative stress-activated BCL10 expression and p38 MAPK activation. © 2017 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

  7. Nut traits and nutritional composition of hazelnut (Corylus avellana L.) as influenced by zinc fertilization.

    PubMed

    Özenç, Nedim; Özenç, Damla Bender

    2015-07-01

    Zinc is an essential element for plants and its deficiency is a widespread problem throughout the world, causing decreased yields and nutritional quality. In this study the effect of zinc fertilization on some nut traits and the nutritional composition of 'Tombul' hazelnut (Corylus avellana L.) variety cultivated in the Black Sea region of Turkey was investigated and the contribution of this nut to human nutrition determined. Trials were carried out at 'Tombul' hazelnut orchards, and zinc fertilizers were applied at 0, 0.2, 0.4, 0.8 and 1.6 kg Zn ha(-1) in three consecutive years. Significant differences in some nut traits and mineral composition (protein, total oil, ash, kernel percentage, empty and wrinkled nuts, copper, boron, manganese and molybdenum) were observed with zinc fertilizer applications. In terms of daily nutritional element requirements, 100 g of hazelnut provided about 44.74% phosphorus, 13.39% potassium, 19.32% calcium, 37.49% magnesium, 0.19% sodium, 51.63% iron, 25.73% zinc and 14.05% boron of the recommended daily amounts (RDAs), while copper, manganese and molybdenum contents exceeded their RDAs. In order to improve some nut traits and the mineral composition of hazelnut, 0.8 and 1.6 kg Zn ha(-1) fertilizations could be recommended in practice. © 2014 Society of Chemical Industry.

  8. The effect of a moderate zinc deficiency and dietary fat source on the activity and expression of the Δ(3)Δ (2)-enoyl-CoA isomerase in the liver of growing rats.

    PubMed

    Justus, Jennifer; Weigand, Edgar

    2014-06-01

    Auxiliary enzymes participate in β-oxidation of unsaturated fatty acids. The objective of the study was to investigate the impact of a moderate zinc deficiency and a high intake of polyunsaturated fat on Δ(3)Δ(2)-enoyl-CoA isomerase (ECI) in the liver and other tissues. Five groups of eight weanling rats each were fed moderately zinc-deficient (ZD) or zinc-adequate (ZA) semisynthetic diets (7 or 50 mg Zn/kg) enriched with 22 % cocoa butter (CB) or 22 % safflower oil (SO) for 4 weeks: (1) ZD-CB, fed free choice; (2) ZA-CBR, ZA-CB diet fed in equivalent amounts consumed by the ZD-CB group; (3) ZD-SO, fed free choice; (4) ZA-SOR, ZA-SO diet fed in equivalent amounts consumed by the ZD-SO group; and (5) ZA-SO, fed free choice. Growth and Zn status markers were markedly reduced in the ZD groups. ECI activity in the liver of the animals fed the ZD- and ZA-SO diets were significantly higher (approximately 2- and 3-fold, respectively) as compared with the CB-fed animals, whereas activities in extrahepatic tissues (kidneys, heart, skeletal muscle, testes, adipose tissue) were not altered by dietary treatments. Transcript levels of the mitochondrial Eci gene in the liver did not significantly differ between ZD and ZA rats, but were 1.6-fold higher in the ZA-SO- than in the ZD-CB-fed animals (P < 0.05). It is concluded that diets enriched with safflower oil as a source high in linoleic acid induce markedly increased hepatic ECI activities and that a moderate Zn deficiency does not affect transcription of the mitochondrial Eci gene in the liver.

  9. Effect of controlled zinc release on bone mineral density from injectable Zn-containing beta-tricalcium phosphate suspension in zinc-deficient diseased rats.

    PubMed

    Otsuka, Makoto; Ohshita, Yuko; Marunaka, Sunao; Matsuda, Yoshihia; Ito, Atsuo; Ichinose, Noboru; Otsuka, Kuniko; Higuchi, William I

    2004-06-01

    The purpose of this study was to evaluate the efficacy of zinc (Zn)-containing beta-tricalcium phosphate (Zn-TCP) in correcting the bone mineral deficiency noted in osteoporosis using ovariectomized rat model. Four rats were used for each of the four experimental groups: D0, D10, D20, and N10. The rats in D0, D10, and D20 groups were ovariectomized, and fed a vitamin D-, Ca-, and Zn-deficient diet, and induced Zn-deficient osteoporoses for 9 weeks. In contrast, the N10 group was the normal rats fed normal healthy diet for 9 weeks. D0 group was injected with pure beta-TCP suspension, D10 and D20 groups were injected with suspensions containing 10 mg of 10 mol % (6.17 wt % Zn) and 20 mol % (12.05 wt % Zn) Zn-TCP, respectively, and the healthy group, N10 were injected with 10 mol %. Zn-TCP suspensions. Injections were administered intramuscularly in the left thigh once a week in all rats, and fed a vitamin D- and Zn-deficient diet for 9 weeks. The plasma calcium (Ca) and Zn levels, plasma alkaline phosphatase activity (ALP) and bone mineral density (BMD) of the lumbar vertebra and femora were measured. The plasma Zn levels in all the rats were between 1.1 and 2.8 microg/mL. The areas under the curves for the Ca, Zn, and ALP (Ca-AUC, Zn-AUC, and ALP-AUC) levels between 0 and 63 days were calculated. Results for the AUCs were as follows: (1) the Zn-AUCs were in the order of N10 = D20 > D10 > D0; (2) the Ca-AUCs for D0, D10 groups were significantly lower than that for the N10 group; (3) the ALP-AUCs for the D10 and D20 groups were significantly higher than that for the N10 group, and that of the D0 group was in between those. The body weight of D10 and D20 groups significantly increased with time, that of the D0 group increased slightly, and that of the N10 group remained unchanged for the entire experimental period. The BMD of the lumbar vertebrae of the D10 and D20 groups (about 100 mg/cm(2)) was significantly higher than that of the D0 group but lower than that of

  10. A role for the Drosophila zinc transporter Zip88E in protecting against dietary zinc toxicity.

    PubMed

    Richards, Christopher D; Warr, Coral G; Burke, Richard

    2017-01-01

    Zinc absorption in animals is thought to be regulated in a local, cell autonomous manner with intestinal cells responding to dietary zinc content. The Drosophila zinc transporter Zip88E shows strong sequence similarity to Zips 42C.1, 42C.2 and 89B as well as mammalian Zips 1, 2 and 3, suggesting that it may act in concert with the apically-localised Drosophila zinc uptake transporters to facilitate dietary zinc absorption by importing ions into the midgut enterocytes. However, the functional characterisation of Zip88E presented here indicates that Zip88E may instead play a role in detecting and responding to zinc toxicity. Larvae homozygous for a null Zip88E allele are viable yet display heightened sensitivity to elevated levels of dietary zinc. This decreased zinc tolerance is accompanied by an overall decrease in Metallothionein B transcription throughout the larval midgut. A Zip88E reporter gene is expressed only in the salivary glands, a handful of enteroendocrine cells at the boundary between the anterior and middle midgut regions, and in two parallel strips of sensory cell projections connecting to the larval ventral ganglion. Zip88E expression solely in this restricted subset of cells is sufficient to rescue the Zip88E mutant phenotype. Together, our data suggest that Zip88E may be functioning in a small subset of cells to detect excessive zinc levels and induce a systemic response to reduce dietary zinc absorption and hence protect against toxicity.

  11. Zinc monotherapy increases serum brain-derived neurotrophic factor (BDNF) levels and decreases depressive symptoms in overweight or obese subjects: a double-blind, randomized, placebo-controlled trial.

    PubMed

    Solati, Zahra; Jazayeri, Shima; Tehrani-Doost, Mehdi; Mahmoodianfard, Salma; Gohari, Mahmood Reza

    2015-05-01

    Previous studies have shown a positive effect of zinc as an adjunctive therapy on reducing depressive symptoms. However, to our knowledge, no study has examined the effect of zinc monotherapy on mood. The aim of the present study was to determine the effects of zinc monotherapy on depressive symptoms and serum brain-derived neurotrophic factor (BDNF) levels in overweight or obese subjects. Fifty overweight or obese subjects were randomly assigned into two groups and received either 30 mg zinc or placebo daily for 12 weeks. At baseline and post-intervention, depression severity was assessed using Beck depression inventory II (BDI II), and serum BDNF and zinc levels were determined by enzyme-linked immunosorbent assay and atomic absorption spectrophotometry, respectively. The trial was completed with 46 subjects. After a 12-week supplementation, serum zinc and BDNF levels increased significantly in the zinc-supplemented group compared with the placebo group. BDI scores declined in both the groups at the end of the study, but reduction in the zinc-supplemented group was significantly higher than the placebo group. More analysis revealed that following supplementation, BDI scores decreased in subgroup of subjects with depressive symptoms (BDI ≥ 10) (n = 30), but did not change in the subgroup of non-depressed subjects (BDI < 10) (n = 16). Moreover, a significant inverse correlation was observed between serum BDNF levels and depression severity in all participants. Interestingly, a significant positive correlation was found between serum BDNF and zinc levels at baseline. Zinc monotherapy improves mood in overweight or obese subjects most likely through increasing BDNF levels.

  12. Fishy Business: Effect of Omega-3 Fatty Acids on Zinc Transporters and Free Zinc Availability in Human Neuronal Cells

    PubMed Central

    De Mel, Damitha; Suphioglu, Cenk

    2014-01-01

    Omega-3 (ω-3) fatty acids are one of the two main families of long chain polyunsaturated fatty acids (PUFA). The main omega-3 fatty acids in the mammalian body are α-linolenic acid (ALA), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). Central nervous tissues of vertebrates are characterized by a high concentration of omega-3 fatty acids. Moreover, in the human brain, DHA is considered as the main structural omega-3 fatty acid, which comprises about 40% of the PUFAs in total. DHA deficiency may be the cause of many disorders such as depression, inability to concentrate, excessive mood swings, anxiety, cardiovascular disease, type 2 diabetes, dry skin and so on. On the other hand, zinc is the most abundant trace metal in the human brain. There are many scientific studies linking zinc, especially excess amounts of free zinc, to cellular death. Neurodegenerative diseases, such as Alzheimer’s disease, are characterized by altered zinc metabolism. Both animal model studies and human cell culture studies have shown a possible link between omega-3 fatty acids, zinc transporter levels and free zinc availability at cellular levels. Many other studies have also suggested a possible omega-3 and zinc effect on neurodegeneration and cellular death. Therefore, in this review, we will examine the effect of omega-3 fatty acids on zinc transporters and the importance of free zinc for human neuronal cells. Moreover, we will evaluate the collective understanding of mechanism(s) for the interaction of these elements in neuronal research and their significance for the diagnosis and treatment of neurodegeneration. PMID:25195602

  13. Fishy business: effect of omega-3 fatty acids on zinc transporters and free zinc availability in human neuronal cells.

    PubMed

    De Mel, Damitha; Suphioglu, Cenk

    2014-08-15

    Omega-3 (ω-3) fatty acids are one of the two main families of long chain polyunsaturated fatty acids (PUFA). The main omega-3 fatty acids in the mammalian body are α-linolenic acid (ALA), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). Central nervous tissues of vertebrates are characterized by a high concentration of omega-3 fatty acids. Moreover, in the human brain, DHA is considered as the main structural omega-3 fatty acid, which comprises about 40% of the PUFAs in total. DHA deficiency may be the cause of many disorders such as depression, inability to concentrate, excessive mood swings, anxiety, cardiovascular disease, type 2 diabetes, dry skin and so on. On the other hand, zinc is the most abundant trace metal in the human brain. There are many scientific studies linking zinc, especially excess amounts of free zinc, to cellular death. Neurodegenerative diseases, such as Alzheimer's disease, are characterized by altered zinc metabolism. Both animal model studies and human cell culture studies have shown a possible link between omega-3 fatty acids, zinc transporter levels and free zinc availability at cellular levels. Many other studies have also suggested a possible omega-3 and zinc effect on neurodegeneration and cellular death. Therefore, in this review, we will examine the effect of omega-3 fatty acids on zinc transporters and the importance of free zinc for human neuronal cells. Moreover, we will evaluate the collective understanding of mechanism(s) for the interaction of these elements in neuronal research and their significance for the diagnosis and treatment of neurodegeneration.

  14. Micronutrient Deficiencies and Plasmodium vivax Malaria among Children in the Brazilian Amazon

    PubMed Central

    Benzecry, Silvana Gomes; Alexandre, Márcia Almeida; Vítor-Silva, Sheila; Salinas, Jorge Luis; de Melo, Gisely Cardoso; Marinho, Helyde Albuquerque; Paes, Ângela Tavares; de Siqueira, André Machado; Monteiro, Wuelton Marcelo; Lacerda, Marcus Vinícius Guimarães; Leite, Heitor Pons

    2016-01-01

    Background There is a growing body of evidence linking micronutrient deficiencies and malaria incidence arising mostly from P. falciparum endemic areas. We assessed the impact of micronutrient deficiencies on malaria incidence and vice versa in the Brazilian state of Amazonas. Methodology/Principal Findings We evaluated children <10 years old living in rural communities in the state of Amazonas, Brazil, from May 2010 to May 2011. All children were assessed for sociodemographic, anthropometric and laboratory parameters, including vitamin A, beta-carotene, zinc and iron serum levels at the beginning of the study (May 2010) and one year later (May 2011). Children were followed in between using passive surveillance for detection of symptomatic malaria. Those living in the study area at the completion of the observation period were reassessed for micronutrient levels. Univariate Cox-proportional Hazards models were used to assess whether micronutrient deficiencies had an impact on time to first P. vivax malaria episode. We included 95 children median age 4.8 years (interquartile range [IQR]: 2.3–6.6), mostly males (60.0%) and with high maternal illiteracy (72.6%). Vitamin A deficiencies were found in 36% of children, beta-carotene deficiency in 63%, zinc deficiency in 61% and iron deficiency in 51%. Most children (80%) had at least one intestinal parasite. During follow-up, 16 cases of vivax malaria were diagnosed amongst 13 individuals. Micronutrient deficiencies were not associated with increased malaria incidence: vitamin A deficiency [Hazard ratio (HR): 1.51; P-value: 0.45]; beta-carotene [HR: 0.47; P-value: 0.19]; zinc [HR: 1.41; P-value: 0.57] and iron [HR: 2.31; P-value: 0.16]). Upon reevaluation, children with al least one episode of malaria did not present significant changes in micronutrient levels. Conclusion Micronutrient serum levels were not associated with a higher malaria incidence nor the malaria episode influenced micronutrient levels. Future studies

  15. Application of zinc isotope tracer technology in tracing soil heavy metal pollution

    NASA Astrophysics Data System (ADS)

    Norbu, Namkha; Wang, Shuguang; Xu, Yan; Yang, Jianqiang; Liu, Qiang

    2017-08-01

    Recent years the soil heavy metal pollution has become increasingly serious, especially the zinc pollution. Due to the complexity of this problem, in order to prevent and treat the soil pollution, it's crucial to accurately and quickly find out the pollution sources and control them. With the development of stable isotope tracer technology, it's able to determine the composition of zinc isotope. Based on the theory of zinc isotope tracer technique, and by means of doing some latest domestic and overseas literature research about the zinc isotope multi-receiving cups of inductively coupled plasma mass spectrometer (MC-ICP-MS) testing technology, this paper summarized the latest research results about the pollution tracer of zinc isotope, and according to the deficiencies and existing problems of previous research, made outlooks of zinc isotope fractionation mechanism, repository establishment and tracer multiple solutions.

  16. Antithrombin deficiency and decreased protein C activity in a young man with venous thromboembolism: a case report.

    PubMed

    Wang, Dong; Tian, Min; Cui, Guanglin; Wang, Dao Wen

    2018-06-01

    Antithrombin and protein C are two crucial members in the anticoagulant system and play important roles in hemostasis. Mutations in SERPINC1 and PROC lead to deficiency or dysfunction of the two proteins, which could result in venous thromboembolism (VTE). Here, we report a Chinese 22-year-old young man who developed recurrent and serious VTE in cerebral veins, visceral veins, and deep veins of the lower extremity. Laboratory tests and direct sequencing of PROC and SERPINC1 were conducted for the patient and his family members. Coagulation tests revealed that the patient presented type I antithrombin deficiency combined with decreased protein C activity resulting from a small insertion mutation c.848_849insGATGT in SERPINC1 and a short deletion variant c.572_574delAGA in PROC. This combination of the two mutations was absent in 400 healthy subjects each from southern and northern China. Then, we summarized all the mutations of the SERPINC1 and PROC gene reported in the Chinese Han population. This study demonstrates that the combination of antithrombin deficiency and decreased protein C activity can result in severe VTE and that the coexistence of different genetic factors may increase the risk of VTE.

  17. Zinc hazards to plants and animals with emphasis on fishery and wildlife resources

    USGS Publications Warehouse

    Eisler, R.; Cheremisinoff, Paul N.

    1997-01-01

    Ecological and toxicological aspects of zinc in the environment are reviewed with emphasis on natural resources. Subtopics include sources and uses; chemical and biochemical properties; carcinogenicity, mutagenicity, teratogenicity; background concentrations in biological and nonbiological compartments; effects of zinc deficiency; toxic and sublethal effects on terrestrial plants and invertebrates, aquatic organisms, birds, and mammals; and recommendations for the protection of sensitive resources.

  18. Involvement of l-arginine-nitric oxide pathway in anxiolytic-like effects of zinc chloride in rats.

    PubMed

    Navabi, Seyedeh Parisa; Eshagh Harooni, Hooman; Moazedi, Ahmad Ali; Khajepour, Lotfolah; Fathinia, Kosar

    2016-10-01

    Zinc is crucial for normal development of the brain, and Zinc deficiency has been shown to associate with neurological disorders (e.g. anxiety) through interactions with several neurotransmitter systems such as nitric oxide (NO). In this regard, our study aimed to evaluate the possible involvement of l-arginine NO pathway on anxiolytic effects of zinc in adult male rats. Zinc chloride at doses of 2.5 and 10mg/kg (intraperitoneal or ip) or saline (1ml/kg, ip) were injected 30min before the anxiety test. Zinc administrated rats (10mg/kg) were pre-treated with intra-CA1 microinjection of l-arginine in sub-effective dose of 1μg/rat (dorsal hippocampus, vehicle: saline1μl/rat). In addition, zinc chloride and NG-nitro-l-arginine methyl ester (l-NAME) were intraperitoneally co-administrated in sub-effective doses of 2.5mg/kg and 80mg/kg, respectively. The percentage of open arm time (OAT%), percentage of open arm entry (OAE%), as measures of anxiety, and total number of arm entries, as measures of locomotor activity, were recorded. Treatment with zinc (10mg/kg) markedly produced an increase in OAT% and OAE% in the Elevated plus maze test (EPM). A decrease of OAT% and OAE% was shown in groups which received zinc (10mg/kg) and l-arginine (1μg/rat) concomitantly as compared to the control group. Moreover, an increase of OAE% was revealed in the group exposed to Zinc (2.5mg/kg) and l-NAME (80mg/kg) co-administration. Although, Two-way ANOVA showed no significant differences of anxiety indices in rats received drug+zinc chloride in compare to the zinc pretreated with saline group. Anxiolytic- like effect of zinc reversed by nitric oxide precursor l-arginine. Additionally, the synergistic effects of l-NAME and ZnCl 2 were shown in the EPM. Thus our findings suggest that at least in part the anxiolytic effects of zinc can be mediated through the nitric oxide system. Copyright © 2016 Elsevier Masson SAS. All rights reserved.

  19. Effect of dietary phytate on zinc homeostasis in young and elderly Korean women.

    PubMed

    Kim, Jihye; Paik, Hee Young; Joung, Hyojee; Woodhouse, Leslie R; Li, Shanji; King, Janet C

    2007-02-01

    Previous studies suggest that consumption of predominantly plant-based diets with high phytate content contribute to zinc deficiency by inhibiting zinc absorption. Age of the individual may also affect the ability to maintain zinc homeostasis. This study was designed to determine the effect of dietary phytate on zinc homeostasis and to evaluate the effect of age on the capacity to maintain the zinc homeostasis with changes in dietary phytate in young and elderly Korean women. Seven healthy young women (22-24 yr) and 10 healthy elderly women (66-75 yr) were studied consecutively for 3 months in 2 metabolic periods (MP) in two different metabolic units. During MP1 the women consumed a high phytate (HP) diet (P:Zn molar ratio = 23) for 9 days. After a 10 d wash-out period at home eating their usual diets, a lower phytate diet (LP) (P:Zn molar ratio = 10) was fed in MP2 for 9 d. Phytase was added to selected foods in the high phytate diet to reduce the phytate content of the meals in the LP period. The zinc content of both diets was about 6.5 mg/d. Stable isotopes of Zn ((70)Zn) were administered intravenously on d 5 of MP 1 and 2 for measuring endogenous fecal zinc excretion. Plasma samples were also collected on d 5 for measuring plasma zinc concentrations by Inductively Coupled Plasma-Atomic Emission Spectrometry (ICP-AES). 24 hr urine samples were collected for 5 d and complete fecal samples were collected for 9 d after isotope administration. Fractional zinc absorption (FZA) was calculated from mass balance corrected for endogenous fecal zinc (EFZ) excretion and EFZ was determined by using an isotopic dilution technique. Isotopic ratios for FZA and EFZ were measured by Inductively Coupled Plasma-Mass Spectrometry (ICP-MS). Statistical analyses were done using ANOVA. Both the young and elderly women were in negative zinc balance during the HP period. This was due to a significant decrease in FZA and total absorbed zinc (TAZ) with a HP diet (43 vs 22% in young women

  20. Losartan Decreases Cardiac Muscle Fibrosis and Improves Cardiac Function in Dystrophin-Deficient Mdx Mice

    PubMed Central

    Spurney, Christopher F.; Sali, Arpana; Guerron, Alfredo D.; Iantorno, Micaela; Yu, Qing; Gordish-Dressman, Heather; Rayavarapu, Sree; van der Meulen, Jack; Hoffman, Eric P.; Nagaraju, Kanneboyina

    2014-01-01

    Recent studies showed that chronic administration of losartan, an angiotensin II type I receptor antagonist, improved skeletal muscle function in dystrophin-deficient mdx mice. In this study, C57BL/10ScSn-Dmdmdx/J female mice were either untreated or treated with losartan (n = 15) in the drinking water at a dose of 600 mg/L over a 6-month period. Cardiac function was assessed via in vivo high frequency echocardiography and skeletal muscle function was assessed using grip strength testing, Digiscan monitoring, Rotarod timing, and in vitro force testing. Fibrosis was assessed using picrosirius red staining and Image J analysis. Gene expression was evaluated using real-time polymerized chain reaction (RT-PCR). Percentage shortening fraction was significantly decreased in untreated (26.9% ± 3.5%) mice compared to losartan-treated (32.2% ± 4.2%; P < .01) mice. Systolic blood pressure was significantly reduced in losartan-treated mice (56 ± 6 vs 69 ± 7 mm Hg; P < .0005). Percentage cardiac fibrosis was significantly reduced in losartan-treated hearts (P < .05) along with diaphragm (P < .01), extensor digitorum longus (P < .05), and gastrocnemius (P < .05) muscles compared to untreated mdx mice. There were no significant differences in skeletal muscle function between treated and untreated groups. Chronic treatment with losartan decreases cardiac and skeletal muscle fibrosis and improves cardiac systolic function in dystrophin-deficient mdx mice. PMID:21304057

  1. Zinc transporter 3 is involved in learned fear and extinction, but not in innate fear.

    PubMed

    Martel, Guillaume; Hevi, Charles; Friebely, Olivia; Baybutt, Trevor; Shumyatsky, Gleb P

    2010-11-01

    Synaptically released Zn²+ is a potential modulator of neurotransmission and synaptic plasticity in fear-conditioning pathways. Zinc transporter 3 (ZnT3) knock-out (KO) mice are well suited to test the role of zinc in learned fear, because ZnT3 is colocalized with synaptic zinc, responsible for its transport to synaptic vesicles, highly enriched in the amygdala-associated neural circuitry, and ZnT3 KO mice lack Zn²+ in synaptic vesicles. However, earlier work reported no deficiency in fear memory in ZnT3 KO mice, which is surprising based on the effects of Zn²+ on amygdala synaptic plasticity. We therefore reexamined ZnT3 KO mice in various tasks for learned and innate fear. The mutants were deficient in a weak fear-conditioning protocol using single tone-shock pairing but showed normal memory when a stronger, five-pairing protocol was used. ZnT3 KO mice were deficient in memory when a tone was presented as complex auditory information in a discontinuous fashion. Moreover, ZnT3 KO mice showed abnormality in trace fear conditioning and in fear extinction. By contrast, ZnT3 KO mice had normal anxiety. Thus, ZnT3 is involved in associative fear memory and extinction, but not in innate fear, consistent with the role of synaptic zinc in amygdala synaptic plasticity.

  2. Cobalamin Deficiency Results in Increased Production of Formate Secondary to Decreased Mitochondrial Oxidation of One-Carbon Units in Rats.

    PubMed

    MacMillan, Luke; Tingley, Garrett; Young, Sara K; Clow, Kathy A; Randell, Edward W; Brosnan, Margaret E; Brosnan, John T

    2018-03-01

    Formate is produced in mitochondria via the catabolism of serine, glycine, dimethylglycine, and sarcosine. Formate produced by mitochondria may be incorporated into the cytosolic folate pool where it can be used for important biosynthetic reactions. Previous studies from our lab have shown that cobalamin deficiency results in increased plasma formate concentrations. Our goal was to determine the basis for elevated formate in vitamin B-12 deficiency. Male Sprague Dawley rats were randomly assigned to consume either a cobalamin-replete (50 μg cobalamin/kg diet) or -deficient (no added cobalamin) diet for 6 wk. Formate production was measured in vivo and in isolated liver mitochondria from a variety of one-carbon precursors. We also measured the oxidation of [3-14C]-l-serine to 14CO2 in isolated rat liver mitochondria and the expression of hepatic genes involved in one-carbon unit and formate metabolism. Cobalamin-deficient rats produce formate at a rate 55% higher than that of replete rats. Formate production from serine was increased by 60% and from dimethylglycine and sarcosine by ∼200% in liver mitochondria isolated from cobalamin-deficient rats compared with cobalamin-replete rats. There was a 26% decrease in the 14CO2 produced by mitochondria from cobalamin-deficient rats. Gene expression analysis showed that 10-formyltetrahydrofolate dehydrogenase-cytosolic (Aldh1l1) and mitochondrial (Aldh1l2) expression were decreased by 40% and 60%, respectively, compared to control, while 10-formyltetrahydrofolate synthetase, mitochondrial, monofunctional (Mthfd1l) expression was unchanged. We propose that a bifurcation in mitochondrial one-carbon metabolism is a key control mechanism in determining the fate of one-carbon units, to formate or CO2. During cobalamin deficiency in rats the disposition of 10-formyl-tetrahydrofolate carbon is shifted in favor of formate production. This may represent a mechanism to generate more one-carbon units for the replenishment of the S

  3. [Biological diagnosis of iron deficiency in children].

    PubMed

    Thuret, I

    2017-05-01

    Measurement of serum ferritin (SF) is currently the laboratory test recommended for diagnosing iron deficiency. In the absence of an associated disease, a low SF value is an early and highly specific indicator of iron deficiency. The WHO criteria proposed to define depleted storage iron are 12μg/L for children under 5 years and 15μg/L for those over 5 years. A higher threshold of 30μg/L is used in the presence of infection or inflammation. Iron deficiency anemia, with typical low mean corpuscular volume and mean corpuscular hemoglobin, is only present at the end stage of iron deficiency. Other diagnostic tests for iron deficiency including iron parameters (low serum iron, increased total iron-binding capacity, low transferrin saturation) and erythrocyte traits (low mean corpuscular volume, increased zinc protoporphyrin) provide little additional diagnostic value over SF. In children, serum soluble transferrin receptor (sTfR) has been reported to be a sensitive indicator of iron deficiency and is relatively unaffected by inflammation. On the other hand, sTfR is directly related to extent of erythroid activity and not commonly used in clinical practice. In population surveys, approaches based on combinations of markers have been explored to improve the specificity and sensitivity of diagnostic. In addition to Hb value determination, a combination of parameters (among transferrin saturation, zinc protoporphyrin, mean corpuscular volume or serum ferritin) was generally used to assess iron deficiency. More recently sTfR/ ferritin index were evaluated, sTfR in conjunction with SF allowing to better distinguishing iron deficiency from inflammatory anemia. Also, hepcidin measurements appeared an interesting marker for diagnosing iron deficiency and identifying individuals in need of iron supplementation in populations where inflammatory or infectious diseases are frequently encountered. Reticulocyte Hb content (CHr) determination is an early parameter of iron deficiency

  4. Response of extracellular zinc in the ventral hippocampus against novelty stress.

    PubMed

    Takeda, Atsushi; Sakurada, Naomi; Kanno, Shingo; Minami, Akira; Oku, Naoto

    2006-10-01

    An extensive neuronal activity takes place in the hippocampus during exploratory behavior. However, the role of hippocampal zinc in exploratory behavior is poorly understood. To analyze the response of extracellular zinc in the hippocampus against novelty stress, rats were placed for 50 min in a novel environment once a day for 8 days. Extracellular glutamate in the hippocampus was increased during exploratory behavior on day 1, whereas extracellular zinc was decreased. The same phenomenon was observed during exploratory behavior on day 2 and extracellular zinc had returned to the basal level during exploratory behavior on day 8. To examine the significance of the decrease in extracellular zinc in exploratory activity, exploratory behavior was observed during perfusion with 1 mm CaEDTA, a membrane-impermeable zinc chelator. Locomotor activity in the novel environment was decreased by perfusion with CaEDTA. The decrease in extracellular zinc and the increase in extracellular glutamate in exploratory period were abolished by perfusion with CaEDTA. These results suggest that zinc uptake by hippocampal cells is linked to exploratory activity and is required for the activation of the glutamatergic neurotransmitter system. The zinc uptake may be involved in the response to painless psychological stress or in the cognitive processes.

  5. The efficacy of a neonatal screening programme in decreasing the hospitalization rate of patients with G6PD deficiency in southern Iran.

    PubMed

    Cohan, Nader; Karimi, Mehran; Khalili, Amir Hossein; Falahzadeh, Mohammad Hossein; Samadi, Behrang; Mahdavi, Mohammad Reza

    2010-01-01

    To investigate whether a neonatal screening programme for G6PD deficiency has decreased hospitalization for acute haemolytic attack in the Fars province of southern Iran. A total of 850 patients registered with G6PD deficiency were included in the study. Variables including age, sex, time and cause of hospitalization, cause of haemolytic crisis, positive history of blood transfusion, G6PD enzyme deficiency, blood urea nitrogen (BUN) and creatinine were recorded based on a standard questionnaire. All patients were analysed for G6PD enzyme level based on a quantitative test. Five hundred and fifty-three patients were hospitalized before the introduction of the neonatal screening programme (2001-2004) and 297 afterwards (2005-2008). Of those patients hospitalized after the introduction of the screening programme, 237 were wrongly classified as normal and 60 were recorded as having G6PD enzyme deficiency by the neonatal screening programme. The main causes of haemolytic crisis in G6PD-deficient patients were fava bean consumption (88.2%), underlying infection (10.9%) and drugs (0.8%). Our study showed the effectiveness of the neonatal screening programme in decreasing the hospitalization rate.

  6. Zinc in Pancreatic Islet Biology, Insulin Sensitivity, and Diabetes

    PubMed Central

    Maret, Wolfgang

    2017-01-01

    About 20 chemical elements are nutritionally essential for humans with defined molecular functions. Several essential and nonessential biometals are either functional nutrients with antidiabetic actions or can be diabetogenic. A key question remains whether changes in the metabolism of biometals and biominerals are a consequence of diabetes or are involved in its etiology. Exploration of the roles of zinc (Zn) in this regard is most revealing because 80 years of scientific discoveries link zinc and diabetes. In pancreatic β- and α-cells, zinc has specific functions in the biochemistry of insulin and glucagon. When zinc ions are secreted during vesicular exocytosis, they have autocrine, paracrine, and endocrine roles. The membrane protein ZnT8 transports zinc ions into the insulin and glucagon granules. ZnT8 has a risk allele that predisposes the majority of humans to developing diabetes. In target tissues, increased availability of zinc enhances the insulin response by inhibiting protein tyrosine phosphatase 1B, which controls the phosphorylation state of the insulin receptor and hence downstream signalling. Inherited diseases of zinc metabolism, environmental exposures that interfere with the control of cellular zinc homeostasis, and nutritional or conditioned zinc deficiency influence the patho-biochemistry of diabetes. Accepting the view that zinc is one of the many factors in multiple gene-environment interactions that cause the functional demise of β-cells generates an immense potential for treating and perhaps preventing diabetes. Personalized nutrition, bioactive food, and pharmaceuticals targeting the control of cellular zinc in precision medicine are among the possible interventions. PMID:28401081

  7. Effects of separate delivery of zinc or zinc and vitamin A on hemoglobin response, growth, and diarrhea in young Peruvian children receiving iron therapy for anemia.

    PubMed

    Alarcon, Karl; Kolsteren, Patrick W; Prada, Ana M; Chian, Ana M; Velarde, Ruth E; Pecho, Iris L; Hoeree, Tom F

    2004-11-01

    Anemia is the most prevalent nutritional deficiency in the world. Attempts to improve iron indexes are affected by deficiency of and interaction between other micronutrients. Our goal was to assess whether zinc added to iron treatment alone or with vitamin A improves iron indexes and affects diarrheal episodes. This was a randomized, placebo-controlled, double-blind trial conducted in Peru. Anemic children aged 6-35 mo were assigned to 3 treatment groups: ferrous sulfate (FS; n = 104), ferrous sulfate and zinc sulfate (FSZn; n = 109), and ferrous sulfate, zinc sulfate, and vitamin A (FSZnA; n = 110). Vitamin A or its placebo was supplied only once; iron and zinc were provided under supervision >/=1 h apart 6 d/wk for 18 wk. The prevalence of anemia was 42.97%. The increase in hemoglobin in the FS group (19.5 g/L) was significantly less than that in the other 2 groups (24.0 and 23.8 g/L in the FSZn and FSZnA groups, respectively). The increase in serum ferritin in the FS group (24.5 mug/L) was significantly less than that in the other 2 groups (33.0 and 30.8 mug/L in the FSZn and FSZnA groups, respectively). The median duration of diarrhea and the mean number of stools per day was significantly higher in the FS group than in other 2 groups (P < 0.005). Adding zinc to iron treatment increases hemoglobin response, improves iron indexes, and has positive effects on diarrhea. No additional effect of vitamin A was found.

  8. Genomics of mineral nutrient biofortification: calcium, iron and zinc

    USDA-ARS?s Scientific Manuscript database

    Dietary deficiencies affect nearly half of the people on the planet, who simply do not receive sufficient nutrition from the food they buy or grow. Inadequate calcium, iron, and zinc consumption create short and long term health problems, which in turn can magnify and stagnate national development. ...

  9. Role of zinc in chronic gastritis.

    PubMed

    Marjanović, Ksenija; Dovhanj, Jasna; Kljaić, Ksenija; Sakić, Katarina; Kondza, Goran; Tadzić, Refmir; Vcev, Aleksandar

    2010-06-01

    Oxidative stress occurs in inflammation of gastric mucosa. The role of zinc in modulating oxidative stress has recently been recognized. Zn deficiency results in an increased sensitivity to oxidative stress and have a higher risk of musoca damage in inflammation. The aim of this study was to determine wheather chronic inflammation affects on the concentration of Zn2+ ions in gastric mucosa of patients with chronic gastritis. Forthy-three patients with chronic gastitis were enrolled. Patients were endoscoped. Histology and scoring of gastritis was performed following the guidelines of the updated Sydney system. Endoscopic finding of mucosa were scored according to a Lanza scoring system. The diagnosis of Helicobacter pylori (H. pylori) infection, histopathologic changes, intensity of inflammation and zinc concentration were determined from biopsies of gastric mucosa. The atomic absorption spectrophotometer was used to determine tissue concentrations of zinc. Twenty of 43 patients with chronic gastritis were uninfected by H. pylori. There was no statistically significant difference in tissue concentrations of zinc between H. pylori-positive and H. pylori-negative patients. From those infected patients 53.3% had chronic active gastritis. There was no statistically significant difference in tissue concentrations of zinc between patients with chronic active gastritis and patients with chronic inactive gastritis (p = 0.966). Zn in antrum showed positive correlation with density of H. pylori in antrum (Spearman' rho = 0.481, p = 0.020), negative correlation with density of H. pylori in corpus (Spearman' rho = -0.492, p = 0.017) and with zinc in corpus (Spearman' rho = 0.631, p =0.001). Tissue concentration of zinc was not affected by chronic inflammation of gastric mucosa in patients with chronic gastritis.

  10. Physiological roles of zinc transporters: molecular and genetic importance in zinc homeostasis.

    PubMed

    Hara, Takafumi; Takeda, Taka-Aki; Takagishi, Teruhisa; Fukue, Kazuhisa; Kambe, Taiho; Fukada, Toshiyuki

    2017-03-01

    Zinc (Zn) is an essential trace mineral that regulates the expression and activation of biological molecules such as transcription factors, enzymes, adapters, channels, and growth factors, along with their receptors. Zn deficiency or excessive Zn absorption disrupts Zn homeostasis and affects growth, morphogenesis, and immune response, as well as neurosensory and endocrine functions. Zn levels must be adjusted properly to maintain the cellular processes and biological responses necessary for life. Zn transporters regulate Zn levels by controlling Zn influx and efflux between extracellular and intracellular compartments, thus, modulating the Zn concentration and distribution. Although the physiological functions of the Zn transporters remain to be clarified, there is growing evidence that Zn transporters are related to human diseases, and that Zn transporter-mediated Zn ion acts as a signaling factor, called "Zinc signal". Here we describe critical roles of Zn transporters in the body and their contribution at the molecular, biochemical, and genetic levels, and review recently reported disease-related mutations in the Zn transporter genes.

  11. RP105 deficiency attenuates early atherosclerosis via decreased monocyte influx in a CCR2 dependent manner.

    PubMed

    Wezel, Anouk; van der Velden, Daniël; Maassen, Johanna M; Lagraauw, H Maxime; de Vries, Margreet R; Karper, Jacco C; Kuiper, Johan; Bot, Ilze; Quax, Paul H A

    2015-01-01

    Toll like receptor 4 (TLR4) plays a key role in inflammation and previously it was established that TLR4 deficiency attenuates atherosclerosis. RadioProtective 105 (RP105) is a structural homolog of TLR4 and an important regulator of TLR4 signaling, suggesting that RP105 may also be an important effector in atherosclerosis. We thus aimed to determine the role of RP105 in atherosclerotic lesion development using RP105 deficient mice on an atherosclerotic background. Atherosclerosis was induced in Western-type diet fed low density lipoprotein receptor deficient (LDLr(-/-)) and LDLr/RP105 double knockout (LDLr(-/-)/RP105(-/-)) mice by means of perivascular carotid artery collar placement. Lesion size was significantly reduced by 58% in LDLr(-/-)/RP105(-/-) mice, and moreover, plaque macrophage content was markedly reduced by 40%. In a model of acute peritonitis, monocyte influx was almost 3-fold reduced in LDLr(-/-)/RP105(-/-) mice (P = 0.001), while neutrophil influx remained unaltered, suggestive of an altered migratory capacity of monocytes upon deletion of RP105. Interestingly, in vitro stimulation of monocytes with LPS induced a downregulation of CCR2, a chemokine receptor crucially involved in monocyte influx to atherosclerotic lesions, which was more pronounced in LDLr(-/-)/RP105(-/-) monocytes as compared to LDLr(-/-) monocytes. We here show that RP105 deficiency results in reduced early atherosclerotic plaque development with a marked decrease in lesional macrophage content, which may be due to disturbed migration of RP105 deficient monocytes resulting from CCR2 downregulation. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

  12. Zinc and its transporters, pancreatic beta cells, and insulin metabolism

    USDA-ARS?s Scientific Manuscript database

    Zinc is an essential trace metal for life. Two families of zinc transporters, SLC30A (ZnT) and SLC39A (ZIP) are required for maintaining cellular zinc homeostasis. ZnTs function to decrease cytoplasmic zinc concentrations whereas ZIPs do the opposite. Expression of zinc transporters can be tissue/ce...

  13. Bioavailability of zinc oxide added to corn tortilla is similar to that of zinc sulfate and is not affected by simultaneous addition of iron

    PubMed Central

    Rosado, Jorge L.; Díaz, Margarita; Muñoz, Elsa; Westcott, Jamie L.; González, Karla E.; Krebs, Nancy F.; Caamaño, María C.; Hambidge, Michael

    2013-01-01

    Background Corn tortilla is the staple food of Mexico and its fortification with zinc, iron, and other micronutrients is intended to reduce micronutrient deficiencies. However, no studies have been performed to determine the relative amount of zinc absorbed from the fortified product and whether zinc absorption is affected by the simultaneous addition of iron. Objective To compare zinc absorption from corn tortilla fortified with zinc oxide versus zinc sulfate and to determine the effect of simultaneous addition of two doses of iron on zinc bioavailability. Methods A randomized, double-blind, crossover design was carried out in two phases. In the first phase, 10 adult women received corn tortillas with either 20 mg/kg of zinc oxide added, 20 mg/kg of zinc sulfate added, or no zinc added. In the second phase, 10 adult women received corn tortilla with 20 mg/kg of zinc oxide added and either with no iron added or with iron added at one of two different levels. Zinc absorption was measured by the stable isotope method. Results The mean (± SEM) fractional zinc absorption from unfortified tortilla, tortilla fortified with zinc oxide, and tortilla fortified with zinc sulfate did not differ among treatments: 0.35 ± 0.07, 0.36 ± 0.05, and 0.37 ± 0.07, respectively. The three treatment groups with 0, 30, and 60 mg/kg of added iron had similar fractional zinc absorption (0.32 ± 0.04, 0.33 ± 0.02, and 0.32 ± 0.05, respectively) and similar amounts of zinc absorbed (4.8 ± 0.7, 4.5 ± 0.3, and 4.8 ± 0.7 mg/day, respectively). Conclusions Since zinc oxide is more stable and less expensive and was absorbed equally as well as zinc sulfate, we suggest its use for corn tortilla fortification. Simultaneous addition of zinc and iron to corn tortilla does not modify zinc bioavailability at iron doses of 30 and 60 mg/kg of corn flour. PMID:23424892

  14. Education and micronutrient deficiencies: an ecological study exploring interactions between women's schooling and children's micronutrient status.

    PubMed

    Harding, Kassandra L; Aguayo, Victor M; Masters, William A; Webb, Patrick

    2018-04-10

    Formal education can be a nutrition-sensitive intervention that supports the scale-up and impact of nutrition-specific actions. Maternal education has long been linked to child survival, growth, and development while adult earnings and nutrition are tied to years in school as a child. However, less is known about the relationship between maternal education and the micronutrient status of children, women and the general population. Using country-level data and an ecological study design, we explored the global associations between women's educational attainment and: a) anemia and vitamin A deficiency (VAD) in children aged 6-59 months; b) anemia in non-pregnant women; and c) zinc deficiency, urinary iodine excretion (UIE), and the proportion of infants protected against iodine deficiency in the general population Cross-sectional relationships (2005-2013) were assessed using linear regression models. Percentage of women without schooling was negatively associated with all outcomes. Number of years of schooling among women was positively associated with all outcomes except for UIE and the proportion of infants protected against iodine deficiency. Income level was a significant effect modifier of the effect of years of women's schooling on child anemia as well as of the proportion of women without formal education on zinc deficiency in the population. The relationship was strongest in low-income countries for child anemia, and was not significant in upper middle-income countries. For zinc deficiency, the relationship was not significant in low or lower middle income countries, which may suggest that a minimum threshold of resources needs to be reached before education can influence zinc status. While relationships between maternal schooling and micronutrient outcomes vary around the globe, more schooling is generally linked to lower rates of deficiency. These findings draw policy-relevant connections between formal education and anemia and micronutrient status

  15. A concentrated electrolyte for zinc hexacyanoferrate electrodes in aqueous rechargeable zinc-ion batteries

    NASA Astrophysics Data System (ADS)

    Kim, D.; Lee, C.; Jeong, S.

    2018-01-01

    In this study, a concentrated electrolyte was applied in an aqueous rechargeable zinc-ion battery system with a zinc hexacyanoferrate (ZnHCF) electrode to improve the electrochemical performance by changing the hydration number of the zinc ions. To optimize the active material, ZnHCF was synthesized using aqueous solutions of zinc nitrate with three different concentrations. The synthesized materials exhibited some differences in structure, crystallinity, and particle size, as observed by X-ray diffraction and scanning electron microscopy. Subsequently, these well-structured materials were applied in electrochemical tests. A more than two-fold improvement in the charge/discharge capacities was observed when the concentrated electrolyte was used instead of the dilute electrolyte. Additionally, the cycling performance observed in the concentrated electrolyte was superior to that in the dilute electrolyte. This improvement in the electrochemical performance may result from a decrease in the hydration number of the zinc ions in the concentrated electrolyte.

  16. Zinc in gut-brain interaction in autism and neurological disorders.

    PubMed

    Vela, Guillermo; Stark, Peter; Socha, Michael; Sauer, Ann Katrin; Hagmeyer, Simone; Grabrucker, Andreas M

    2015-01-01

    A growing amount of research indicates that abnormalities in the gastrointestinal (GI) system during development might be a common factor in multiple neurological disorders and might be responsible for some of the shared comorbidities seen among these diseases. For example, many patients with Autism Spectrum Disorder (ASD) have symptoms associated with GI disorders. Maternal zinc status may be an important factor given the multifaceted effect of zinc on gut development and morphology in the offspring. Zinc status influences and is influenced by multiple factors and an interdependence of prenatal and early life stress, immune system abnormalities, impaired GI functions, and zinc deficiency can be hypothesized. In line with this, systemic inflammatory events and prenatal stress have been reported to increase the risk for ASD. Thus, here, we will review the current literature on the role of zinc in gut formation, a possible link between gut and brain development in ASD and other neurological disorders with shared comorbidities, and tie in possible effects on the immune system. Based on these data, we present a novel model outlining how alterations in the maternal zinc status might pathologically impact the offspring leading to impairments in brain functions later in life.

  17. Zinc in Gut-Brain Interaction in Autism and Neurological Disorders

    PubMed Central

    Vela, Guillermo; Stark, Peter; Socha, Michael; Sauer, Ann Katrin; Hagmeyer, Simone; Grabrucker, Andreas M.

    2015-01-01

    A growing amount of research indicates that abnormalities in the gastrointestinal (GI) system during development might be a common factor in multiple neurological disorders and might be responsible for some of the shared comorbidities seen among these diseases. For example, many patients with Autism Spectrum Disorder (ASD) have symptoms associated with GI disorders. Maternal zinc status may be an important factor given the multifaceted effect of zinc on gut development and morphology in the offspring. Zinc status influences and is influenced by multiple factors and an interdependence of prenatal and early life stress, immune system abnormalities, impaired GI functions, and zinc deficiency can be hypothesized. In line with this, systemic inflammatory events and prenatal stress have been reported to increase the risk for ASD. Thus, here, we will review the current literature on the role of zinc in gut formation, a possible link between gut and brain development in ASD and other neurological disorders with shared comorbidities, and tie in possible effects on the immune system. Based on these data, we present a novel model outlining how alterations in the maternal zinc status might pathologically impact the offspring leading to impairments in brain functions later in life. PMID:25878905

  18. Zinc and homocysteine levels in polycystic ovarian syndrome patients with insulin resistance.

    PubMed

    Guler, Ismail; Himmetoglu, Ozdemir; Turp, Ahmet; Erdem, Ahmet; Erdem, Mehmet; Onan, M Anıl; Taskiran, Cagatay; Taslipinar, Mine Yavuz; Guner, Haldun

    2014-06-01

    In this study, our objective was to evaluating the value of serum zinc levels as an etiologic and prognostic marker in patients with polycystic ovarian syndrome. We conducted a prospective study, including 53 women with polycystic ovarian syndrome and 33 healthy controls. We compared serum zinc levels, as well as clinical and metabolic features, of the cases. We also compared serum zinc levels between patients with polycystic ovarian syndrome with insulin resistance. Mean zinc levels were found to be significantly lower in patients with polycystic ovarian syndrome than healthy controls. Multiple logistic regression analysis of significant metabolic variables between polycystic ovarian syndrome and control groups (serum zinc level, body mass index, the ratio of triglyceride/high-density lipoprotein cholesterol, and homocysteine) revealed that zinc level was the most significant variable to predict polycystic ovarian syndrome. Mean serum zinc levels tended to be lower in patients with polycystic ovarian syndrome with impaired glucose tolerance than patients with normal glucose tolerance, but the difference was not statistically significant. In conclusion, zinc deficiency may play a role in the pathogenesis of polycystic ovarian syndrome and may be related with its long-term metabolic complications.

  19. Changes in zinc status and zinc transporters expression in whole blood of patients with Systemic Inflammatory Response Syndrome (SIRS).

    PubMed

    Florea, Daniela; Molina-López, Jorge; Hogstrand, Christer; Lengyel, Imre; de la Cruz, Antonio Pérez; Rodríguez-Elvira, Manuel; Planells, Elena

    2018-09-01

    Critically ill patients develop severe stress, inflammation and a clinical state that may raise the utilization and metabolic replacement of many nutrients and especially zinc, depleting their body reserves. This study was designed to assess the zinc status in critical care patients with systemic inflammatory response syndrome (SIRS), comparing them with a group of healthy people, and studying the association with expression of zinc transporters. This investigation was a prospective, multicentre, comparative, observational and analytic study. Twelve critically ill patients from different hospitals and 12 healthy subjects from Granada, Spain, all with informed consent were recruited. Data on daily nutritional assessment, ICU severity scores, inflammation, clinical and nutritional parameters, plasma and blood cell zinc concentrations, and levels of transcripts for zinc transporters in whole blood were taken at admission and at the seventh day of the ICU stay. Zinc levels on critical ill patient are diminish comparing with the healthy control (HS: 0.94 ± 0.19; CIPF: 0.67 ± 0.16 mg/dL). The 58% of critical ill patients showed zinc plasma deficiency at beginning of study while 50.0% of critical ill after 7 days of ICU stay. ZnT7, ZIP4 and ZIP9 were the zinc transporters with highest expression in whole blood. In general, all zinc transporters were significantly down-regulated (P < 0.05) in the critical ill population at admission in comparison with healthy subjects. Severity scores and inflammation were significantly associated (P < 0.05) with zinc plasma levels, and zinc transporters ZIP3, ZIP4, ZIP8, ZnT6, ZnT7. Expression of 11 out of 24 zinc transporters was analysed, and ZnT1, ZnT4, ZnT5 and ZIP4, which were downregulated by more than 3-fold in whole blood of patients. In summary, in our study an alteration of zinc status was related with the severity-of-illness scores and inflammation in critical ill patients since admission in ICU stay. SIRS

  20. Modulating the immune response by oral zinc supplementation: a single approach for multiple diseases.

    PubMed

    Overbeck, Silke; Rink, Lothar; Haase, Hajo

    2008-01-01

    Zinc is required for multiple cellular tasks, and especially the immune system depends on a sufficient availability of this essential trace element. During the last decades, many studies attempted to affect the outcome of various diseases by zinc supplementation. These efforts either aimed at supporting immunity by zinc administration or at correcting a loss of zinc secondary to the disease to restore the zinc-dependent functions of the immune system. This review aims to summarize the respective findings and to discuss possible molecular mechanisms by which zinc could influence viral, bacterial, and parasitic infections, autoimmune diseases, and the response to vaccination. Zinc supplementation in diseases such as diarrhea, chronic hepatitis C, shigellosis, leprosy, tuberculosis, pneumonia, acute lower respiratory infection, and leishmaniasis seems beneficial. In contrast, the results for the common cold and malaria are still not conclusive, and zinc was ineffective in most vaccination and rheumatoid arthritis studies. For AIDS and type 1 diabetes, zinc supplementation may even be a risk factor for increased mortality or deterioration of the glucose metabolism, respectively. In these cases, zinc supplementation should be used with care and limited to clearly zinc-deficient individuals.

  1. Efficacy of zinc sulfate supplement on febrile seizure recurrence prevention in children with normal serum zinc level: A randomised clinical trial.

    PubMed

    Fallah, Razieh; Sabbaghzadegan, Saeideh; Karbasi, Sedighah Akhavan; Binesh, Fariba

    2015-01-01

    Serum zinc level might be related to pathogenesis of febrile seizure (FS). The purpose of this study was to evaluate efficacy and safety of oral zinc supplementation on FS recurrence prevention in non-zinc-deficient children. In a randomized clinical study, one hundred 18 to 60 mo old children with normal zinc level with first simple FS were referred to Shahid Sadoughi Hospital, Yazd, Iran from May 2012 to June 2013, were randomly assigned to two groups to receive 2 mg/kg/d zinc sulfate for six consecutive months or placebo as control group and were followed up for 1 y for FS recurrence. 41 girls and 59 boys with mean age of 2.47 ± 1.01 y were evaluated. Race, mean weight, height and body fat were similar in both groups. FS recurrence occurred in 19 children (38%) in the control group [95% confidence interval (CI): 19.45%-53.95%] and in 11 children (22%) in the zinc sulfate (95% CI: 57.47%-89.13%) groups, respectively; and the zinc group had lower FS recurrence (P = 0.03). The mean serum zinc level before intervention was lower in children with FS recurrence (72.43 ± 14.58 μg/dL versus 96.33 ± 12.69 μg/dL, P = 0.04). Gastrointestinal side effects (vomiting in five children, heartburn in two children and abdominal pain in one child) were seen in 16% of the zinc group and vomiting occurred in two children (4%) in control group and frequency of adverse events was similar in the two groups (P = 0.1). Zinc supplementation should be considered as effective and safe in prevention of FS recurrence. Copyright © 2015 Elsevier Inc. All rights reserved.

  2. Zinc treatment increases the titre of ‘Candidatus Liberibacter asiaticus’ in Huanglongbing-affected citrus plants while affecting the bacterial microbiomes

    USDA-ARS?s Scientific Manuscript database

    Huanglongbing (HLB)-affected citrus often display zinc deficiency symptoms. In this study, supplemental zinc was applied to citrus to determine its effect on Candidatus Liberibacter asiaticus (Las) titer, HLB symptoms, and leaf microbiome. HLB-affected citrus were treated with various amounts of zi...

  3. Evaluation of the serum zinc level in erosive and non-erosive oral lichen planus.

    PubMed

    Gholizadeh, N; Mehdipour, M; Najafi, Sh; Bahramian, A; Garjani, Sh; Khoeini Poorfar, H

    2014-06-01

    Lichen planus is a chronic inflammatory immunologic-based disease involving skin and mucosa. This disease is generally divided into two categories: erosive and non-erosive. Many etiologic factors are deliberated regarding the disease; however, the disorders of immune system and the role of cytotoxic T-lymphocytes and monocytes are more highlighted. Zinc is an imperative element for the growth of epithelium and its deficiency induces the cytotoxic activity of T-helper2 cells, which seems to be associated with lichen planus. This study was aimed to evaluate the levels of serum zinc in erosive and non-erosive oral lichen planus (OLP) and to compare it with the healthy control group to find out any feasible inference. A total of 22 patients with erosive oral lichen planus, 22 patients with non erosive OLP and 44 healthy individuals as the control group were recruited in this descriptive-comparative study. All the participants were selected from the referees to the department of oral medicine, school of dentistry, Tabriz University of Medical Sciences. Serum zinc level was examined for all the individuals with liquid-stat kit (Beckman Instruments Inc.; Carlsbad, CA). Data were analyzed by adopting the ANOVA and Tukey tests, using SPSS 16 statistical software. The mean age of patients with erosive and non-erosive LP was 41.7 and 41.3 years, respectively. The mean age of the healthy control group was 34.4 years .The mean serum zinc levels in the erosive and non erosive lichen planus groups and control groups were 8.3 (1.15), 11.15 (0.92) and 15.74 (1.75) μg/dl respectively. The difference was statistically significant (p< 0.05). The serum zinc levels were decreased in patients with erosive oral lichen planus. This finding may probably indicate the promising role of zinc in development of oral lichen planus.

  4. The relationship between zinc intake and growth in children aged 1-8 years: a systematic review and meta-analysis.

    PubMed

    Stammers, A L; Lowe, N M; Medina, M W; Patel, S; Dykes, F; Pérez-Rodrigo, C; Serra-Majam, L; Nissensohn, M; Moran, V H

    2015-02-01

    It is estimated that zinc deficiency affects 17% of the world's population, and because of periods of rapid growth children are at an increased risk of deficiency, which may lead to stunting. This paper presents a systematic review and meta-analysis of the randomised controlled trials (RCTs) that assess zinc intake and growth in children aged 1-8 years. This review is part of a larger systematic review by the European Micronutrient Recommendations Aligned Network of Excellence that aims to harmonise the approach to setting micronutrient requirements for optimal health in European populations (www.eurreca.org). Searches were performed of literature published up to and including December 2013 using MEDLINE, Embase and the Cochrane Library databases. Included studies were RCTs in apparently healthy child populations aged from 1 to 8 years that supplied zinc supplements either as capsules or as part of a fortified meal. Pooled meta-analyses were performed when appropriate. Nine studies met the inclusion criteria. We found no significant effect of zinc supplementation of between 2 weeks and 12 months duration on weight gain, height for age, weight for age, length for age, weight for height (WHZ) or WHZ scores in children aged 1-8 years. Many of the children in the included studies were already stunted and may have been suffering from multiple micronutrient deficiencies, and therefore zinc supplementation alone may have only a limited effect on growth.

  5. Thiol peroxidase deficiency leads to increased mutational load and decreased fitness in Saccharomyces cerevisiae.

    PubMed

    Kaya, Alaattin; Lobanov, Alexei V; Gerashchenko, Maxim V; Koren, Amnon; Fomenko, Dmitri E; Koc, Ahmet; Gladyshev, Vadim N

    2014-11-01

    Thiol peroxidases are critical enzymes in the redox control of cellular processes that function by reducing low levels of hydroperoxides and regulating redox signaling. These proteins were also shown to regulate genome stability, but how their dysfunction affects the actual mutations in the genome is not known. Saccharomyces cerevisiae has eight thiol peroxidases of glutathione peroxidase and peroxiredoxin families, and the mutant lacking all these genes (∆8) is viable. In this study, we employed two independent ∆8 isolates to analyze the genome-wide mutation spectrum that results from deficiency in these enzymes. Deletion of these genes was accompanied by a dramatic increase in point mutations, many of which clustered in close proximity and scattered throughout the genome, suggesting strong mutational bias. We further subjected multiple lines of wild-type and ∆8 cells to long-term mutation accumulation, followed by genome sequencing and phenotypic characterization. ∆8 lines showed a significant increase in nonrecurrent point mutations and indels. The original ∆8 cells exhibited reduced growth rate and decreased life span, which were further reduced in all ∆8 mutation accumulation lines. Although the mutation spectrum of the two independent isolates was different, similar patterns of gene expression were observed, suggesting the direct contribution of thiol peroxidases to the observed phenotypes. Expression of a single thiol peroxidase could partially restore the growth phenotype of ∆8 cells. This study shows how deficiency in nonessential, yet critical and conserved oxidoreductase function, leads to increased mutational load and decreased fitness. Copyright © 2014 by the Genetics Society of America.

  6. Vitamin D deficiency decreases adiposity in rats and causes altered expression of uncoupling proteins and steroid receptor coactivator3.

    PubMed

    Bhat, Mehrajuddin; Noolu, Bindu; Qadri, Syed S Y H; Ismail, Ayesha

    2014-10-01

    The vitamin D endocrine system is functional in the adipose tissue, as demonstrated in vitro, in cultured adipocytes, and in vivo in mutant mice that developed altered lipid metabolism and fat storage in the absence of either 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] or the vitamin D receptor. The aim of the present study was to examine the role of vitamin D and calcium on body adiposity in a diet-induced vitamin D deficient rat model. Vitamin D-deficient rats gained less weight and had lower amounts of visceral fat. Consistent with reduced adipose tissue mass, the vitamin D-deficient rats had low circulating levels of leptin, which reflects body fat stores. Expression of vitamin D and calcium sensing receptors, and that of genes involved in adipogenesis such as peroxisome proliferator-activated receptor, fatty acid synthase and leptin were significantly reduced in white adipose tissue of deficient rats compared to vitamin D-sufficient rats. Furthermore, the expression of uncoupling proteins (Ucp1 and Ucp2) was elevated in the white adipose tissue of the deficient rat indicative of higher energy expenditure, thereby leading to a lean phenotype. Expression of the p160 steroid receptor coactivator3 (SRC3), a key regulator of adipogenesis in white adipose tissue was decreased in vitamin D-deficient state. Interestingly, most of the changes observed in vitamin D deficient rats were corrected by calcium supplementation alone. Our data demonstrates that dietary vitamin D and calcium regulate adipose tissue function and metabolism. Copyright © 2014 Elsevier Ltd. All rights reserved.

  7. Hematopoietic Sphingosine 1-Phosphate Lyase Deficiency Decreases Atherosclerotic Lesion Development in LDL-Receptor Deficient Mice

    PubMed Central

    Bot, Martine; Van Veldhoven, Paul P.; de Jager, Saskia C. A.; Johnson, Jason; Nijstad, Niels; Van Santbrink, Peter J.; Westra, Marijke M.; Van Der Hoeven, Gerd; Gijbels, Marion J.; Müller-Tidow, Carsten; Varga, Georg; Tietge, Uwe J. F.; Kuiper, Johan; Van Berkel, Theo J. C.; Nofer, Jerzy-Roch

    2013-01-01

    Aims Altered sphingosine 1-phosphate (S1P) homeostasis and signaling is implicated in various inflammatory diseases including atherosclerosis. As S1P levels are tightly controlled by S1P lyase, we investigated the impact of hematopoietic S1P lyase (Sgpl1−/−) deficiency on leukocyte subsets relevant to atherosclerosis. Methods and Results LDL receptor deficient mice that were transplanted with Sgpl1−/− bone marrow showed disrupted S1P gradients translating into lymphopenia and abrogated lymphocyte mitogenic and cytokine response as compared to controls. Remarkably however, Sgpl1−/− chimeras displayed mild monocytosis, due to impeded stromal retention and myelopoiesis, and plasma cytokine and macrophage expression patterns, that were largely compatible with classical macrophage activation. Collectively these two phenotypic features of Sgpl1 deficiency culminated in diminished atherogenic response. Conclusions Here we not only firmly establish the critical role of hematopoietic S1P lyase in controlling S1P levels and T cell trafficking in blood and lymphoid tissue, but also identify leukocyte Sgpl1 as critical factor in monocyte macrophage differentiation and function. Its, partly counterbalancing, pro- and anti-inflammatory activity spectrum imply that intervention in S1P lyase function in inflammatory disorders such as atherosclerosis should be considered with caution. PMID:23700419

  8. Marginal Vitamin B-6 Deficiency Decreases Plasma (n-3) and (n-6) PUFA Concentrations in Healthy Men and Women123

    PubMed Central

    Zhao, Mei; Lamers, Yvonne; Ralat, Maria A.; Coats, Bonnie S.; Chi, Yueh-Yun; Muller, Keith E.; Bain, James R.; Shankar, Meena N.; Newgard, Christopher B.; Stacpoole, Peter W.; Gregory, Jesse F.

    2012-01-01

    Previous animal studies showed that severe vitamin B-6 deficiency altered fatty acid profiles of tissue lipids, often with an increase of linoleic acid and a decrease of arachidonic acid. However, little is known about the extent to which vitamin B-6 deficiency affects human fatty acid profiles. The aim of this study was to determine the effects of marginal vitamin B-6 deficiency on fatty acid profiles in plasma, erythrocytes, and peripheral blood mononuclear cells (PBMC) of healthy adults fed a 28-d, low-vitamin B-6 diet. Healthy participants (n = 23) received a 2-d, controlled, vitamin B-6–adequate diet followed by a 28-d, vitamin B-6–restricted diet to induce a marginal deficiency. Plasma HDL and LDL cholesterol concentrations, FFA concentrations, and erythrocyte and PBMC membrane fatty acid compositions did not significantly change from baseline after the 28-d restriction. Plasma total arachidonic acid, EPA, and DHA concentrations decreased from (mean ± SD) 548 ± 96 to 490 ± 94 μmol/L, 37 ± 13 to 32 ± 13 μmol/L, and 121 ± 28 to 109 ± 28 μmol/L [positive false discovery rate (pFDR) adjusted P < 0.05], respectively. The total (n-6):(n-3) PUFA ratio in plasma exhibited a minor increase from 15.4 ± 2.8 to 16.6 ± 3.1 (pFDR adjusted P < 0.05). These data indicate that short-term vitamin B-6 restriction decreases plasma (n-3) and (n-6) PUFA concentrations and tends to increase the plasma (n-6):(n-3) PUFA ratio. Such changes in blood lipids may be associated with the elevated risk of cardiovascular disease in vitamin B-6 insufficiency. PMID:22955512

  9. ZINC-DEFICIENCY ENHANCES PRO-INFLAMMATORY RESPONSES AFTER OZONE EXPOSURE

    EPA Science Inventory

    Epidemiological and controlled exposure studies have demonstrated that humans are differentially susceptible to adverse health effects induced by exposure to ozone. Serum analysis of vitamins and trace elements have shown that the elderly (people >65 years) are deficient in sever...

  10. Carbohydrate metabolism in erythrocytes of copper deficient rats.

    PubMed

    Brooks, S P J; Cockell, K A; Dawson, B A; Ratnayake, W M N; Lampi, B J; Belonje, B; Black, D B; Plouffe, L J

    2003-11-01

    Dietary copper deficiency is known to adversely affect the circulatory system of fructose-fed rats. Part of the problem may lie in the effect of copper deficiency on intermediary metabolism. To test this, weanling male Long-Evans rats were fed for 4 or 8 weeks on sucrose-based diets containing low or adequate copper content. Copper deficient rats had significantly lower plasma and tissue copper as well as lower plasma copper, zinc-superoxide dismutase activity. Copper deficient rats also had a significantly higher heart:body weight ratio when compared to pair-fed controls. Direct measurement of glycolysis and pentose phosphate pathway flux in erythrocytes using (13)C NMR showed no differences in carbon flux from glucose or fructose to pyruvate but a significantly higher flux through the lactate dehydrogenase locus in copper deficient rats (approximately 1.3 times, average of glucose and glucose + fructose measurements). Copper-deficient animals had significantly higher erythrocyte concentrations of glucose, fructose, glyceraldehyde 3-phosphate and NAD(+). Liver metabolite levels were also affected by copper deficiency being elevated in glycogen and fructose 1-phosphate content. The results show small changes in carbohydrate metabolism of copper deficient rats.

  11. Finger millet (Eleucine coracana) flour as a vehicle for fortification with zinc.

    PubMed

    Tripathi, Bhumika; Platel, Kalpana

    2010-01-01

    Millets, being less expensive compared to cereals and the staple for the poorer sections of population, could be the choice for fortification with micronutrients such as zinc. In view of this, finger millet, widely grown and commonly consumed in southern India, was explored as a vehicle for fortification with zinc in this investigation. Finger millet flour fortified with either zinc oxide or zinc stearate so as to provide 50mg zinc per kg flour, was specifically examined for the bioaccessibility of the fortified mineral, as measured by in vitro simulated gastrointestinal digestion procedure and storage stability. Addition of the zinc salts increased the bioaccessible zinc content by 1.5-3 times that of the unfortified flour. Inclusion of EDTA along with the fortified salt significantly enhanced the bioaccessibility of zinc from the fortified flours, the increase being three-fold. Inclusion of citric acid along with the zinc salt and EDTA during fortification did not have any additional beneficial effect on zinc bioaccessiblity. Moisture and free fatty acid contents of the stored fortified flours indicated the keeping quality of the same, up to 60 days. Both zinc oxide and zinc stearate were equally effective as fortificants, when used in combination with EDTA as a co-fortificant. The preparation of either roti or dumpling from the fortified flours stored up to 60 days did not result in any significant compromise in the bioaccessible zinc content. Thus, the present study has revealed that finger millet flour can effectively be used as a vehicle for zinc fortification to derive additional amounts of bioaccessible zinc, with reasonably good storage stability, to combat zinc deficiency. Copyright 2009 Elsevier GmbH. All rights reserved.

  12. Differential changes in photosynthetic capacity, 77 K chlorophyll fluorescence and chloroplast ultrastructure between Zn-efficient and Zn-inefficient rice genotypes (Oryza sativa) under low zinc stress.

    PubMed

    Chen, Wenrong; Yang, Xiaoe; He, Zhenli; Feng, Ying; Hu, Fenghong

    2008-01-01

    The relationship of zinc (Zn) efficiency in rice to differential tolerance of photosynthetic capacity and chloroplast function to low Zn stress was studied using Zn-efficient (IR8192) and Zn-inefficient (Erjiufeng) rice genotypes (Oryza sativa L.). Zinc deficiency caused extensive declines in leaf chlorophyll (Chl) content, ratios of chl a:b, Pn, Fv/Fm and Fv/Fo, indicating that the intrinsic quantum efficiency of the photosystem II (PSII) units was damaged. A greater decline was observed in the inefficient genotype (Erjiufeng) than the efficient genotype (IR8192). The 77 K chl fluorescence emission spectrum revealed that Zn deficiency blocked energy spillover from PSII to PSI and more excitation energy was distributed to PSII in IR8192 than Erjiufeng. The spectrum of Zn-deficient Erjiufeng was completely disordered, implying that the photosynthetic centers were seriously damaged. Electron microscopy showed that Zn deficiency caused a severe damage to the fine structure of chloroplasts, but IR8192 had a better preserved chloroplast ultrastructure as compared with Erjiufeng. These differences may result from the higher levels of the antioxidant enzyme activities and lower oxidant stress level in IR8192. These results indicate that Zn deficiency decreases leaf photosynthetic capacity primarily by reducing the number of PSII units per unit leaf area, and also reducing the photochemical capacity of the remaining PSII units. Therefore, the maintenance of more efficient photochemical capacity under low Zn stress is a key factor for the high Zn efficiency in rice, which may result from less antioxidant damage caused by low Zn to the chloroplast ultrastructure.

  13. The effect of polymers onto the size of zinc layered hydroxide salt and its calcined product

    NASA Astrophysics Data System (ADS)

    Hussein, Mohd Zobir bin; Ghotbi, Mohammad Yeganeh; Yahaya, Asmah Hj; Abd Rahman, Mohd Zaki

    2009-02-01

    Zinc hydroxide nitrate, a brucite-like layered material was synthesized using pH control method. Poly(vinyl alcohol) and poly(ethylene glycol) were used at various percentages as size decreasing agents during the synthesis of zinc hydroxide nitrate. SEM and PXRD showed the decrease of size and thickness of the resultant zinc hydroxide nitrates. TG and surface area data confirmed the decrease of the particle sizes, too. When zinc hydroxide nitrates were heat treated at 500 °C, the physical properties of nano zinc oxides obtained depended on the parent material, zinc hydroxide nitrate.

  14. Role of zinc in maternal and child mental health1234

    PubMed Central

    Ramirez-Zea, Manuel

    2009-01-01

    Mental health problems in women, children, and adolescents are a significant public health issue. Given current barriers to the effective treatment of these problems, researchers are looking to the field of nutrition for potential alternatives to better understand and address mental health issues. The purpose of this article was to review current evidence on the relation between zinc and mental health disorders with a focus on 2 mental health problems that commonly affect women and children: depression and attention-deficit hyperactivity disorder (ADHD). A literature search of the databases Medline and PsychInfo was conducted with the use of key terms. The review included articles from 1975 to May 2008, but focused on articles published in recent years. Relations between zinc concentrations and behavior in animals; the relation between zinc deficiency, depression, and ADHD in patient and community samples; and the potential biological mechanisms for these relations were explored. The data support a relation between low concentrations of zinc and mental health problems, especially in at-risk populations. Evidence for the potential use of zinc in treating mental health problems comes mainly from patient populations and is strongest when zinc is given in combination with pharmacologic treatment. Less conclusive evidence exists for the effectiveness of zinc alone or in general community samples. Recommendations for further research in this area are provided. PMID:19176735

  15. Zinc supplements for treating thalassaemia and sickle cell disease.

    PubMed

    Swe, Kye Mon Min; Abas, Adinegara B L; Bhardwaj, Amit; Barua, Ankur; Nair, N S

    2013-06-28

    Haemoglobinopathies, inherited disorders of haemoglobin synthesis (thalassaemia) or structure (sickle cell disease), are responsible for significant morbidity and mortality throughout the world. The WHO estimates that, globally, 5% of adults are carriers of a haemoglobin condition, 2.9% are carriers of thalassaemia and 2.3% are carriers of sickle cell disease. Carriers are found worldwide as a result of migration of various ethnic groups to different regions of the world. Zinc is an easily available supplement and intervention programs have been carried out to prevent deficiency in people with thalassaemia or sickle cell anaemia. It is important to evaluate the role of zinc supplementation in the treatment of thalassaemia and sickle cell anaemia to reduce deaths due to complications. To assess the effect of zinc supplementation in the treatment of thalassaemia and sickle cell disease. We searched the Cochrane Cystic Fibrosis and Genetic Disorders Group's Haemoglobinopathies Trials Register comprising references identified from comprehensive electronic database searches and handsearches of relevant journals and abstract books of conference proceedings.Date of most recent search: 01 February 2013. Randomised, placebo-controlled trials of zinc supplements for treating thalassaemia or sickle cell disease administered at least once a week for at least a month. Two review authors assessed the eligibility and risk of bias of the included trials, extracted and analysed data and wrote the review. We summarised results using risk ratios or rate ratios for dichotomous data and mean differences for continuous data. We combined trial results where appropriate. We identified nine trials for inclusion with all nine contributing outcome data. Two trials reported on people with thalassaemia (n = 152) and seven on sickle cell anaemia (n = 307).In people with thalassaemia, in one trial, the serum zinc level value showed no difference between the zinc supplemented group and the

  16. Plasma zinc in institutionalized elderly individuals: Relation with immune and cardiometabolic biomarkers.

    PubMed

    Sales, Márcia Cristina; de Oliveira, Larissa Praça; de Araújo Cabral, Natalia Louise; de Sousa, Sara Estéfani Soares; das Graças Almeida, Maria; Lemos, Telma Maria Araújo Moura; de Oliveira Lyra, Clélia; de Lima, Kenio Costa; Sena-Evangelista, Karine Cavalcanti Mauricio; de Fatima Campos Pedrosa, Lucia

    2018-04-24

    Changes in zinc metabolism caused by aging and the institutionalization process may contribute to zinc deficiency in elderly individuals. Hypozincemia results in changes in glycemic, lipid, and inflammatory profiles. The aim of this study was to evaluate plasma zinc concentrations and their relationships with sociodemographic, dietary, inflammatory, and cardiometabolic biomarkers in institutionalized elderly individuals. A cross-sectional study was carried out including 255 elderly adults living in nursing homes. The associations between plasma zinc and dietary zinc intake, sociodemographic indicators, and glycemic, lipid, and inflammatory biomarkers were evaluated. Independent variables were analyzed according to quartiles of plasma zinc concentrations (Q1: <71.1 μg/dL; Q2: 71.1-83.3 μg/dL; Q3: <83.3-93.7 μg/dL; Q4: >93.7 μg/dL). The relationship between plasma zinc concentrations and predictor variables was also tested. In Q1, higher concentrations of the following variables were observed, compared with those in other quartiles: total cholesterol and low-density lipoprotein cholesterol (LDL-c; Q1 > Q2, Q3, Q4; all p <0.001); triglycerides (Q1 > Q3, Q4; all p < 0.001); interleukin (IL)-6 (Q1 > Q3, Q4; p = 0.024 and p = 0.010, respectively); tumor necrosis factor (TNF)-α (Q1 > Q3, p = 0.003). A significant reduction in plasma zinc concentrations was observed with increasing age-adjusted institutionalization time (Δ = - 0.10; 95% confidence interval [CI]: -0.18 to -0.01). The concentrations of total cholesterol (Δ = - 0.19; 95% CI: -0.23 to -0.15), LDL-c (Δ = - 0.19; 95% CI: -0.23 to -0.15), triglycerides (Δ = - 0.11; 95% CI: -0.16 to -0.06), IL-6 (Δ = - 1.41; 95% CI: -2.64 to -0.18), and TNF-α (Δ = - 1.04; 95% CI: -1.71 to -0.36) were also significantly increased. In conclusion, decreased plasma zinc concentrations were associated with longer institutionalization time and worse

  17. Nutrition Deficiencies in Children With Intestinal Failure Receiving Chronic Parenteral Nutrition.

    PubMed

    Namjoshi, Shweta S; Muradian, Sarah; Bechtold, Hannah; Reyen, Laurie; Venick, Robert S; Marcus, Elizabeth A; Vargas, Jorge H; Wozniak, Laura J

    2017-02-01

    Home parenteral nutrition (PN) is a lifesaving therapy for children with intestinal failure (IF). Our aims were to describe the prevalence of micronutrient deficiencies (vitamin D, zinc, copper, iron, selenium) in a diverse population of children with IF receiving PN and to identify and characterize risk factors associated with micronutrient deficiencies, including hematologic abnormalities. Data were collected on 60 eligible patients through retrospective chart review between May 2012 and February 2015. Descriptive statistics included frequencies, medians, interquartile ranges (IQRs), and odds ratios (ORs). Statistical analyses included χ 2 , Fisher's exact, t tests, and logistic, univariate, and multivariate regressions. Patients were primarily young (median age, 3.3 years; IQR, 0.7-8.4), Latino (62%), and male (56%), with short bowel syndrome (70%). Of 60 study patients, 88% had ≥1 deficiency and 90% were anemic for age. Of 51 patients who had all 5 markers checked, 59% had multiple deficiencies (defined as ≥3). Multivariate analysis shows multiple deficiencies were associated with nonwhite race (OR, 9.4; P = .012) and higher body mass index z score (OR, 2.2; P = .016). Children with severe anemia (hemoglobin <8.5 g/dL) made up 50% of the cohort. Nonwhite race (OR, 6.6; P = .037) and zinc deficiency (OR, 11; P = .003) were multivariate predictors of severe anemia. Micronutrient deficiency and anemia are overwhelmingly prevalent in children with IF using chronic PN. This emphasizes the importance of universal surveillance and supplementation to potentially improve quality of life and developmental outcomes. Future research should investigate how racial disparities might contribute to nutrition outcomes for children using chronic PN.

  18. Zinc transporters and dysregulated channels in cancers

    PubMed Central

    Pan, Zui; Choi, Sangyong; Ouadid-Ahidouch, Halima; Yang, Jin-Ming; Beattie, John H.; Korichneva, Irina

    2016-01-01

    As a nutritionally essential metal ion, zinc (Zn) not only constitutes a structural element for more than 3000 proteins but also plays important regulatory functions in cellular signal transduction. Zn homeostasis is tightly controlled by regulating the flux of Zn across cell membranes through specific transporters, i.e. ZnT and ZIP family proteins. Zn deficiency and malfunction of Zn transporters have been associated with many chronic diseases including cancer. However, the mechanisms underlying Zn regulatory functions in cellular signaling and their impact on the pathogenesis and progression of cancers remain largely unknown. In addition to these acknowledged multifunctions, Zn modulates a wide range of ion channels that in turn may also play an important role in cancer biology. The goal of this review is to propose how zinc deficiency, through modified Zn homeostasis, transporter activity and the putative regulatory function of Zn can influence ion channel activity, and thereby contribute to carcinogenesis and tumorigenesis. This review intends to stimulate interest in, and support for research into the understanding of Zn-modulated channels in cancers, and to search for novel biomarkers facilitating effective clinical stratification of high risk cancer patients as well as improved prevention and therapy in this emerging field. PMID:27814637

  19. Ascorbic acid deficiency decreases hepatic cytochrome P-450, especially CYP2B1/2B2, and simultaneously induces heme oxygenase-1 gene expression in scurvy-prone ODS rats.

    PubMed

    Kobayashi, Misato; Hoshinaga, Yukiko; Miura, Natsuko; Tokuda, Yuki; Shigeoka, Shigeru; Murai, Atsushi; Horio, Fumihiko

    2014-01-01

    The mechanisms underlying the decrease in hepatic cytochrome P-450 (CYP) content in ascorbic acid deficiency was investigated in scurvy-prone ODS rats. First, male ODS rats were fed a diet containing sufficient ascorbic acid (control) or a diet without ascorbic acid (deficient) for 18 days, with or without the intraperitoneal injection of phenobarbital. Ascorbic acid deficiency decreased hepatic microsomal total CYP content, CYP2B1/2B2 protein, and mitochondrial cytochrome oxidase (COX) complex IV subunit I protein, and simultaneously increased heme oxygenase-1 protein in microsomes and mitochondria. Next, heme oxygenase-1 inducers, that is lipopolysaccharide and hemin, were administered to phenobaribital-treated ODS rats fed sufficient ascorbic acid. The administration of these inducers decreased hepatic microsomal total CYP content, CYP2B1/2B2 protein, and mitochondrial COX complex IV subunit I protein. These results suggested that the stimulation of hepatic heme oxygenase-1 expression by ascorbic acid deficiency caused the decrease in CYP content in liver.

  20. High-performance varistors simply by hot-dipping zinc oxide thin films in Pr6O11: Influence of temperature

    PubMed Central

    Wang, Yang; Peng, Zhijian; Wang, Qi; Wang, Chengbiao; Fu, Xiuli

    2017-01-01

    High-performance ZnO-Pr6O11 thin-film varistors were fabricated simply by hot-dipping oxygen-deficient zinc oxide thin films in Pr6O11 powder. The films had a composition of ZnO0.81 and a thickness of about 200 nm, which were deposited by radio frequency magnetron sputtering a sintered zinc oxide ceramic target. Special attention was paid on the temperature dependence of the varistors. In 50 min with hot-dipping temperature increased from 300–700 °C, the nonlinear coefficient (α) of the varistors increased, but with higher temperature it decreased again. Correspondingly, the leakage current (IL) decreased first and then increased, owing mainly to the formation and destroying of complete zinc oxide/Pr6O11 grain boundaries. The breakdown field (E1mA) decreased monotonously from 0.02217 to 0.01623 V/nm with increasing temperature (300–800 °C), due to the decreased number of effective grain boundaries in the varistors. The varistors prepared at 700 °C exhibited the optimum nonlinear properties with the highest α = 39.29, lowest IL = 0.02736 mA/cm2, and E1mA = 0.01757 V/nm. And after charge-discharge at room temperature for 1000 times, heating at 100 or 250 °C for up to 100 h, or applying at up to 250 °C, the varistors still performed well. Such nanoscaled thin-film varistors will be very promising in electrical/electronic devices working at low voltage. PMID:28155890

  1. ZNT7 binds to CD40 and influences CD154-triggered p38 MAPK activity in B lymphocytes-a possible regulatory mechanism for zinc in immune function

    USDA-ARS?s Scientific Manuscript database

    Zinc deficiency impairs immune system leading to frequent infections. Although it is known that zinc plays critical roles in maintaining healthy immune function, the underlying molecular targets are largely unknown. In this study, we showed that zinc is important for the CD154-CD40-mediated activati...

  2. Effects of cadmium and zinc on solar-simulated light-irradiated cells: potential role of zinc-metallothionein in zinc-induced genoprotection.

    PubMed

    Jourdan, Eric; Emonet-Piccardi, Nathalie; Didier, Christine; Beani, Jean-Claude; Favier, Alain; Richard, Marie-Jeanne

    2002-09-15

    Zinc is an essential oligoelement for cell growth and cell survival and has been demonstrated to protect cells from oxidative stress induced by UVA or from genotoxic stress due to UVB. In a recent work we demonstrated that the antioxidant role of zinc could be related to its ability to induce metallothioneins (MTs). In this study we identified the mechanism of zinc protection against solar-simulated light (SSL) injury. Cultured human keratinocytes (HaCaT) were used to examine MTs expression and localization in response to solar-simulated radiation. We found translocation to the nucleus, with overexpression of MTs in irradiated cells, a novel observation. The genoprotective effect of zinc was dependent on time and protein synthesis. DNA damage was significantly decreased after 48 h of ZnCl(2) (100 microM) treatment and is inhibited by actinomycin D. ZnCl(2) treatment (100 microM) led to an intense induction, redistribution, and accumulation of MT in the nucleus of irradiated cells. MT expression correlated with the time period of ZnCl(2) treatment. CdCl(2), a potent MT inducer, did not show any genoprotection, although the MTs were expressed in the nucleus. Overall our findings demonstrate that MTs could be a good candidate for explaining the genoprotection mediated by zinc on irradiated cells.

  3. An MSC2 Promoter-lacZ Fusion Gene Reveals Zinc-Responsive Changes in Sites of Transcription Initiation That Occur across the Yeast Genome

    PubMed Central

    Wu, Yi-Hsuan; Taggart, Janet; Song, Pamela Xiyao; MacDiarmid, Colin; Eide, David J.

    2016-01-01

    The Msc2 and Zrg17 proteins of Saccharomyces cerevisiae form a complex to transport zinc into the endoplasmic reticulum. ZRG17 is transcriptionally induced in zinc-limited cells by the Zap1 transcription factor. In this report, we show that MSC2 mRNA also increases (~1.5 fold) in zinc-limited cells. The MSC2 gene has two in-frame ATG codons at its 5’ end, ATG1 and ATG2; ATG2 is the predicted initiation codon. When the MSC2 promoter was fused at ATG2 to the lacZ gene, we found that unlike the chromosomal gene this reporter showed a 4-fold decrease in lacZ mRNA in zinc-limited cells. Surprisingly, β-galactosidase activity generated by this fusion gene increased ~7 fold during zinc deficiency suggesting the influence of post-transcriptional factors. Transcription of MSC2ATG2-lacZ was found to start upstream of ATG1 in zinc-replete cells. In zinc-limited cells, transcription initiation shifted to sites just upstream of ATG2. From the results of mutational and polysome profile analyses, we propose the following explanation for these effects. In zinc-replete cells, MSC2ATG2-lacZ mRNA with long 5’ UTRs fold into secondary structures that inhibit translation. In zinc-limited cells, transcripts with shorter unstructured 5’ UTRs are generated that are more efficiently translated. Surprisingly, chromosomal MSC2 did not show start site shifts in response to zinc status and only shorter 5’ UTRs were observed. However, the shifts that occur in the MSC2ATG2-lacZ construct led us to identify significant transcription start site changes affecting the expression of ~3% of all genes. Therefore, zinc status can profoundly alter transcription initiation across the yeast genome. PMID:27657924

  4. Biochemical indicators of root damage in rice (Oryza sativa) genotypes under zinc deficiency stress.

    PubMed

    Lee, Jae-Sung; Wissuwa, Matthias; Zamora, Oscar B; Ismail, Abdelbagi M

    2017-11-01

    Zn deficiency is one of the major soil constraints currently limiting rice production. Although recent studies demonstrated that higher antioxidant activity in leaf tissue effectively protects against Zn deficiency stress, little is known about whether similar tolerance mechanisms operate in root tissue. In this study we explored root-specific responses of different rice genotypes to Zn deficiency. Root solute leakage and biomass reduction, antioxidant activity, and metabolic changes were measured using plants grown in Zn-deficient soil and hydroponics. Solute leakage from roots was higher in sensitive genotypes and linked to membrane damage caused by Zn deficiency-induced oxidative stress. However, total root antioxidant activity was four-fold lower than in leaves and did not differ between sensitive and tolerant genotypes. Root metabolite analysis using gas chromatography-mass spectrometry and high performance liquid chromatography indicated that Zn deficiency triggered the accumulation of glycerol-3-phosphate and acetate in sensitive genotypes, while less or no accumulation was seen in tolerant genotypes. We suggest that these metabolites may serve as biochemical indicators of root damage under Zn deficiency.

  5. Intrinsic functional defects of type 2 innate lymphoid cells impair innate allergic inflammation in promyelocytic leukemia zinc finger (PLZF)-deficient mice.

    PubMed

    Verhoef, Philip A; Constantinides, Michael G; McDonald, Benjamin D; Urban, Joseph F; Sperling, Anne I; Bendelac, Albert

    2016-02-01

    The transcription factor promyelocytic leukemia zinc finger (PLZF) is transiently expressed during development of type 2 innate lymphoid cells (ILC2s) but is not present at the mature stage. We hypothesized that PLZF-deficient ILC2s have functional defects in the innate allergic response and represent a tool for studying innate immunity in a mouse with a functional adaptive immune response. We determined the consequences of PLZF deficiency on ILC2 function in response to innate and adaptive immune stimuli by using PLZF(-/-) mice and mixed wild-type:PLZF(-/-) bone marrow chimeras. PLZF(-/-) mice, wild-type littermates, or mixed bone marrow chimeras were treated with the protease allergen papain or the cytokines IL-25 and IL-33 or infected with the helminth Nippostrongylus brasiliensis to induce innate type 2 allergic responses. Mice were sensitized with intraperitoneal ovalbumin-alum, followed by intranasal challenge with ovalbumin alone, to induce adaptive TH2 responses. Lungs were analyzed for immune cell subsets, and alveolar lavage fluid was analyzed for ILC2-derived cytokines. In addition, ILC2s were stimulated ex vivo for their capacity to release type 2 cytokines. PLZF-deficient lung ILC2s exhibit a cell-intrinsic defect in the secretion of IL-5 and IL-13 in response to innate stimuli, resulting in defective recruitment of eosinophils and goblet cell hyperplasia. In contrast, the adaptive allergic inflammatory response to ovalbumin and alum was unimpaired. PLZF expression at the innate lymphoid cell precursor stage has a long-range effect on the functional properties of mature ILC2s and highlights the importance of these cells for innate allergic responses in otherwise immunocompetent mice. Copyright © 2015 American Academy of Allergy, Asthma & Immunology. All rights reserved.

  6. Identification of membrane proteome of Paracoccidioides lutzii and its regulation by zinc

    PubMed Central

    de Curcio, Juliana Santana; Silva, Marielle Garcia; Silva Bailão, Mirelle Garcia; Báo, Sônia Nair; Casaletti, Luciana; Bailão, Alexandre Mello; de Almeida Soares, Célia Maria

    2017-01-01

    Aim: During infection development in the host, Paracoccidioides spp. faces the deprivation of micronutrients, a mechanism called nutritional immunity. This condition induces the remodeling of proteins present in different metabolic pathways. Therefore, we attempted to identify membrane proteins and their regulation by zinc in Paracoccidioides lutzii. Materials & methods: Membranes enriched fraction of yeast cells of P. lutzii were isolated, purified and identified by 2D LC–MS/MS detection and database search. Results & conclusion: Zinc deprivation suppressed the expression of membrane proteins such as glycoproteins, those involved in cell wall synthesis and those related to oxidative phosphorylation. This is the first study describing membrane proteins and the effect of zinc deficiency in their regulation in one member of the genus Paracoccidioides. PMID:29134119

  7. Vitamin B-12 Deficiency in Children Is Associated with Grade Repetition and School Absenteeism, Independent of Folate, Iron, Zinc, or Vitamin A Status Biomarkers.

    PubMed

    Duong, Minh-Cam; Mora-Plazas, Mercedes; Marín, Constanza; Villamor, Eduardo

    2015-07-01

    Micronutrients are essential to neurocognitive development; yet their role in educational outcomes is unclear. We examined the associations of micronutrient status biomarkers with the risk of grade repetition and rates of school absenteeism in a cohort of school children. We recruited 3156 children aged 5-12 y from public schools in Bogota, Colombia. Circulating ferritin, hemoglobin, zinc, vitamin A, and vitamin B-12; erythrocyte folate; and mean corpuscular volume (MCV) were measured in blood samples obtained at the beginning of the year. Absenteeism was recorded weekly during the school year, and grade repetition was determined the next year. Risk ratios for grade repetition and rate ratios for absenteeism were estimated by categories of micronutrient status indicators with use of Poisson regression, adjusting for potential confounders. The risk of grade repetition was 4.9%, and the absenteeism rate was 3.8 d per child-year of observation. Vitamin B-12 deficiency (<148 pmol/L) was associated with an adjusted 2.36-fold greater risk of grade repetition (95% CI: 1.03, 5.41; P = 0.04) compared with plasma concentrations ≥148 pmol/L. Other micronutrients were not related to grade repetition. Vitamin B-12 deficiency was also associated with school absenteeism rates. Compared with children with plasma vitamin B-12 concentrations ≥148 pmol/L, vitamin B-12-deficient children had a 1.89-times higher adjusted rate (95% CI: 1.53, 2.34; P < 0.0001). Anemia was related to a 72% higher rate (95% CI: 48%, 99%; P < 0.0001), whereas every 5-fL difference in MCV was associated with a 7% lower adjusted rate (95% CI: 4%, 10%; P < 0.0001). Vitamin B-12 deficiency was associated with risk of grade repetition and school absenteeism rates in school children from Bogota, Colombia. The effects of correcting vitamin B-12 deficiency on educational outcomes and neurocognitive development of school children need to be determined in intervention studies. © 2015 American Society for

  8. Subacute Zinc Administration and L-NAME Caused an Increase of NO, Zinc, Lipoperoxidation, and Caspase-3 during a Cerebral Hypoxia-Ischemia Process in the Rat

    PubMed Central

    Blanco-Alvarez, Victor Manuel; Lopez-Moreno, Patricia; Soto-Rodriguez, Guadalupe; Martinez-Fong, Daniel; Rubio, Hector; Gonzalez-Barrios, Juan Antonio; Piña-Leyva, Celia; Torres-Soto, Maricela; Gomez-Villalobos, María de Jesus; Hernandez-Baltazar, Daniel; Eguibar, José Ramon; Ugarte, Araceli; Cebada, Jorge

    2013-01-01

    Zinc or L-NAME administration has been shown to be protector agents, decreasing oxidative stress and cell death. However, the treatment with zinc and L-NAME by intraperitoneal injection has not been studied. The aim of our work was to study the effect of zinc and L-NAME administration on nitrosative stress and cell death. Male Wistar rats were treated with ZnCl2 (2.5 mg/kg each 24 h, for 4 days) and N-ω-nitro-L-arginine-methyl ester (L-NAME, 10 mg/kg) on the day 5 (1 hour before a common carotid-artery occlusion (CCAO)). The temporoparietal cortex and hippocampus were dissected, and zinc, nitrites, and lipoperoxidation were assayed at different times. Cell death was assayed by histopathology using hematoxylin-eosin staining and caspase-3 active by immunostaining. The subacute administration of zinc before CCAO decreases the levels of zinc, nitrites, lipoperoxidation, and cell death in the late phase of the ischemia. L-NAME administration in the rats treated with zinc showed an increase of zinc levels in the early phase and increase of zinc, nitrites, and lipoperoxidation levels, cell death by necrosis, and the apoptosis in the late phase. These results suggest that the use of these two therapeutic strategies increased the injury caused by the CCAO, unlike the alone administration of zinc. PMID:23997853

  9. Interdependence of free zinc changes and protein complex assembly - insights into zinc signal regulation.

    PubMed

    Kocyła, Anna; Adamczyk, Justyna; Krężel, Artur

    2018-01-24

    Cellular zinc (Zn(ii)) is bound with proteins that are part of the proteomes of all domains of life. It is mostly utilized as a catalytic or structural protein cofactor, which results in a vast number of binding architectures. The Zn(ii) ion is also important for the formation of transient protein complexes with a Zn(ii)-dependent quaternary structure that is formed upon cellular zinc signals. The mechanisms by which proteins associate with and dissociate from Zn(ii) and the connection with cellular Zn(ii) changes remain incompletely understood. In this study, we aimed to examine how zinc protein domains with various Zn(ii)-binding architectures are formed under free Zn(ii) concentration changes and how formation of the Zn(ii)-dependent assemblies is related to the protein concentration and reactivity. To accomplish these goals we chose four zinc domains with different Zn(ii)-to-protein binding stoichiometries: classical zinc finger (ZnP), LIM domain (Zn 2 P), zinc hook (ZnP 2 ) and zinc clasp (ZnP 1 P 2 ) folds. Our research demonstrated a lack of changes in the saturation level of intraprotein zinc binding sites, despite various peptide concentrations, while homo- and heterodimers indicated a concentration-dependent tendency. In other words, at a certain free Zn(ii) concentration, the fraction of a formed dimeric complex increases or decreases with subunit concentration changes. Secondly, even small or local changes in free Zn(ii) may significantly affect protein saturation depending on its architecture, function and subcellular concentration. In our paper, we indicate the importance of interdependence of free Zn(ii) availability and protein subunit concentrations for cellular zinc signal regulation.

  10. Deficiency of slow skeletal muscle troponin T causes atrophy of type I slow fibres and decreases tolerance to fatigue.

    PubMed

    Wei, Bin; Lu, Yingru; Jin, J-P

    2014-03-15

    The total loss of slow skeletal muscle troponin T (ssTnT encoded by TNNT1 gene) due to a nonsense mutation in codon Glu(180) causes a lethal form of recessively inherited nemaline myopathy (Amish nemaline myopathy, ANM). To investigate the pathogenesis and muscle pathophysiology of ANM, we studied the phenotypes of partial and total loss of ssTnT in Tnnt1 gene targeted mice. An insertion of neomycin resistance cassette in intron 10 of Tnnt1 gene caused an approximately 60% decrease in ssTnT protein expression whereas cre-loxP-mediated deletion of exons 11-13 resulted in total loss of ssTnT, as seen in ANM muscles. In diaphragm and soleus muscles of the knockdown and knockout mouse models, we demonstrated that ssTnT deficiency resulted in significantly decreased levels of other slow fibre-specific myofilament proteins whereas fast fibre-specific myofilament proteins were increased correspondingly. Immunohistochemical studies revealed that ssTnT deficiency produced significantly smaller type I slow fibres and compensatory growth of type II fast fibres. Along with the slow fibre atrophy and the changes in myofilament protein isoform contents, ssTnT deficiency significantly reduced the tolerance to fatigue in soleus muscle. ssTnT-deficient soleus muscle also contains significant numbers of small-sized central nuclei type I fibres, indicating active regeneration. The data provide strong support for the essential role of ssTnT in skeletal muscle function and the causal effect of its loss in the pathology of ANM. This observation further supports the hypothesis that the function of slow fibres can be restored in ANM patients if a therapeutic supplement of ssTnT is achieved.

  11. Deficiency of slow skeletal muscle troponin T causes atrophy of type I slow fibres and decreases tolerance to fatigue

    PubMed Central

    Wei, Bin; Lu, Yingru; Jin, J-P

    2014-01-01

    The total loss of slow skeletal muscle troponin T (ssTnT encoded by TNNT1 gene) due to a nonsense mutation in codon Glu180 causes a lethal form of recessively inherited nemaline myopathy (Amish nemaline myopathy, ANM). To investigate the pathogenesis and muscle pathophysiology of ANM, we studied the phenotypes of partial and total loss of ssTnT in Tnnt1 gene targeted mice. An insertion of neomycin resistance cassette in intron 10 of Tnnt1 gene caused an approximately 60% decrease in ssTnT protein expression whereas cre-loxP-mediated deletion of exons 11–13 resulted in total loss of ssTnT, as seen in ANM muscles. In diaphragm and soleus muscles of the knockdown and knockout mouse models, we demonstrated that ssTnT deficiency resulted in significantly decreased levels of other slow fibre-specific myofilament proteins whereas fast fibre-specific myofilament proteins were increased correspondingly. Immunohistochemical studies revealed that ssTnT deficiency produced significantly smaller type I slow fibres and compensatory growth of type II fast fibres. Along with the slow fibre atrophy and the changes in myofilament protein isoform contents, ssTnT deficiency significantly reduced the tolerance to fatigue in soleus muscle. ssTnT-deficient soleus muscle also contains significant numbers of small-sized central nuclei type I fibres, indicating active regeneration. The data provide strong support for the essential role of ssTnT in skeletal muscle function and the causal effect of its loss in the pathology of ANM. This observation further supports the hypothesis that the function of slow fibres can be restored in ANM patients if a therapeutic supplement of ssTnT is achieved. PMID:24445317

  12. Expression of the ZNT1 Zinc Transporter from the Metal Hyperaccumulator Noccaea caerulescens Confers Enhanced Zinc and Cadmium Tolerance and Accumulation to Arabidopsis thaliana

    PubMed Central

    Schat, Henk; Aarts, Mark G. M.

    2016-01-01

    Prompt regulation of transition metal transporters is crucial for plant zinc homeostasis. NcZNT1 is one of such transporters, found in the metal hyperaccumulator Brassicaceae species Noccaea caerulescens. It is orthologous to AtZIP4 from Arabidopsis thaliana, an important actor in Zn homeostasis. We examined if the NcZNT1 function contributes to the metal hyperaccumulation of N. caerulescens. NcZNT1 was found to be a plasma-membrane located metal transporter. Constitutive overexpression of NcZNT1 in A. thaliana conferred enhanced tolerance to exposure to excess Zn and Cd supply, as well as increased accumulation of Zn and Cd and induction of the Fe deficiency response, when compared to non-transformed wild-type plants. Promoters of both genes were induced by Zn deficiency in roots and shoots of A. thaliana. In A. thaliana, the AtZIP4 and NcZNT1 promoters were mainly active in cortex, endodermis and pericycle cells under Zn deficient conditions. In N. caerulescens, the promoters were active in the same tissues, though the activity of the NcZNT1 promoter was higher and not limited to Zn deficient conditions. Common cis elements were identified in both promoters by 5’ deletion analysis. These correspond to the previously determined Zinc Deficiency Responsive Elements found in A. thaliana to interact with two redundantly acting transcription factors, bZIP19 and bZIP23, controlling the Zn deficiency response. In conclusion, these results suggest that NcZNT1 is an important factor in contributing to Zn and Cd hyperaccumulation in N. caerulescens. Differences in cis- and trans-regulators are likely to account for the differences in expression between A. thaliana and N. caerulescens. The high, constitutive NcZNT1 expression in the stele of N. caerulescens roots implicates its involvement in long distance root-to-shoot metal transport by maintaining a Zn/Cd influx into cells responsible for xylem loading. PMID:26930473

  13. Effects of Zinc Chelators on Aflatoxin Production in Aspergillus parasiticus

    PubMed Central

    Wee, Josephine; Day, Devin M.; Linz, John E.

    2016-01-01

    Zinc concentrations strongly influence aflatoxin accumulation in laboratory media and in food and feed crops. The presence of zinc stimulates aflatoxin production, and the absence of zinc impedes toxin production. Initial studies that suggested a link between zinc and aflatoxin biosynthesis were presented in the 1970s. In the present study, we utilized two zinc chelators, N,N,N′,N′-tetrakis (2-pyridylmethyl) ethane-1,2-diamine (TPEN) and 2,3-dimercapto-1-propanesulfonic acid (DMPS) to explore the effect of zinc limitation on aflatoxin synthesis in Aspergillus parasiticus. TPEN but not DMPS decreased aflatoxin biosynthesis up to six-fold depending on whether A. parasiticus was grown on rich or minimal medium. Although we observed significant inhibition of aflatoxin production by TPEN, no detectable changes were observed in expression levels of the aflatoxin pathway gene ver-1 and the zinc binuclear cluster transcription factor, AflR. Treatment of growing A. parasiticus solid culture with a fluorescent zinc probe demonstrated an increase in intracellular zinc levels assessed by increases in fluorescent intensity of cultures treated with TPEN compared to controls. These data suggest that TPEN binds to cytoplasmic zinc therefore limiting fungal access to zinc. To investigate the efficacy of TPEN on food and feed crops, we found that TPEN effectively decreases aflatoxin accumulation on peanut medium but not in a sunflower seeds-derived medium. From an application perspective, these data provide the basis for biological differences that exist in the efficacy of different zinc chelators in various food and feed crops frequently contaminated by aflatoxin. PMID:27271668

  14. Plasticity of DNA methylation and gene expression under zinc deficiency in Arabidopsis roots.

    PubMed

    Chen, Xiaochao; Schönberger, Brigitte; Menz, Jochen; Ludewig, Uwe

    2018-05-25

    DNA methylation is a heritable chromatin modification that maintains chromosome stability, regulates transposon silencing and appears to be involved in gene expression in response to environmental conditions. Environmental stress alters DNA methylation patterns that are correlated with gene expression differences. Here, genome-wide differential DNA-methylation was identified upon prolonged Zn deficiency, leading to hypo- and hyper-methylated chromosomal regions. Preferential CpG methylation changes occurred in gene promoters and gene bodies, but did not overlap with transcriptional start sites. Methylation changes were also prominent in transposable elements. By contrast, non-CG methylation differences were exclusively found in promoters of protein coding genes and in transposable elements. Strongly Zn deficiency-induced genes and their promoters were mostly non-methylated, irrespective of Zn supply. Differential DNA methylation in the CpG and CHG, but not in the CHH context, was found close to a few up-regulated Zn-deficiency genes. However, the transcriptional Zn-deficiency response in roots appeared little correlated with associated DNA methylation changes in promoters or gene bodies. Furthermore, under Zn deficiency, developmental defects were identified in an Arabidopsis mutant lacking non-CpG methylation. The root methylome thus responds specifically to a micro-nutrient deficiency and is important for efficient Zn utilization at low availability, but the relationship of differential methylation and differentially expressed genes is surprisingly poor.

  15. Characterization of the Bacillus stearothermophilus manganese superoxide dismutase gene and its ability to complement copper/zinc superoxide dismutase deficiency in Saccharomyces cerevisiae

    SciTech Connect

    Bowler, C.; Inze, D.; Van Camp, W.

    1990-03-01

    Recombinant clones containing the manganese superoxide dismutase (MnSOD) gene of Bacillus stearothermophilus were isolated with an oligonucleotide probe designed to match a part of the previously determined amino acid sequence. Complementation analyses, performed by introducing each plasmid into a superoxide dismutase-deficient mutant of Escherichia coli, allowed us to define the region of DNA which encodes the MnSOD structural gene and to identify a promoter region immediately upstream from the gene. These data were subsequently confirmed by DNA sequencing. Since MnSOD is normally restricted to the mitochondria in eucaryotes, we were interested (i) in determining whether B. stearothermophilus MnSOD could functionmore » in eucaryotic cytosol and (ii) in determining whether MnSOD could replace the structurally unrelated copper/zinc superoxide dismutase (Cu/ZnSOD) which is normally found there. To test this, the sequence encoding bacterial MnSOD was cloned into a yeast expression vector and subsequently introduced into a Cu/ZnSOD-deficient mutant of the yeast Saccharomyces cerevisiae. Functional expression of the protein was demonstrated, and complementation tests revealed that the protein was able to provide tolerance at wild-type levels to conditions which are normally restrictive for this mutant. Thus, in spite of the evolutionary unrelatedness of these two enzymes, Cu/ZnSOD can be functionally replaced by MnSOD in yeast cytosol.« less

  16. Blood zinc levels in nursing women from different regions of the West Bank of Palestine.

    PubMed

    Shawahna, Ramzi; Zyoud, Ahed; Jallad, Donia; Hadwan, Labebah; Ihssan, Neeran; Hilal, Hikmat

    2017-07-06

    Pregnant and nursing women are at higher risk of zinc deficiency which can have detrimental consequences on health. We assessed blood zinc levels in 72 nursing women from the West Bank of Palestine and investigated the association between sociodemographic variables and blood zinc levels. Blood samples were analyzed for their zinc contents using graphite furnace atomic absorption spectrophotometry. Blood and data collection were performed between July and December 2016. The median blood zinc level was 4.53 mg/L (interquartile range of 0.38 mg/L). In unadjusted analyses, blood zinc levels were higher in nursing women who lived in cities (p-value <.001), had higher household income (p-value <.001), whose husbands had a white collar job (p-value <.05), were nonsmokers (p-value <.05), did not use hair dyes (p-value <.05), and consumed energy beverages (p-value <.001). Multiple linear analysis showed that living in cities and consuming energy beverages remained significantly associated with higher blood zinc levels (p-value <.05). Blood zinc levels were in the range previously reported for similar non-malnourished populations. Nursing women living in cities and those consuming energy beverages tended to have higher blood zinc levels. Urbanized lifestyle might have enhanced blood zinc levels in nursing women.

  17. Effect of low zinc intake and oral contraceptive agents on nitrogen utilization and clinical findings in young women.

    PubMed

    Hess, F M; King, J C; Margen, S

    1977-12-01

    In a previous paper we reported that serum, urine and fecal zinc levels fell markedly in women taking a combination oral contraceptive agent (+OCA) and in women with normal menstrual cycles (-OCA) when they consumed a low-zinc diet (less than 0.2 mg/day) for 35 days. We evaluated other biochemical and clinical data in order to determine if depletion of accessible body zinc and/or physiologic adjustment to conserve body zinc stores had occurred. Neither low zinc intake nor oral contraceptive use appeared to influence nitrogen balance or body weight. Use of contraceptive drugs appeared to influence the response of blood parameters to zinc depletion. Serum transferrin and cholesterol declined significantly in the -OCA group, whereas alkaline phosphatase and gamma-globulin changed significantly in both groups. Clinical problems developed in all the subjects with serum zinc levels below 50 microgram/dl during the study; three of the six with serum zinc levels above 50 microgram/dl also complained of clinical symptoms. The results suggest that zinc deficiency through depletion of accessible body zinc stores developed during the 35-day study.

  18. Zinc supplementation leads to immune modulation and improved survival in a juvenile model of murine sepsis.

    PubMed

    Ganatra, Hammad A; Varisco, Brian M; Harmon, Kelli; Lahni, Patrick; Opoka, Amy; Wong, Hector R

    2017-01-01

    Children with severe sepsis are known to have altered zinc homeostasis and decreased circulating zinc levels, suggesting a role for zinc supplementation to improve outcomes. We tested the hypothesis that zinc supplementation would improve survival in a juvenile model of polymicrobial sepsis. Juvenile (13-14-d-old) C57BL/6 mice were treated with 10 mg/kg of zinc via i.p. injections (or vehicle) for 3 d prior to induction of polymicrobial sepsis via i.p. cecal slurry injections. Survival after sepsis was followed for 3 d, and bacterial clearance, ex vivo phagocytosis, systemic inflammatory markers and neutrophil extracellular trap (NET) formation were quantified. We found a significant survival benefit and decreased bacterial burden among zinc supplemented mice when compared with the control group. Zinc supplementation also resulted in enhanced phagocytic activity, greater neutrophil recruitment in the peritoneal cavity and NET formation, suggesting a possible mechanism for improved bacterial clearance and survival. We also noted decreased serum cytokine levels and decreased myeloperoxidase activity in lung tissue following zinc supplementation, suggesting attenuation of the systemic inflammatory response. In conclusion, zinc supplementation improves bacterial clearance, and hence survival, in juvenile mice with polymicrobial sepsis.

  19. A potential role for zinc transporter 7 in testosterone synthesis in mouse Leydig tumor cells.

    PubMed

    Chu, Qingqing; Chi, Zhi-Hong; Zhang, Xiuli; Liang, Dan; Wang, Xuemei; Zhao, Yue; Zhang, Li; Zhang, Ping

    2016-06-01

    Previous studies have demonstrated that zinc (Zn) is an essential trace element which is involved in male reproduction. The zinc transporter (ZnT) family, SLC30a, is involved in the maintenance of Zn homeostasis and in mediating intracellular signaling events; however, relatively little is known regarding the effect of ZnTs on testosterone synthesis. Thus, in the present study, we aimed to determine the effect of Zn transporter 7 (ZnT7) on testosterone synthesis in male CD-1 mice and mouse Leydig cells. The findings of the present study revealed that the concentrations of Zn in the testes and Leydig cells were significantly lower in mice fed a Zn-deficient diet compared with the control mice fed a Zn-adequate diet. In addition, ZnT7 was principally expressed and colocalized with steroidogenic acute regulatory protein (StAR) in the Leydig cells of male CD-1 mice. ZnT7 expression was downregulated in the mice fed a Zn-deficient diet, which led to decreases in the expression of the enzymes involved in testosterone synthesis namely cholesterol side‑chain cleavage enzyme (P450scc) and 3β-hydroxysteroid dehydrogenase/D5-D4 isomerase (3β-HSD) as well as decreased serum testosterone levels. These results suggested that Znt7 may be involved in testosterone synthesis in the mouse testes. To examine this hypothesis, we used the mouse Leydig tumor cell line (MLTC-1 cell line) in which the ZnT7 gene had been silenced, in order to gauge the impact of changes in ZnT7 expression on testosterone secretion and the enzymes involved in testosterone synthesis. The results demonstrated that ZnT7 gene silencing downregulated the expression of StAR, P450scc and 3β-HSD as well as progesterone concentrations in the human chorionic gonadotrophin (hCG)-stimulated MLTC-1 cells. Taken together, these findings reveal that ZnT7 may play an important role in the regulation of testosterone synthesis by modulating steroidogenic enzymes, and may represent a therapeutic target in

  20. Biofortified indica rice attains iron and zinc nutrition dietary targets in the field

    USDA-ARS?s Scientific Manuscript database

    Iron (Fe) and zinc (Zn) deficiencies are the most prevalent micronutrient malnutrition globally1. Fe in rice has proven efficacious in improving serum ferritin concentration and body Fe levels2. Rapid progress in biofortification demonstrates the feasibility to enhance Fe in polished rice by expre...

  1. Low zinc levels may contribute to gynecomastia in puberty.

    PubMed

    Erkekoglu, Pinar; Durmaz, Erdem; Kızılgün, Murat; Özmert, Elif N; Derman, Orhan; Yurdakök, Kadriye; Kocer-Gumusel, Belma

    2017-12-01

    This study aimed to determine whether there were any differences in trace element levels between adolescent boys with gynecomastia and control boys and to determine the correlations between the levels of trace elements and body mass index (BMI) and sex hormones. The pubertal gynecomastia group comprised of 41 patients (mean age=13.2 ±0.9 years), who were admitted to Hacettepe University İhsan Doğramacı Children's Hospital in Ankara. Control group comprised of 21 healthy male children. Analyses of trace element levels were performed atomic absorption spectrometry. The mean zinc level of control group was 101.33±16.87μg/dL and the mean zinc level of gynecomastia group was 81.36±17,43μg/dL (20% lower in gynecomastia patients, p=0.0001). However, the mean copper and manganese levels of gynecomastia patients were not statistically different than the control group. There were significant positive correlations between plasma zinc and total testosterone levels in gynecomastia group (r=0.592; p<0.05). There was a significant negative correlation between plasma zinc levels and BMI (r=-0.311; p<0.05). These results indicate that zinc deficiency might be one of the underlying factors of gynecomastia, the importance of which needs to be further elucidated. Copyright © 2017 Elsevier GmbH. All rights reserved.

  2. Intrauterine Zn Deficiency Favors Thyrotropin-Releasing Hormone-Increasing Effects on Thyrotropin Serum Levels and Induces Subclinical Hypothyroidism in Weaned Rats.

    PubMed

    Alcántara-Alonso, Viridiana; Alvarez-Salas, Elena; Matamoros-Trejo, Gilberto; de Gortari, Patricia

    2017-10-18

    Individuals who consume a diet deficient in zinc (Zn-deficient) develop alterations in hypothalamic-pituitary-thyroid axis function, i.e., a low metabolic rate and cold insensitivity. Although those disturbances are related to primary hypothyroidism, intrauterine or postnatal Zn-deficient adults have an increased thyrotropin (TSH) concentration, but unchanged thyroid hormone (TH) levels and decreased body weight. This does not support the view that the hypothyroidism develops due to a low Zn intake. In addition, intrauterine or postnatal Zn-deficiency in weaned and adult rats reduces the activity of pyroglutamyl aminopeptidase II (PPII) in the medial-basal hypothalamus (MBH). PPII is an enzyme that degrades thyrotropin-releasing hormone (TRH). This hypothalamic peptide stimulates its receptor in adenohypophysis, thereby increasing TSH release. We analyzed whether earlier low TH is responsible for the high TSH levels reported in adults, or if TRH release is enhanced by Zn deficiency at weaning. Dams were fed a 2 ppm Zn-deficient diet in the period from one week prior to gestation and up to three weeks after delivery. We found a high release of hypothalamic TRH, which along with reduced MBH PPII activity, increased TSH levels in Zn-deficient pups independently of changes in TH concentration. We found that primary hypothyroidism did not develop in intrauterine Zn-deficient weaned rats and we confirmed that metal deficiency enhances TSH levels since early-life, favoring subclinical hypothyroidism development which remains into adulthood.

  3. Longitudinal changes in zinc transport kinetics, metallothionein, and zinc transporter expression in a blood-brain barrier model in response to a moderately excessive zinc environment$

    PubMed Central

    Gauthier, Nicole A.; Karki, Shakun; Olley, Bryony J.; Thomas, W. Kelly

    2008-01-01

    A blood-brain barrier (BBB) model composed of porcine brain capillary endothelial cells (BCEC) was exposed to a moderately excessive zinc environment (50 µmol Zn/L) in cell culture and longitudinal measurements were made of zinc transport kinetics, ZnT-1 (SLC30A1) expression, and changes in the protein concentration of metallothionein (MT), ZnT-1, ZnT-2 (SLC30A2), and Zip1 (SLC39A1). Zinc release by cells of the BBB model was significantly increased after 12–24 h of exposure, but decreased back to control levels after 48–96 h, as indicated by transport across the BBB from both the ablumenal (brain) and lumenal (blood) directions. Expression of ZnT-1, the zinc export protein, increased 169% within 12 h, but was no longer different from controls after 24 h. Likewise, ZnT-1 protein content increased transiently after 12 h of exposure but returned to control levels by 24 h. Capacity for zinc uptake and retention increased from both the lumenal and ablumenal directions within 12–24 h of exposure and remained elevated. MT and ZnT-2 were elevated within 12 h and remained elevated throughout the study. Zip1 was unchanged by the treatment. The BBB’s response to a moderately high zinc environment was dynamic and involved multiple mechanisms. The initial response was to increase the cell’s capacity to sequester zinc with additional MT and increase zinc export with the ZnT-1 protein. But, the longer term strategy involved increasing ZnT-2 transporters, presumably to sequester zinc into intracellular vesicles as a mechanism to protect the brain and maintain brain zinc homeostasis. PMID:18061429

  4. Influence of carotene-rich vegetable meals on the prevalence of anaemia and iron deficiency in Filipino schoolchildren.

    PubMed

    Maramag, C C; Ribaya-Mercado, J D; Rayco-Solon, P; Solon, J A A; Tengco, L W; Blumberg, J B; Solon, F S

    2010-05-01

    To determine the effects of eating carotene-rich green and yellow vegetables on the prevalence of anaemia, iron deficiency and iron-deficiency anaemia in schoolchildren. Schoolchildren (n=104), aged 9-12 years, received standardized meals containing 4.2 mg of provitamin A carotenoids/day (mainly beta-carotene) from yellow and green leafy vegetables and at least 7 g dietary fat/day. The meals were provided three times/day, 5 days/week, for 9 weeks at school. Before and after the dietary intervention, total-body vitamin A pool size was assessed by using the deuterated-retinol-dilution method; serum retinol and beta-carotene concentrations were measured by high-performance liquid chromatography; and whole blood haemoglobin (Hb) and zinc protoporphyrin (ZnPP) concentrations were measured by using a photometer and a hematofluorometer, respectively. After 9 weeks, the mean total-body vitamin A pool size increased twofold (95% confidence interval (CI): -0.11, -0.07 micromol retinol; P<0.001), and serum beta-carotene concentration increased fivefold (95% CI: -0.97, -0.79 micromol/l; P<0.001). Blood Hb (95% CI: -1.02, -0.52 g per 100 ml; P<0.001) and ZnPP increased (95% CI: -11.82, -4.57 microol/mol haem; P<0.001). The prevalence of anaemia (Hb<11.5 g per 100 ml) decreased from 12.5 to 1.9% (P<0.001). There were no significant changes in the prevalence of iron deficiency or iron-deficiency anaemia. Ingestion of carotene-rich yellow and green leafy vegetables improves the total-body vitamin A pool size and Hb concentration, and decreases anaemia rates in Filipino schoolchildren, with no effect on iron deficiency or iron-deficiency anaemia rates.

  5. Zinc electrode and rechargeable zinc-air battery

    DOEpatents

    Ross, Jr., Philip N.

    1989-01-01

    An improved zinc electrode is disclosed for a rechargeable zinc-air battery comprising an outer frame and a porous foam electrode support within the frame which is treated prior to the deposition of zinc thereon to inhibit the formation of zinc dendrites on the external surface thereof. The outer frame is provided with passageways for circulating an alkaline electrolyte through the treated zinc-coated porous foam. A novel rechargeable zinc-air battery system is also disclosed which utilizes the improved zinc electrode and further includes an alkaline electrolyte within said battery circulating through the passageways in the zinc electrode and an external electrolyte circulation means which has an electrolyte reservoir external to the battery case including filter means to filter solids out of the electrolyte as it circulates to the external reservoir and pump means for recirculating electrolyte from the external reservoir to the zinc electrode.

  6. Decreased GABA-A binding on FMZ-PET in succinic semialdehyde dehydrogenase deficiency.

    PubMed

    Pearl, P L; Gibson, K M; Quezado, Z; Dustin, I; Taylor, J; Trzcinski, S; Schreiber, J; Forester, K; Reeves-Tyer, P; Liew, C; Shamim, S; Herscovitch, P; Carson, R; Butman, J; Jakobs, C; Theodore, W

    2009-08-11

    Succinic semialdehyde dehydrogenase (SSADH) deficiency is an autosomal recessive disorder of GABA metabolism characterized by elevated levels of GABA and gamma-hydroxybutyric acid. Clinical findings include intellectual impairment, hypotonia, hyporeflexia, hallucinations, autistic behaviors, and seizures. Autoradiographic labeling and slice electrophysiology studies in the murine model demonstrate use-dependent downregulation of GABA(A) receptors. We studied GABA(A) receptor activity in human SSADH deficiency utilizing [(11)C]-flumazenil (FMZ)-PET. FMZ binding was measured in 7 patients, 10 unaffected parents, and 8 healthy controls. Data analysis was performed using a reference region compartmental model, with time-activity curve from pons as the input function. Relative parametric binding potential (BP(ND)) was derived, with MRI-based pixel by pixel partial volume correction, in regions of interest drawn on coregistered MRI. In amygdala, hippocampus, cerebellar vermis, frontal, parietal, and occipital cortex, patients with SSADH deficiency had significant reductions in FMZ BP(ND) compared to parents and controls. Mean cortical values were 6.96 +/- 0.79 (controls), 6.89 +/- 0.71 (parents), and 4.88 +/- 0.77 (patients) (F ratio 16.1; p < 0.001). There were no differences between controls and parents in any cortical region. Succinic semialdehyde dehydrogenase (SSADH) deficient patients show widespread reduction in BZPR binding on [(11)C]-flumazenil-PET. Our results suggest that high endogenous brain GABA levels in SSADH deficiency downregulate GABA(A)-BZPR binding site availability. This finding suggests a potential mechanism for neurologic dysfunction in a serious neurodevelopmental disorder, and suggests that PET may be useful to translate studies in animal models to human disease.

  7. Zinc as an adjunct therapy in the management of severe pneumonia among Gambian children: randomized controlled trial.

    PubMed

    Howie, Stephen; Bottomley, Christian; Chimah, Osaretin; Ideh, Readon; Ebruke, Bernard; Okomo, Uduak; Onyeama, Charles; Donkor, Simon; Rodrigues, Onike; Tapgun, Mary; Janneh, Marie; Oluwalana, Claire; Kuti, Bankole; Enwere, Godwin; Esangbedo, Pamela; Doherty, Conor; Mackenzie, Grant; Greenwood, Brian; Corrah, Tumani; Prentice, Andrew; Adegbola, Richard; Zaman, Syed

    2018-06-01

    The benefit of zinc as an adjunct therapy for severe pneumonia is not established. We assessed the benefit of adjunct zinc therapy for severe pneumonia in children and determined whether the study children were zinc deficient. This was a randomized, parallel group, double-blind, placebo-controlled trial with an allocation ratio of 1:1 conducted in children with severe pneumonia to evaluate the efficacy of daily zinc as an adjunct treatment in preventing 'treatment failure' (presence of any sign of severe pneumonia) on day-5 and day-10 and in reducing the time to resolution of signs of severe pneumonia. Six hundred and four children 2-59 months of age presenting with severe pneumonia at six urban and rural health care facilities in The Gambia were individually randomised to receive placebo (n = 301) or zinc (n = 303) for seven days. To determine if the study children were zinc deficient, supplementation was continued in a randomly selected subgroup of 121 children from each arm for six months post-enrolment, and height-gain, nutritional status, plasma zinc concentrations, and immune competence were compared. Percentage of treatment failure were similar in placebo and zinc arms both on day 5 (14.0% vs 14.1%) and day 10 (5.2% vs 5.9%). The time to recovery from lower chest wall indrawing and sternal retraction was longer in the placebo compared to zinc arm (24.4 vs 23.0 hours; P  = 0.011 and 18.7 vs 11.0 hours; P  = 0.006 respectively). The time to resolution for all respiratory symptoms of severity was not significantly different between placebo and zinc arms (42.3 vs 30.9 hours respectively; P  = 0.242). In the six months follow-up sub-group, there was no significant difference in height gain, height-for-age and weight-for-height Z-scores, mid upper arm circumference, plasma zinc concentrations, and anergy at six months post-enrolment. In this population, zinc given as an adjunct treatment for severe pneumonia showed no benefit in treatment

  8. Copper/zinc superoxide dismutase insufficiency impairs progesterone secretion and fertility in female mice.

    PubMed

    Noda, Yoshihiro; Ota, Kuniaki; Shirasawa, Takuji; Shimizu, Takahiko

    2012-01-01

    Copper/zinc superoxide dismutase (CuZn-SOD, SOD1) is one of the major antioxidant enzymes, and is localized in the cytoplasm to scavenge superoxide. To investigate the physiological role of SOD1 in the ovaries, we analyzed the fertility of Sod1-deficient female mice. To evaluate their hormonal metabolism, we measured pituitary and ovarian hormone levels in the plasma of the mutant mice. Plasma follicle-stimulating hormone, luteinizing hormone, and estradiol were not altered in the mutant compared to the wild-type females, while the plasma progesterone level was significantly reduced in the mutant females. Furthermore, the mutant mice showed decreased progesterone secretion under the condition of superovulation. In a histochemical analysis, we observed a remarkable reduction in the corpus luteum area in the mutant ovaries without atrophic changes. The mutant mice also displayed enhanced superoxide generation in the region surrounding the corpora lutea, which was associated with increased apoptotic cells and suppressed vasculature. These results suggested that SOD1 deficiency dysregulated luteal formation because of increased superoxide generation in the ovary. In vitro fertilization experiments showed no abnormal fertilization of Sod1-deficient oocytes. In addition, when Sod1-deficient embryos were transferred into the oviducts of wild-type females, mutant embryos developed at a normal rate, indicating that SOD1 deficiency in embryos did not cause miscarriage in the uterus of wild-type females. These results indicated that increased intracellular ROS impaired luteal formation and progesterone production in the mutant females, thus suggesting that SOD1 plays a crucial role in both the luteal function and the maintenance of fertility in female mice.

  9. The effect of zinc limitation on the transcriptome of Pseudomonas fluorescens Pf-5

    USDA-ARS?s Scientific Manuscript database

    Pseudomonas fluorescens Pf-5 is a soil bacterium that can protect several plant species from diseases caused by fungal and bacterial pathogens. Zinc is a vital micronutrient for bacteria but is deficient in some soil environments and toxic in large quantities. Hence, bacteria have evolved elaborate ...

  10. Zinc Promotes Adipose-Derived Mesenchymal Stem Cell Proliferation and Differentiation towards a Neuronal Fate.

    PubMed

    Moon, Mi-Young; Kim, Hyun Jung; Choi, Bo Young; Sohn, Min; Chung, Tae Nyoung; Suh, Sang Won

    2018-01-01

    Zinc is an essential element required for cell division, migration, and proliferation. Under zinc-deficient conditions, proliferation and differentiation of neural progenitors are significantly impaired. Adipose-derived mesenchymal stem cells (AD-MSCs) are multipotent stem cells that can differentiate into neurons. The aim of this study was to evaluate the effect of zinc on AD-MSC proliferation and differentiation. We initially examined the effect of zinc on stem cell proliferation at the undifferentiated stage. AD-MSCs showed high proliferation rates on day 6 in 30  μ M and 100  μ M of ZnCl 2 . Zinc chelation inhibited AD-MSC proliferation via downregulation of ERK1/2 activity. We then assessed whether zinc was involved in cell migration and neurite outgrowth during differentiation. After three days of neuronal differentiation, TUJ-1-positive cells were observed, implying that AD-MSCs had differentiated into early neuron or neuron-like cells. Neurite outgrowth was increased in the zinc-treated group, while the CaEDTA-treated group showed diminished, shrunken neurites. Furthermore, we showed that zinc promoted neurite outgrowth via the inactivation of RhoA and led to the induction of neuronal gene expression (MAP2 and nestin) in differentiated stem cells. Taken together, zinc promoted AD-MSC proliferation and affected neuronal differentiation, mainly by increasing neurite outgrowth.

  11. Zinc Promotes Adipose-Derived Mesenchymal Stem Cell Proliferation and Differentiation towards a Neuronal Fate

    PubMed Central

    Moon, Mi-Young; Kim, Hyun Jung; Choi, Bo Young; Sohn, Min

    2018-01-01

    Zinc is an essential element required for cell division, migration, and proliferation. Under zinc-deficient conditions, proliferation and differentiation of neural progenitors are significantly impaired. Adipose-derived mesenchymal stem cells (AD-MSCs) are multipotent stem cells that can differentiate into neurons. The aim of this study was to evaluate the effect of zinc on AD-MSC proliferation and differentiation. We initially examined the effect of zinc on stem cell proliferation at the undifferentiated stage. AD-MSCs showed high proliferation rates on day 6 in 30 μM and 100 μM of ZnCl2. Zinc chelation inhibited AD-MSC proliferation via downregulation of ERK1/2 activity. We then assessed whether zinc was involved in cell migration and neurite outgrowth during differentiation. After three days of neuronal differentiation, TUJ-1-positive cells were observed, implying that AD-MSCs had differentiated into early neuron or neuron-like cells. Neurite outgrowth was increased in the zinc-treated group, while the CaEDTA-treated group showed diminished, shrunken neurites. Furthermore, we showed that zinc promoted neurite outgrowth via the inactivation of RhoA and led to the induction of neuronal gene expression (MAP2 and nestin) in differentiated stem cells. Taken together, zinc promoted AD-MSC proliferation and affected neuronal differentiation, mainly by increasing neurite outgrowth. PMID:29765417

  12. Inhibition of vaccinia virus maturation by zinc chloride.

    PubMed Central

    Katz, E; Margalith, E

    1981-01-01

    Zinc chloride (0.1 mM) inhibited by 96.4% the growth of vaccinia virus in HeLa cells. Approximately 50% inhibition in formation of particles that sedimented in sucrose gradients similarly to vaccinia virions occurred in the presence of zinc ions. Whereas the synthesis of the viral deoxyribonucleic acid was not affected by zinc chloride, a decrease in the overall synthesis of viral polypeptides and inhibition of the cleavage of precursors to the core polypeptides were observed. Images PMID:7347557

  13. Zinc and Copper Metabolism and Risk of Autism: a reply to Sayehmiri et al.

    PubMed

    Fluegge Ba, Keith

    2017-01-01

    Sayehmiri et al. recently conducted a meta-analysis to explore the relationship between zinc and copper metabolism and autism spectrum disorders (ASD). Recent reports have elucidated a full behavioral profile of mice exposed to prenatal zinc deficiency and documented a phenotype similar to that found in autism spectrum disorders (ASD). These studies suggest that significant alterations in Zn metabolism may be an important nutritional component in the development of ASD. The idea that prenatal zinc deficiency may be to blame is cursorily challenged. Epidemiological studies show that high-income countries with a low estimated prevalence of inadequate zinc intake report the highest prevalence of ASD. Consistent with other reports indicating a link between air pollution and ASD, it has recently been proposed that use of the herbicide, glyphosate, in agriculture may serve as an instrumental variable in predicting later neurodevelopmental impairment via emissions of the agricultural air pollutant, nitrous oxide (N2O). Work in anesthesiology has demonstrated the neurological effects from subanesthetic doses of N2O, including its inhibition of the alpha 7 nicotinic acetylcholine receptor (α7), a receptor coupled to both central nitric oxide (NO) metabolism and peripheral anti-inflammation. This correspondence explores how the aforementioned nutritional phenotypes found by Sayehmiri et al. in their systematic review may be a compensatory mechanism to counter the effects (namely, α7 inhibition) of air pollutant exposures occurring during the most critical stages of fetal development.

  14. Effects of Zn Deficiency and Bicarbonate on the Growth and Photosynthetic Characteristics of Four Plant Species

    PubMed Central

    Zhao, Kuan; Wu, Yanyou

    2017-01-01

    Calcareous soils are characterized by low nutrient contents, high bicarbonate (HCO3−) content, and high alkalinity. The effects of HCO3− addition under zinc-sufficient (+Zn) and zinc-deficient (−Zn) conditions on the growth and photosynthetic characteristics of seedlings of two Moraceae species (Broussonetia papyrifera and Morus alba) and two Brassicaceae species (Orychophragmus violaceus and Brassica napus) were investigated. These four species were hydroponically grown in nutrient solution with 0 mM Zn (−Zn) or 0.02 mM Zn (+Zn) and 0 mM or 10 mM HCO3−. The photosynthetic response to HCO3− treatment, Zn deficiency, or both varied according to plant species. Of the four species, Broussonetia papyrifera showed the best adaptability to Zn deficiency for both the 0 mM and 10 mM HCO3− treatments due to its strong growth and minimal inhibition of photosynthesis and photosystem II (PS II). Brassica napus was sensitive to Zn deficiency, HCO3− treatment, or both as evidenced by the considerable inhibition of photosynthesis and high PS II activity. The results indicated different responses of various plant species to Zn deficiency and excess HCO3−. Broussonetia papyrifera was shown to have potential as a pioneer species in karst regions. PMID:28076430

  15. [Immune, inflammatory, and nutritional protein profile in children with iron deficiency in Côte d'Ivoire].

    PubMed

    Yapi, Houphouët Félix; Ahiboh, Hugues; Yayo, Eric; Edjeme, Angele; Attoungbre-Hauhouot, Marie Laure; Allico, Joseph Djaman; Monnet, Dagui

    2009-01-01

    not differ significantly. The reduced IgG associated with iron deficiency may be attributed to the role that iron plays in the proliferation and maturation of lymphocytes. Reduced iron levels would thus lead to slowing down the hematopoietic mechanism, resulting in a decrease in B lymphocyte production and thus inevitably a reduction in IgG synthesis. The reduction in albumin and TBPA associated with the iron deficiency but in the absence of any sign of malnutrition (W/H > 96%) or inflammatory risk (PINI < 2) in either study group shows that iron may play a dominant role during protein synthesis. Iron deficiency might limit the energy of cellular tissues, leading to a reduction in RNA activity (transcription and translation), which would in turn decrease ribosome activity in tissues and thus reduce amino acid synthesis in cells, resulting in the reduction observed in protein synthesis. The lack of difference between the study groups in inflammatory proteins, notably CRP and alpha1-GPA, indicates that iron deficiency does not appear to be related to an inflammatory process. This study of children without any apparent clinical signs of iron deficiency shows that such a deficiency may be associated with a disruption in protein production. The proteins concerned include IgG, TBPA and albumin. The public authorities should pay particular attention to improving children's diets, especially their micronutrient levels, including for iron, vitamin A and zinc.

  16. Vitamin D Decreases Serum VEGF Correlating with Clinical Improvement in Vitamin D-Deficient Women with PCOS: A Randomized Placebo-Controlled Trial.

    PubMed

    Irani, Mohamad; Seifer, David B; Grazi, Richard V; Irani, Sara; Rosenwaks, Zev; Tal, Reshef

    2017-03-28

    Vascular endothelial growth factor (VEGF) has been suggested to play a role in the pathophysiology of polycystic ovary syndrome (PCOS) and may contribute to increased risk of ovarian hyperstimulation syndrome (OHSS) in affected individuals. Vitamin D (VitD) supplementation improves multiple clinical parameters in VitD-deficient women with PCOS and decreases VEGF levels in several other pathologic conditions. Unveiling the basic mechanisms underlying the beneficial effects of vitamin D on PCOS may enhance our understanding of the pathophysiology of this syndrome. It may also suggest a new treatment for PCOS that can improve it through the same mechanism as vitamin D and can be given regardless of vitamin D levels. Therefore, we aimed to explore the effect of VitD supplementation on serum VEGF levels and assess whether changes in VEGF correlate with an improvement in characteristic clinical abnormalities of PCOS. This is a randomized placebo-controlled trial conducted between October 2013 and March 2015. Sixty-eight VitD-deficient women with PCOS were recruited. Women received either 50,000 IU of oral VitD3 or placebo once weekly for 8 weeks. There was a significant decrease in serum VEGF levels (1106.4 ± 36.5 to 965.3 ± 42.7 pg·mL -1 ; p < 0.001) in the VitD group. Previously reported findings of this trial demonstrated a significant decrease in the intermenstrual intervals, Ferriman-Gallwey hirsutism score, and triglycerides following VitD supplementation. Interestingly, ∆VEGF was positively correlated with ∆triglycerides ( R ² = 0.22; p = 0.02) following VitD supplementation. In conclusion, VitD replacement significantly decreases serum VEGF levels correlating with a decrease in triglycerides in women with PCOS. This is a novel molecular explanation for the beneficial effects of VitD treatment. It also suggests the need to investigate a potential role of VitD treatment in reducing the incidence or severity of OHSS in VitD-deficient women with PCOS.

  17. Vacuolar zinc transporter Zrc1 is required for detoxification of excess intracellular zinc in the human fungal pathogen Cryptococcus neoformans.

    PubMed

    Cho, Minsu; Hu, Guanggan; Caza, Mélissa; Horianopoulos, Linda C; Kronstad, James W; Jung, Won Hee

    2018-01-01

    Zinc is an important transition metal in all living organisms and is required for numerous biological processes. However, excess zinc can also be toxic to cells and cause cellular stress. In the model fungus Saccharomyces cerevisiae, a vacuolar zinc transporter, Zrc1, plays important roles in the storage and detoxification of excess intracellular zinc to protect the cell. In this study, we identified an ortholog of the S. cerevisiae ZRC1 gene in the human fungal pathogen Cryptococcus neoformans. Zrc1 was localized in the vacuolar membrane in C. neoformans, and a mutant lacking ZRC1 showed significant growth defects under high-zinc conditions. These results suggested a role for Zrc1 in zinc detoxification. However, contrary to our expectation, the expression of Zrc1 was induced in cells grown in zinc-limited conditions and decreased upon the addition of zinc. These expression patterns were similar to those of Zip1, the high-affinity zinc transporter in the plasma membrane of C. neoformans. Furthermore, we used the zrc1 mutant in a murine model of cryptococcosis to examine whether a mammalian host could inhibit the survival of C. neoformans using zinc toxicity. We found that the mutant showed no difference in virulence compared with the wildtype strain. This result suggests that Zrc1-mediated zinc detoxification is not required for the virulence of C. neoformans, and imply that zinc toxicity may not be an important aspect of the host immune response to the fungus.

  18. Dietary and non-dietary factors associated with serum zinc in Indian women.

    PubMed

    Herbst, Catherine A; Menon, Kavitha C; Ferguson, Elaine L; Thomson, Christine D; Bailey, Karl; Gray, Andrew R; Zodpey, Sanjay; Saraf, Abhay; Das, Prabir Kumar; Skeaff, Sheila A

    2014-10-01

    Women in low-income settings, common in India, are at risk of inadequate zinc intake due to poor diet quality and low consumption of flesh foods rich in zinc. The aims of this study were to assess the prevalence of zinc status of non-pregnant rural and tribal women living in central India and to identify dietary and non-dietary factors associated with the biochemical zinc status of these women. Rural and tribal non-pregnant women 18-30 years of age were selected using proportion to population sampling near Nagpur, Maharashtra, India. Sociodemographic, biochemical (serum zinc), clinical, and dietary data (1-day interactive 24-h recall) were collected. The mean age of women (n = 109; rural = 52; tribal = 56) was 23.2 years and mean BMI was 17.9 kg/m(2). The majority of the participants identified as being non-vegetarian (72 %). The mean ± SD serum zinc concentration was 10.8 ± 1.6 μmol/L, and 52 % of participants had a low serum zinc concentration according to the International Zinc Nutrition Consultative Group (IZiNCG). The median (first and third quartile) energy, zinc intake, and phytate/zinc molar ratio was 5.4 (4.2, 6.7) MJ/day, 5.3 (3.8, 7.0) mg/day, and 26 (22, 28), respectively. Zinc intakes were well below IZiNCG recommendations for dietary zinc of 9 mg/day for non-pregnant women aged 14-18 years and 7 mg/day for non-pregnant women aged ≥ 19 years. Using linear regression analysis to identify non-dietary and dietary factors associated with serum zinc, a significant association was only found for current lactation (p = 0.012) and energy intake (p < 0.001). Diets low in energy with poor bioavailability of dietary zinc are likely to be the primary cause of the high proportion of Indian women with zinc deficiency.

  19. The Effect of Low Dose Iron and Zinc Intake on Child Micronutrient Status and Development during the First 1000 Days of Life: A Systematic Review and Meta-Analysis.

    PubMed

    Petry, Nicolai; Olofin, Ibironke; Boy, Erick; Donahue Angel, Moira; Rohner, Fabian

    2016-11-30

    Adequate supply of micronutrients during the first 1000 days is essential for normal development and healthy life. We aimed to investigate if interventions administering dietary doses up to the recommended nutrient intake (RNI) of iron and zinc within the window from conception to age 2 years have the potential to influence nutritional status and development of children. To address this objective, a systematic review and meta-analysis of randomized and quasi-randomized fortification, biofortification, and supplementation trials in women (pregnant and lactating) and children (6-23 months) delivering iron or zinc in doses up to the recommended nutrient intake (RNI) levels was conducted. Supplying iron or zinc during pregnancy had no effects on birth outcomes. There were limited or no data on the effects of iron/zinc during pregnancy and lactation on child iron/zinc status, growth, morbidity, and psychomotor and mental development. Delivering up to 15 mg iron/day during infancy increased mean hemoglobin by 4 g/L ( p < 0.001) and mean serum ferritin concentration by 17.6 µg/L ( p < 0.001) and reduced the risk for anemia by 41% ( p < 0.001), iron deficiency by 78% (ID; p < 0.001) and iron deficiency anemia by 80% (IDA; p < 0.001), but had no effect on growth or psychomotor development. Providing up to 10 mg of additional zinc during infancy increased plasma zinc concentration by 2.03 µmol/L ( p < 0.001) and reduced the risk of zinc deficiency by 47% ( p < 0.001). Further, we observed positive effects on child weight for age z -score (WAZ) ( p < 0.05), weight for height z -score (WHZ) ( p < 0.05), but not on height for age z -score (HAZ) or the risk for stunting, wasting, and underweight. There are no studies covering the full 1000 days window and the effects of iron and zinc delivered during pregnancy and lactation on child outcomes are ambiguous, but low dose daily iron and zinc use during 6-23 months of age has a positive effect on child iron and zinc status.

  20. A moderate increase in dietary zinc reduces DNA strand breaks in leukocytes and alters plasma proteins without changing plasma zinc concentrations123

    PubMed Central

    Zyba, Sarah J; Killilea, David W; Holland, Tai C; Kim, Elijah; Moy, Adrian; Sutherland, Barbara; Shigenaga, Mark K

    2017-01-01

    Background: Food fortification has been recommended to improve a population’s micronutrient status. Biofortification techniques modestly elevate the zinc content of cereals, but few studies have reported a positive impact on functional indicators of zinc status. Objective: We determined the impact of a modest increase in dietary zinc that was similar to that provided by biofortification programs on whole-body and cellular indicators of zinc status. Design: Eighteen men participated in a 6-wk controlled consumption study of a low-zinc, rice-based diet. The diet contained 6 mg Zn/d for 2 wk and was followed by 10 mg Zn/d for 4 wk. To reduce zinc absorption, phytate was added to the diet during the initial period. Indicators of zinc homeostasis, including total absorbed zinc (TAZ), the exchangeable zinc pool (EZP), plasma and cellular zinc concentrations, zinc transporter gene expression, and other metabolic indicators (i.e., DNA damage, inflammation, and oxidative stress), were measured before and after each dietary-zinc period. Results: TAZ increased with increased dietary zinc, but plasma zinc concentrations and EZP size were unchanged. Erythrocyte and leukocyte zinc concentrations and zinc transporter expressions were not altered. However, leukocyte DNA strand breaks decreased with increased dietary zinc, and the level of proteins involved in DNA repair and antioxidant and immune functions were restored after the dietary-zinc increase. Conclusions: A moderate 4-mg/d increase in dietary zinc, similar to that which would be expected from zinc-biofortified crops, improves zinc absorption but does not alter plasma zinc. The repair of DNA strand breaks improves, as do serum protein concentrations that are associated with the DNA repair process. This trial was registered at clinicaltrials.gov as NCT02861352. PMID:28003206

  1. Zinc Levels in Left Ventricular Hypertrophy.

    PubMed

    Huang, Lei; Teng, Tianming; Bian, Bo; Yao, Wei; Yu, Xuefang; Wang, Zhuoqun; Xu, Zhelong; Sun, Yuemin

    2017-03-01

    Zinc is one of the most important trace elements in the body and zinc homeostasis plays a critical role in maintaining cellular structure and function. Zinc dyshomeostasis can lead to many diseases, such as cardiovascular disease. Our aim was to investigate whether there is a relationship between zinc and left ventricular hypertrophy (LVH). A total of 519 patients was enrolled and their serum zinc levels were measured in this study. We performed analyses on the relationship between zinc levels and LVH and the four LV geometry pattern patients: normal LV geometry, concentric remodeling, eccentric LVH, and concentric LVH. We performed further linear and multiple regression analyses to confirm the relationship between zinc and left ventricular mass (LVM), left ventricular mass index (LVMI), and relative wall thickness (RWT). Our data showed that zinc levels were 710.2 ± 243.0 μg/L in the control group and were 641.9 ± 215.2 μg/L in LVH patients. We observed that zinc levels were 715 ± 243.5 μg/L, 694.2 ± 242.7 μg/L, 643.7 ± 225.0 μg/L, and 638.7 ± 197.0 μg/L in normal LV geometry, concentric remodeling, eccentric LVH, and concentric LVH patients, respectively. We further found that there was a significant inverse linear relationship between zinc and LVM (p = 0.001) and LVMI (p = 0.000) but did not show a significant relationship with RWT (p = 0.561). Multiple regression analyses confirmed that the linear relationship between zinc and LVM and LVMI remained inversely significant. The present study revealed that serum zinc levels were significantly decreased in the LVH patients, especially in the eccentric LVH and concentric LVH patients. Furthermore, zinc levels were significantly inversely correlated with LVM and LVMI.

  2. Zinc Bioavailability from Phytate-Rich Foods and Zinc Supplements. Modeling the Effects of Food Components with Oxygen, Nitrogen, and Sulfur Donor Ligands.

    PubMed

    Tang, Ning; Skibsted, Leif H

    2017-10-04

    Aqueous solubility of zinc phytate (K sp = (2.6 ± 0.2) × 10 -47 mol 7 /L 7 ), essential for zinc bioavailability from plant foods, was found to decrease with increasing temperature corresponding to ΔH dis of -301 ± 22 kJ/mol and ΔS dis of -1901 ± 72 J/(mol K). Binding of zinc to phytate was found to be exothermic for the stronger binding site and endothermic for the weaker binding site. The solubility of the slightly soluble zinc citrate and insoluble zinc phytate was found to be considerably enhanced by the food components with oxygen donor, nitrogen donor, and sulfur donor ligands. The driving force for the enhanced solubility is mainly due to the complex formation between zinc and the investigated food components rather than ligand exchange and ternary complex formation as revealed by quantum mechanical calculations and isothermal titration calorimetry. Histidine and citrate are promising ligands for improving zinc absorption from phytate-rich foods.

  3. Prognostic value of serum zinc levels in patients with acute HC/zinc chloride smoke inhalation

    PubMed Central

    Xie, Fei; Zhang, Xingang; Xie, Lixin

    2017-01-01

    Abstract Hexachloroethane (HC)/zinc chloride (ZnCl, smoke bomb) exposure in the military setting results in lung injury which is uncommon and has been rarely described in previous studies. The aim of this study is to investigate the correlation between the serum zinc in patients with HC/ZnCl smoke inhalation lung injury and disease severity. A total of 15 patients with HC/ZnCl-related conditions were recruited in this study. The serum zinc level and the pulmonary function tests and liver function tests including total lung capacity (TLC), forced vital capacity (FVC), forced expiratory pressure in 1 second (FEV1), alanine aminotransferase (ALT), and aspartate transaminase (AST) were analyzed. Eleven cases had mild clinical manifestations. Four cases rapidly developed features typical of severe adult respiratory distress syndrome. The level of serum zinc was increased, but FVC, FEV1, and TLC was decreased significantly in the moderate and severe cases. In addition, the serum zinc level correlated well with the TLC, FVC, and FEV1 (r = −0.587, −0.626, −0.617, respectively; P = .027, .017, .019, respectively). The 4 cases in moderate and severe group had delayed impairment of liver functions after the accident. This study suggested that the serum zinc level may be associated with the severity of lung and liver injuries after HC/ZnCl smoke inhalation. PMID:28953660

  4. Effect of oral zinc supplementation upon Taenia crassiceps murine cysticercosis.

    PubMed

    Fragoso, G; Lastra, M D; Aguilar, A E; Pastelin, R; Rosas, G; Meneses, G; Sciutto, E; Lamoyi, E

    2001-10-01

    The effect of zinc supplementation on Taenia crassiceps murine cysticercosis was studied in susceptible BALB/cAnN mice. Female offspring of mice supplemented with high zinc throughout gestation and lactation were intraperitoneally infected with T. crassiceps cysticerci. Offspring from nonsupplemented mothers were used as controls. Significantly fewer parasites were recovered from zinc-supplemented mice (Zsm) 30 days after infection. Increased resistance was not related to the IgG antibody response. At early stages of infection, T cells from Zsm proliferated to T. crassiceps antigens, whereas cells from control mice did not respond. Infection caused in both groups a decrease in CD3+ cell percentages, which was more pronounced in the controls, and paralleled by a decrease in CD8+ cells; CD3+ and CD8+ percentages returned to normal levels at later stages of infection. In contrast, the CD4+ subpopulation only decreased in control mice. Intracellular cytokine determinations indicate that zinc supplementation favored a stronger and persistent type-1 T cell response in cysticerci-infected mice, which probably participates in the observed increased resistance.

  5. Is There a Relationship between Zinc and the Peculiar Comorbidities of Down Syndrome?

    ERIC Educational Resources Information Center

    Romano, Corrado; Pettinato, Rosa; Ragusa, Letizia; Barone, Concetta; Alberti, Antonino; Failla, Pinella

    2002-01-01

    A comparison was made between a range of clinical and biochemical variables and zinc levels in 120 individuals with Down syndrome. No significant differences were found between the normal-zinc and low-zinc groups, except for IgG4 which was, unexpectedly, significantly decreased in the group with normal zinc levels. (Contains references.)…

  6. Zinc lozenges and the common cold: a meta-analysis comparing zinc acetate and zinc gluconate, and the role of zinc dosage.

    PubMed

    Hemilä, Harri

    2017-05-01

    To compare the efficacy of zinc acetate lozenges with zinc gluconate lozenges in common cold treatment and to examine the dose-dependency of the effect. Meta-analysis. Placebo-controlled zinc lozenge trials, in which the zinc dose was > 75 mg/day. The pooled effect of zinc lozenges on common cold duration was calculated by using inverse-variance random-effects method. Seven randomised trials with 575 participants with naturally acquired common colds. Duration of the common cold. The mean common cold duration was 33% (95% CI 21% to 45%) shorter for the zinc groups of the seven included trials. Three trials that used lozenges composed of zinc acetate found that colds were shortened by 40% and four trials that used zinc gluconate by 28%. The difference between the two salts was not significant: 12 percentage points (95% CI: -12 to + 36). Five trials used zinc doses of 80-92 mg/day, common cold duration was reduced by 33%, and two trials used zinc doses of 192-207 mg/day and found an effect of 35%. The difference between the high-dose and low-dose zinc trials was not significant: 2 percentage points (95% CI: -29 to + 32). Properly composed zinc gluconate lozenges may be as effective as zinc acetate lozenges. There is no evidence that zinc doses over 100 mg/day might lead to greater efficacy in the treatment of the common cold. Common cold patients may be encouraged to try zinc lozenges for treating their colds. The optimal lozenge composition and dosage scheme need to be investigated further.

  7. Alterations of zinc homeostasis in response to Cryptococcus neoformans in a murine macrophage cell line.

    PubMed

    Dos Santos, Francine Melise; Piffer, Alícia Corbellini; Schneider, Rafael de Oliveira; Ribeiro, Nicole Sartori; Garcia, Ane Wichine Acosta; Schrank, Augusto; Kmetzsch, Lívia; Vainstein, Marilene Henning; Staats, Charley Christian

    2017-05-01

    To evaluate alterations of zinc homeostasis in macrophages exposed to Cryptococcus neoformans. Materials & methods: Using a fluorescent zinc probe-based flow cytometry and atomic absorption spectrometry, zinc levels were evaluated in J774.A1 cell lines exposed to C. neoformans H99 cells. The transcription profile of macrophage zinc related homeostasis genes - metallothioneins and zinc transporters (ZnTs) of the SLC30 and SLC39 (Zrt-Irt-protein) families - was analyzed by quantitative PCR. Macrophage intracellular labile zinc levels decreased following exposure to C. neoformans. A significant decrease in transcription levels was detected in specific ZnTs from both the Zrt-Irt-protein and ZnT families, especially 24 h after infection. These findings suggest that macrophages may exhibit zinc depletion in response to C. neoformans infection.

  8. The linoleic acid: dihomo-y-linolenic acid ratio (LA:DGLA)— an emerging biomarker of Zn status

    USDA-ARS?s Scientific Manuscript database

    Zinc (Zn) deficiency is a common aliment predicted to affect 17% of the world’s population. Zinc is a vital micronutrient used for over 300 enzymatic reactions and multiple biochemical and structural processes in the body. Although whole blood, plasma, and urine zinc decrease in severe zinc deficien...

  9. A mixed valence zinc dithiolene system with spectator metal and reactor ligands.

    PubMed

    Ratvasky, Stephen C; Mogesa, Benjamin; van Stipdonk, Michael J; Basu, Partha

    2016-08-16

    Neutral complexes of zinc with N,N'-diisopropylpiperazine-2,3-dithione ( i Pr 2 Dt 0 ) and N,N'-dimethylpiperazine-2,3-dithione (Me 2 Dt 0 ) with chloride or maleonitriledithiolate (mnt 2- ) as coligands have been synthesized and characterized. The molecular structures of these zinc complexes have been determined using single crystal X-ray diffractometry. Complexes recrystallize in monoclinic P type systems with zinc adopting a distorted tetrahedral geometry. Two zinc complexes with mixed-valent dithiolene ligands exhibit ligand-to-ligand charge transfer bands. Optimized geometries, molecular vibrations and electronic structures of charge-transfer complexes were calculated using density functional theory (B3LYP/6-311G+(d,p) level). Redox orbitals are shown to be almost exclusively ligand in nature, with a HOMO based heavily on the electron-rich maleonitriledithiolate ligand, and a LUMO comprised mostly of the electron-deficient dithione ligand. Charge transfer is thus believed to proceed from dithiolate HOMO to dithione LUMO, showing ligand-to-ligand redox interplay across a d 10 metal.

  10. Zinc oxide nanoparticles as a substitute for zinc oxide or colistin sulfate: Effects on growth, serum enzymes, zinc deposition, intestinal morphology and epithelial barrier in weaned piglets

    PubMed Central

    Zhang, Ligen; Su, Weipeng; Ying, Zhixiong; He, Jintian; Zhang, Lili; Zhong, Xiang; Wang, Tian

    2017-01-01

    The objective of this study was to evaluate effects of zinc oxide nanoparticles (nano-ZnOs) as a substitute for colistin sulfate (CS) and/or zinc oxide (ZnO) on growth performance, serum enzymes, zinc deposition, intestinal morphology and epithelial barrier in weaned piglets. A total of 216 crossbred Duroc×(Landrace×Yorkshire) piglets weaned at 23 days were randomly assigned into 3 groups, which were fed with basal diets supplemented with 20 mg/kg CS (CS group), 20mg/kg CS+3000 mg/kg ZnO (CS+ZnO group), and 1200 mg/kg nano-ZnOs (nano-ZnO group) for 14 days. Results indicated that compared to CS group, supplementation of 1200 mg/kg nano-ZnOs (about 30 nm) significantly increased final body weight and average daily gain, and 3000 mg/kg ZnO plus colistin sulfate significantly increased average daily gain and decreased diarrhea rate in weaned piglets. There was no significant difference in growth performance and diarrhea rate between nano-ZnO and CS+ZnO groups. Supplementation of nano-ZnOs did not affect serum enzymes (glutamic oxalacetic transaminase, glutamic-pyruvic transaminase, and lactate dehydrogenase), but significantly increased plasma and tissue zinc concentrations (liver, tibia), improved intestinal morphology (increased duodenal and ileal villus length, crypt depth, and villus surface), enhanced mRNA expression of ZO-1 in ileal mucosa, and significantly decreased diamine oxidase activity in plasma, total aerobic bacterial population in MLN as compared to CS group. Effects of nano-ZnOs on serum enzymes, intestinal morphology, and mRNA expressions of tight junction were similar to those of high dietary ZnO plus colistin sulfate, while nano-ZnOs significantly reduced zinc concentrations of liver, tibia, and feces, and decreased total aerobic bacterial population in MLN as compared to CS+ZnO group. These results suggested that nano-ZnOs (1200 mg/kg) might be used as a substitute for colistin sulfate and high dietary ZnO in weaned piglets. PMID:28704517

  11. Zinc oxide nanoparticles as a substitute for zinc oxide or colistin sulfate: Effects on growth, serum enzymes, zinc deposition, intestinal morphology and epithelial barrier in weaned piglets.

    PubMed

    Wang, Chao; Zhang, Ligen; Su, Weipeng; Ying, Zhixiong; He, Jintian; Zhang, Lili; Zhong, Xiang; Wang, Tian

    2017-01-01

    The objective of this study was to evaluate effects of zinc oxide nanoparticles (nano-ZnOs) as a substitute for colistin sulfate (CS) and/or zinc oxide (ZnO) on growth performance, serum enzymes, zinc deposition, intestinal morphology and epithelial barrier in weaned piglets. A total of 216 crossbred Duroc×(Landrace×Yorkshire) piglets weaned at 23 days were randomly assigned into 3 groups, which were fed with basal diets supplemented with 20 mg/kg CS (CS group), 20mg/kg CS+3000 mg/kg ZnO (CS+ZnO group), and 1200 mg/kg nano-ZnOs (nano-ZnO group) for 14 days. Results indicated that compared to CS group, supplementation of 1200 mg/kg nano-ZnOs (about 30 nm) significantly increased final body weight and average daily gain, and 3000 mg/kg ZnO plus colistin sulfate significantly increased average daily gain and decreased diarrhea rate in weaned piglets. There was no significant difference in growth performance and diarrhea rate between nano-ZnO and CS+ZnO groups. Supplementation of nano-ZnOs did not affect serum enzymes (glutamic oxalacetic transaminase, glutamic-pyruvic transaminase, and lactate dehydrogenase), but significantly increased plasma and tissue zinc concentrations (liver, tibia), improved intestinal morphology (increased duodenal and ileal villus length, crypt depth, and villus surface), enhanced mRNA expression of ZO-1 in ileal mucosa, and significantly decreased diamine oxidase activity in plasma, total aerobic bacterial population in MLN as compared to CS group. Effects of nano-ZnOs on serum enzymes, intestinal morphology, and mRNA expressions of tight junction were similar to those of high dietary ZnO plus colistin sulfate, while nano-ZnOs significantly reduced zinc concentrations of liver, tibia, and feces, and decreased total aerobic bacterial population in MLN as compared to CS+ZnO group. These results suggested that nano-ZnOs (1200 mg/kg) might be used as a substitute for colistin sulfate and high dietary ZnO in weaned piglets.

  12. The Effects of Supplemental Zinc and Honey on Wound Healing in Rats

    PubMed Central

    Sazegar, Ghasem; Seyed Reza, Attarzadeh Hosseini; Behravan, Effat

    2011-01-01

    Objective(s) Clinicians have long been searching for ways to obtain "super normal" wound healing. Zinc supplementation improves the healing of open wounds. Honey can improve the wound healing with its antibacterial properties. Giving supplemental zinc to normal rats can increase the wound tensile strength. This work is to study the concurrent effects of zinc and honey in wound healing of normal rats. Materials and Methods One hundred and seventy two young rats were randomly divided into four groups: control, zinc-supplement, applied honey, zinc-supplement and applied honey. Two areas of skin about 4 cm² were excised. The wound area was measured every 2 days. After 3 weeks, all animals were killed and tensile strength of wounds, zinc concentration of blood and histological improvement of wounds were evaluated. The results were analyzed using two-way ANOVA and the mean differences were tested. Results It was found that honey could inhibit the bacterial growth in skin excisions. The tensile strength was increased significantly in the second to fourth groups at 21st day (P< 0.001). Also there was a significant increase in tensile strength at the same time in the fourth group. The results of the histological study showed a considerable increase in the collagen fibers, re-epithelialization and re-vascularization in the second to fourth groups. Conclusion The results of the present study indicate that zinc sulfate could retard re-epithelialization, but when used with natural honey (administered topically) it could have influent wound healing in non-zinc-deficient subjects as well. PMID:23493488

  13. Compromised zinc status of experimental rats as a consequence of prolonged iron & calcium supplementation.

    PubMed

    Jayalakshmi, S; Platel, Kalpana

    2016-02-01

    Iron supplementation is usually given to pregnant and lactating women who may also have marginal deficiency of zinc. The negative impact of supplemental iron and calcium on zinc status is a cause of concern. The present investigation was undertaken to examine the effect of inclusion of iron and calcium in the diet at supplementary levels on zinc status of experimental rats. Groups of experimental rats were maintained on diets supplemented with iron (Molar ratio - Zn:Fe 1:30) and calcium (Molar ratio - Zn:Ca 1:667) both individually and in combination for six weeks. Zinc status of these rats was assessed by determining zinc concentration in circulation and in organs, and the activities of zinc containing enzymes in serum and liver. The zinc status of experimental rats receiving supplemental levels of iron and calcium was significantly compromised. Zinc concentration in serum, kidney, spleen and liver was reduced significantly by both these minerals. Six weeks of supplementation of iron and calcium individually, significantly reduced the activity of liver and serum superoxide dismutase and alkaline phosphatase. Activity of liver alcohol dehydrogenase was lowered in calcium supplemented group and in calcium + iron supplemented group, while that of carbonic anhydrase was significantly reduced by iron, calcium and their combination. Supplemental levels of iron and calcium, both individually and in combination, significantly compromised the zinc status of experimental rats. This negative effect of these two minerals was more prominent when these were supplemented for a period of six weeks.

  14. Zinc in an ultraoligotrophic lake food web.

    PubMed

    Montañez, Juan Cruz; Arribére, María A; Rizzo, Andrea; Arcagni, Marina; Campbell, Linda; Ribeiro Guevara, Sergio

    2018-06-01

    Zinc (Zn) bioaccumulation and trophic transfer were analyzed in the food web of Lake Nahuel Huapi, a deep, unpolluted ultraoligotrophic system in North Patagonia. Benthic macroinvertebrates, plankton, and native and introduced fish were collected at three sites. The effect of pyroclastic inputs on Zn levels in lacustrine food webs was assessed by studying the impact of the eruption of Puyehue-Cordón Caulle volcanic complex (PCCVC) in 2011, by performing three sampling campaigns immediately before and after the PCCVC eruption, and after 2 years of recovery of the ecosystem. Zinc trophodynamics in L. Nahuel Huapi food web was assessed using nitrogen stable isotopes (δ 15 N). There was no significant increase of Zn concentrations ([Zn]) in L. Nahuel Huapi biota after the PCCVC eruption, despite the evidence of [Zn] increase in lake water that could be associated with volcanic ash leaching. The organisms studied exhibited [Zn] above the threshold level considered for dietary deficiency, regulating Zn adequately even under a catastrophic situations like PCCVC 2011 eruption. Zinc concentrations exhibited a biodilution pattern in the lake's food web. To the best of our knowledge, present research is the first report of Zn biodilution in lacustrine systems, and the first to study Zn transfer in a freshwater food web including both pelagic and benthic compartments.

  15. Facilitated citrate-dependent iron translocation increases rice endosperm iron and zinc concentrations.

    PubMed

    Wu, Ting-Ying; Gruissem, Wilhelm; Bhullar, Navreet K

    2018-05-01

    Iron deficiency affects one third of the world population. Most iron biofortification strategies have focused on genes involved in iron uptake and storage but facilitating internal long-distance iron translocation has been understudied for increasing grain iron concentrations. Citrate is a primary iron chelator, and the transporter FERRIC REDUCTASE DEFECTIVE 3 (FRD3) loads citrate into the xylem. We have expressed AtFRD3 in combination with AtNAS1 (NICOTIANAMINE SYNTHASE 1) and PvFER (FERRITIN) or with PvFER alone to facilitate long-distance iron transport together with efficient iron uptake and storage in the rice endosperm. The citrate and iron concentrations in the xylem sap of transgenic plants increased two-fold compared to control plants. Iron and zinc levels increased significantly in polished and unpolished rice grains to more than 70% of the recommended estimated average requirement (EAR) for iron and 140% of the recommended EAR for zinc in polished rice grains. Furthermore, the transformed lines showed normal phenotypic growth, were tolerant to iron deficiency and aluminum toxicity, and had grain cadmium levels similar to control plants. Together, our results demonstrate that deploying FRD for iron biofortification has no obvious anti-nutritive effects and should be considered as an effective strategy for reducing human iron deficiency anemia. Copyright © 2018 The Authors. Published by Elsevier B.V. All rights reserved.

  16. Transfers and transformations of zinc in flow-through wetland microcosms.

    PubMed

    Gillespie, W B; Hawkins, W B; Rodgers, J H; Cano, M L; Dorn, P B

    1999-06-01

    Two microcosm-scale wetlands (570-liter containers) were integratively designed and constructed to investigate transfers and transformations of zinc associated with an aqueous matrix, and to provide future design parameters for pilot-scale constructed wetlands. The fundamental design of these wetland microcosms was based on biogeochemical principles regulating fate and transformations of zinc (pH, redox, etc.). Each wetland consisted of a 45-cm hydrosoil depth inundated with 25 cm of water, and planted with Scirpus californicus. Zinc ( approximately 2 mg/liter) as ZnCl2 was amended to each wetland for 62 days. Individual wetland hydraulic retention times (HRT) were approximately 24 h. Total recoverable zinc was measured daily in microcosm inflow and outflows, and zinc concentrations in hydrosoil and S. californicus tissue were measured pre- and post-treatment. Ceriodaphnia dubia and Pimephales promelas7-day aqueous toxicity tests were performed on wetland inflows and outflows, and Hyalella azteca whole sediment toxicity tests (10-day) were performed pre- and post-treatment. Approximately 75% of total recoverable zinc was transferred from the water column. Toxicity decreased from inflow to outflow based on 7-day C. dubia tests, and survival of H. azteca in hydrosoil was >80%. Data illustrate the ability of integratively designed wetlands to transfer and sequester zinc from the water column while concomitantly decreasing associated toxicity. Copyright 1999 Academic Press.

  17. [Prevalence of iron deficiency].

    PubMed

    Dupont, C

    2017-05-01

    Studies of prévalence in iron deficiency separate iron depletion (defined as decreased blood ferritin) and iron deficiency anemia (defined as blood decrease in both ferritin and hemoglobin). In Europe, most studies are outdated. Prevalence of iron depletion varies from 7 to 18 % and 24 to 36% in toddlers and adolescents, respectively. Prevalence of iron deficiency anemia varies from 2 to 8.5% and 7 to 10% in toddlers and adolescents. In French speaking African countries, Demography Health Surveys show that 80% of children aged 0 to 2 years are anemic, severely for 5 to 9% of them. © 2017 Elsevier Masson SAS. Tous droits réservés.

  18. Zinc Enzymes.

    ERIC Educational Resources Information Center

    Bertini, I.; And Others

    1985-01-01

    Discusses the role of zinc in various enzymes concerned with hydration, hydrolysis, and redox reactions. The binding of zinc to protein residues, properties of noncatalytic zinc(II) and catalytic zinc, and the reactions catalyzed by zinc are among the topics considered. (JN)

  19. A Moderate Zinc Deficiency Does Not Alter Lipid and Fatty Acid Composition in the Liver of Weanling Rats Fed Diets Rich in Cocoa Butter or Safflower Oil

    PubMed Central

    Egenolf, Jennifer

    2017-01-01

    The aim of the study was to examine whether a moderate zinc deficiency alters hepatic lipid composition. Male weanling rats, assigned to five groups (8 animals each), were fed low-carbohydrate high-fat diets supplemented with 7 or 50 mg Zn/kg (LZ or HZ) and 22% cocoa butter (CB) or 22% safflower oil (SF) for four weeks. One group each had free access to the LZ-CB and LZ-SF diets, one group each was restrictedly fed the HZ-CB and HZ-SF diets in matching amounts, and one group had free access to the HZ-SF diet (ad libitum control). The rats fed the LZ diets had significantly lower energy intakes and final body weights than the ad libitum control group, and lower plasma and femur Zn concentrations than the animals consuming the HZ diets. Hepatic cholesterol, triacylglycerol and phospholipid concentrations, and fatty acid composition of hepatic triacylglycerols and phospholipids did not significantly differ between the LZ and their respective HZ groups, but were greatly affected by dietary fat source. In conclusion, the moderate Zn deficiency did not significantly alter liver lipid concentrations and fatty acid composition. PMID:28465837

  20. A Moderate Zinc Deficiency Does Not Alter Lipid and Fatty Acid Composition in the Liver of Weanling Rats Fed Diets Rich in Cocoa Butter or Safflower Oil.

    PubMed

    Weigand, Edgar; Egenolf, Jennifer

    2017-01-01

    The aim of the study was to examine whether a moderate zinc deficiency alters hepatic lipid composition. Male weanling rats, assigned to five groups (8 animals each), were fed low-carbohydrate high-fat diets supplemented with 7 or 50 mg Zn/kg (LZ or HZ) and 22% cocoa butter (CB) or 22% safflower oil (SF) for four weeks. One group each had free access to the LZ-CB and LZ-SF diets, one group each was restrictedly fed the HZ-CB and HZ-SF diets in matching amounts, and one group had free access to the HZ-SF diet (ad libitum control). The rats fed the LZ diets had significantly lower energy intakes and final body weights than the ad libitum control group, and lower plasma and femur Zn concentrations than the animals consuming the HZ diets. Hepatic cholesterol, triacylglycerol and phospholipid concentrations, and fatty acid composition of hepatic triacylglycerols and phospholipids did not significantly differ between the LZ and their respective HZ groups, but were greatly affected by dietary fat source. In conclusion, the moderate Zn deficiency did not significantly alter liver lipid concentrations and fatty acid composition.

  1. Laboratory evaluation of borate/amine/zinc formulations for fungal decay protection

    Treesearch

    George C. Chen; Rebecca E. Ibach

    2010-01-01

    The goals of this study were to evaluate borate/amine/zinc formulations in wood for fungal decay protection as well as the permanence of zinc and boron in wood. Wood treated with each of four formulations of borate/amine/zinc prevented or decreased fungal degradation after a 12-week AWPA Standard soil-block test. For non-leached specimens, wood treated with borax/amine...

  2. Zinc regulates iNOS-derived nitric oxide formation in endothelial cells.

    PubMed

    Cortese-Krott, Miriam M; Kulakov, Larissa; Opländer, Christian; Kolb-Bachofen, Victoria; Kröncke, Klaus-D; Suschek, Christoph V

    2014-01-01

    Aberrant production of nitric oxide (NO) by inducible NO synthase (iNOS) has been implicated in the pathogenesis of endothelial dysfunction and vascular disease. Mechanisms responsible for the fine-tuning of iNOS activity in inflammation are still not fully understood. Zinc is an important structural element of NOS enzymes and is known to inhibit its catalytical activity. In this study we aimed to investigate the effects of zinc on iNOS activity and expression in endothelial cells. We found that zinc down-regulated the expression of iNOS (mRNA+protein) and decreased cytokine-mediated activation of the iNOS promoter. Zinc-mediated regulation of iNOS expression was due to inhibition of NF-κB transactivation activity, as determined by a decrease in both NF-κB-driven luciferase reporter activity and expression of NF-κB target genes, including cyclooxygenase 2 and IL-1β. However, zinc did not affect NF-κB translocation into the nucleus, as assessed by Western blot analysis of nuclear and cytoplasmic fractions. Taken together our results demonstrate that zinc limits iNOS-derived high output NO production in endothelial cells by inhibiting NF-κB-dependent iNOS expression, pointing to a role of zinc as a regulator of iNOS activity in inflammation.

  3. Zinc regulates iNOS-derived nitric oxide formation in endothelial cells

    PubMed Central

    Cortese-Krott, Miriam M.; Kulakov, Larissa; Opländer, Christian; Kolb-Bachofen, Victoria; Kröncke, Klaus-D.; Suschek, Christoph V.

    2014-01-01

    Aberrant production of nitric oxide (NO) by inducible NO synthase (iNOS) has been implicated in the pathogenesis of endothelial dysfunction and vascular disease. Mechanisms responsible for the fine-tuning of iNOS activity in inflammation are still not fully understood. Zinc is an important structural element of NOS enzymes and is known to inhibit its catalytical activity. In this study we aimed to investigate the effects of zinc on iNOS activity and expression in endothelial cells. We found that zinc down-regulated the expression of iNOS (mRNA+protein) and decreased cytokine-mediated activation of the iNOS promoter. Zinc-mediated regulation of iNOS expression was due to inhibition of NF-κB transactivation activity, as determined by a decrease in both NF-κB-driven luciferase reporter activity and expression of NF-κB target genes, including cyclooxygenase 2 and IL-1β. However, zinc did not affect NF-κB translocation into the nucleus, as assessed by Western blot analysis of nuclear and cytoplasmic fractions. Taken together our results demonstrate that zinc limits iNOS-derived high output NO production in endothelial cells by inhibiting NF-κB-dependent iNOS expression, pointing to a role of zinc as a regulator of iNOS activity in inflammation. PMID:25180171

  4. Zinc

    MedlinePlus

    ... Using toothpastes containing zinc, with or without an antibacterial agent, appears to prevent plaque and gingivitis. Some ... is some evidence that zinc has some antiviral activity against the herpes virus. Low zinc levels can ...

  5. A Decrease in Glomerular Endothelial Cells and Endothelial-mesenchymal Transition during Glomerulosclerosis in the Tensin2-deficient Mice (ICGN strain).

    PubMed

    Kato, Takashi; Mizuno, Shinya; Ito, Akihiko

    2014-01-01

    The ICR-derived glomerulonephritis (ICGN) mouse is a unique model of nephrotic syndrome, and albuminuria becomes evident in a neonatal stage, due to a genetic mutation of tensin2. We previously provided evidence that an apparent decrease in nephrin, caused by tensin2-deficiencient states, leads to podocytopathy, albuminuria and eventually, chronic renal failure. In general, glomerular endothelial cells (ECs) function as a barrier through tight attachment of glomerular basement membrane to podocytes, while decreased ECs can worsen renal failure. Nevertheless, it is still unknown whether glomerular ECs are altered under the tensin-2-deficient states during the manifestation of chronic renal failure. Herein, we examined the changes of glomerular ECs, with focus on the expression of PECAM-1 and VE-cadherin (EC-specific markers), or of α-SMA (myofibroblast marker) in this mouse model by histological methods. Compared with the non-nephrotic (+/nep) mice, the nephrotic (nep/nep) mice exhibited the reduced expression of PECAM-1, or of VE-cadherin, in glomerular area. Notably, some glomerular ECs showed the positive stainings for both PECAM-1 and α-SMA, suggesting endothelial-to-mesenchymal transition (EndoMT) during progression of glomerular sclerosis. This is the first report showing that a decrease in glomerular ECs, at least in part, via EndoMT is involved in tensin2-deficient pathological conditions.

  6. Field evidence of cadmium phytoavailability decreased effectively by rape straw and/or red mud with zinc sulphate in a Cd-contaminated calcareous soil.

    PubMed

    Li, Bo; Yang, Junxing; Wei, Dongpu; Chen, Shibao; Li, Jumei; Ma, Yibing

    2014-01-01

    To reduce Cd phytoavailability in calcareous soils, the effects of soil amendments of red mud, rape straw, and corn straw in combination with zinc fertilization on Cd extractability and phytoavailability to spinach, tomato, Chinese cabbage and radish were investigated in a calcareous soil with added Cd at 1.5 mg kg-1. The results showed that water soluble and exchangeable Cd in soils was significantly decreased by the amendments themselves from 26% to 70%, which resulted in marked decrease by approximately from 34% to 77% in Cd concentration in vegetables. The amendments plus Zn fertilization further decreased the Cd concentration in vegetables. Also cruciferous rape straw was more effective than gramineous corn straw. In all treatments, rape straw plus red mud combined with Zn fertilization was most effective in decreasing Cd phytoavailability in soils, and it is potential to be an efficient and cost-effective measure to ensure food safety for vegetable production in mildly Cd-contaminated calcareous soils.

  7. Field Evidence of Cadmium Phytoavailability Decreased Effectively by Rape Straw and/or Red Mud with Zinc Sulphate in a Cd-Contaminated Calcareous Soil

    PubMed Central

    Li, Bo; Yang, Junxing; Wei, Dongpu; Chen, Shibao; Li, Jumei; Ma, Yibing

    2014-01-01

    To reduce Cd phytoavailability in calcareous soils, the effects of soil amendments of red mud, rape straw, and corn straw in combination with zinc fertilization on Cd extractability and phytoavailability to spinach, tomato, Chinese cabbage and radish were investigated in a calcareous soil with added Cd at 1.5 mg kg−1. The results showed that water soluble and exchangeable Cd in soils was significantly decreased by the amendments themselves from 26% to 70%, which resulted in marked decrease by approximately from 34% to 77% in Cd concentration in vegetables. The amendments plus Zn fertilization further decreased the Cd concentration in vegetables. Also cruciferous rape straw was more effective than gramineous corn straw. In all treatments, rape straw plus red mud combined with Zn fertilization was most effective in decreasing Cd phytoavailability in soils, and it is potential to be an efficient and cost-effective measure to ensure food safety for vegetable production in mildly Cd-contaminated calcareous soils. PMID:25303439

  8. Micronutrients and kelp cultures: Evidence for cobalt and manganese deficiency in Southern California deep seawater

    USGS Publications Warehouse

    Kuwabara, J.S.

    1982-01-01

    It has been suggested that naturally occurring copper and zinc concentrations in deep seawater are toxic to marine organisms when the free ion forms are overabundant. The effects of micronutrients on the growth of gametophytes of the ecologically and commercially significant giant kelp (Macrocystis pyrifera) were studied in defined media. The results indicate that toxic copper and zinc ion concentrations as well as cobalt and manganese deficiencies may be among the factors controlling the growth of marine organisms in nature. Copyright ?? 1982 AAAS.

  9. Maternal diets, nutritional status, and zinc in contemporary Mexican infants' teeth: Implications for reconstructing paleodiets.

    PubMed

    Dolphin, Alexis E; Goodman, Alan H

    2009-11-01

    Despite attempts to use zinc (Zn) concentrations in hard tissues to comment upon the degree of carnivory in past populations, zinc has yielded inconsistent trophic level effects. The question of what, if anything, zinc in human enamel reveals regarding past diets is the focus of this research. We test whether the zinc content of deciduous tooth enamel from contemporary Mexican infants varies by maternal dietary variables such as zinc intake, proportion of animal products consumed, and dietary components that are known to impact zinc absorption. Deciduous teeth were collected from former participants in a longitudinal study of maternal and infant diet and function in highland Mexico. The Zn/Ca ratios of both prenatal and postnatal regions of 37 anterior teeth representing 26 individuals were assessed via laser ablation-inductively coupled plasma-mass spectrometry. Maternal dietary data collected during lactation were not correlated with zinc levels in the early postnatal enamel of infants' teeth, which were forming at the same time. In the case of prenatal enamel, zinc values were correlated with the consumption of foods known to influence Zn bioavailability, most notably tortillas (P = 0.008; r = 0.510), but not with meat consumption. Unexpectedly, women who consumed diets with poor zinc bioavailability during pregnancy gave birth to infants whose prenatal enamel demonstrated the highest Zn/Ca ratios, possibly due to enhanced zinc absorption during pregnancy for those mothers suffering most from long-term micronutrient deficiency. These results would suggest that zinc is not a reliable trophic level indicator.

  10. Comparative studies on acid leaching of zinc waste materials

    NASA Astrophysics Data System (ADS)

    Rudnik, Ewa; Włoch, Grzegorz; Szatan, Leszek

    2017-11-01

    Three industrial waste materials were characterized in terms of their elemental and phase compositions, leaching behaviour in 10% sulfuric acid solution as well as leaching thermal effects. Slag from melting of mixed metallic scrap contained about 50% Zn and 10% Pb. It consisted mainly of various oxides and oxy-chlorides of metals. Zinc spray metallizing dust contained about 77% Zn in form of zinc and/or zinc-iron oxides, zinc metal and Zn-Fe intermetallic. Zinc ash from hot dip galvanizing was a mixture of zinc oxide, metallic zinc and zinc hydroxide chloride and contained about 80% Zn. Dissolution efficiency of zinc from the first material was 80% (independently on the solid to liquid ratio, 50-150 kg/m3), while decrease of the efficacy from 80% to 60% with increased solid to liquid ratio for the two remaining materials was observed. Both increase in the temperature (20 °C to 35 °C) and agitation rate (300 rpm to 900 rpm) did not improve seriously the leaching results. In all cases, transfer of zinc ions to the leachate was accompanied by different levels of solution contamination, depending on the type of the waste. Leaching of the materials was exothermic with the similar reaction heats for two high oxide-type products (slag, zinc ash) and higher values for the spray metallizing dust.

  11. The Effect of Low Dose Iron and Zinc Intake on Child Micronutrient Status and Development during the First 1000 Days of Life: A Systematic Review and Meta-Analysis

    PubMed Central

    Petry, Nicolai; Olofin, Ibironke; Boy, Erick; Donahue Angel, Moira; Rohner, Fabian

    2016-01-01

    Adequate supply of micronutrients during the first 1000 days is essential for normal development and healthy life. We aimed to investigate if interventions administering dietary doses up to the recommended nutrient intake (RNI) of iron and zinc within the window from conception to age 2 years have the potential to influence nutritional status and development of