Zinc chloride, zinc oxide, hydrochloric acid exposure and dental erosion in a zinc galvanizing plant in the Netherlands.
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Air Pollutants↗
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Results for “zinc”
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Zinc bioavailability in tetrabasic zinc chloride and the dietary zinc requirement of young chicks fed a soy concentrate diet.
Three chick assays were conducted to determine a bioavailable Zn requirement and to establish a Zn relative bioavailability (RBV) value for tetrabasic Zn chloride [TBZC, i.e., Zn5Cl2(OH)8]. In Assay 1, 8-d-old chicks were fed a Zn-deficient soy concentrate diet (8.8 mg/kg bioavailable Zn) supplemented with 0, 5.81, 10.81, 15.10, and 20.25 mg Zn/kg from ZnSO4.7H2O for 14 d to establish a linear response range and estimate a bioavailable Zn requirement. Weight gain of chicks increased linearly (P < 0.01; r2 = 0.99) when the first three levels of Zn were fed. Broken-line analysis of the weight gain data indicated a bioavailable Zn requirement of 22.4 mg/kg. In Assay 2, RBV of Zn in TBZC was determined by multiple-linear regression slope-ratio methodology. The Zn-deficient basal diet was supplemented with 0, 5.81, and 10.81 mg Zn/kg from ZnSO4.7H2O to produce a linear growth response as determined in Assay 1. The same basal diet was supplemented with 5.38 and 10.81 mg Zn/kg from TBZC. The RBV of Zn in TBZC was found to be 102%, which was not different (P > 0.10) from 100%. A third assay was conducted as described for Assay 2, and the RBV of Zn in TBZC was 111%, which was not different from 100%. In summary, the RBV of Zn in TBZC was not different from that of ZnSO4.7H2O, and the minimal bioavailable Zn requirement for chicks 1 to 3 wk of age fed a soy concentrate diet was estimated at 22.4 mg/kg.
Animal Feed↗
Ruminal distribution of zinc in steers fed a polysaccharide-zinc complex or zinc oxide.
Six Holstein steers (initial BW 335 kg) were used in a replicated 3 x 3 Latin square design to study the distribution of Zn in ruminal contents from a conventional Zn source (ZnO) or Zn sequestered to a polysaccharide (PC-Zn). Treatments consisted of a basal diet (no Zn supplementation) and the basal diet supplemented with Zn from either PC-Zn or ZnO. Steers were provided with 208, 920, or 896 mg of Zn/d from basal, PC-Zn, or ZnO, respectively. On collection day, steers were dosed with 800 mg of Zn from each Zn supplement and whole ruminal contents (WRC) were sampled at 1, 2, 4, 6, and 8 h postdosing. The cell-free (soluble) Zn concentrations in steers fed the PC-Zn or ZnO supplements decreased (P < .05) rapidly after dosing. Mean Zn concentrations of the cell-free fraction were considerably lower than either microbial or particle fractions of WRC. Compared with ZnO, the PC-Zn source resulted in higher (P < .05) cell-free Zn at 1 and 2 h after dosing and higher (P < .05) Zn concentrations (micrograms/gram of DM) in the fluid- and particle-associated microbial and particle fractions. Compared with basal, fluid-associated microbial DM concentration tended to be higher (P < .10) at 6 and 8 h with PC-Zn and ZnO. Results indicate a rapid disappearance of Zn from the soluble fraction and a high concentration of Zn in the DM of the microbial and particle fractions of WRC. Furthermore, PC-Zn resulted in higher levels of Zn in all fractions of WRC, and Zn supplementation tended to increase microbial DM production at later sampling times.
Administration, Oral↗
Comparison of growth performance and zinc absorption, retention, and excretion in weanling pigs fed diets supplemented with zinc-polysaccharide or zinc oxide.
Fifty weanling crossbred pigs averaging 6.2 kg of initial BW and 21 d of age were used in a 5-wk experiment to evaluate lower dietary concentrations of an organic source of Zn as a Zn-polysaccharide (Zn-PS) compared with 2,000 ppm of inorganic Zn as ZnO, with growth performance, plasma concentrations of Zn and Cu, and Zn and Cu balance as the criteria. The pigs were fed individually in metabolism crates, and Zn and Cu balance were measured on individual pigs (10 replications per treatment) from d 22 to 26. The basal Phase 1 (d 0 to 14) and Phase 2 (d 14 to 35) diets contained 125 or 100 ppm added Zn as Zn sulfate, respectively, and met all nutrient requirements. Treatments were the basal Phase 1 and 2 diets supplemented with 0, 150, 300, or 450 ppm of Zn as Zn-PS or 2,000 ppm Zn as ZnO. Blood samples were collected from all pigs on d 7, 14, and 28. For pigs fed increasing Zn as Zn-PS, there were no linear or quadratic responses (P > or = 0.16) in ADG, ADFI, or G:F for Phases 1 or 2 or overall. For single degree of freedom treatment comparisons, Phase 1 ADG and G:F were greater (P < or = 0.05) for pigs fed 2,000 ppm Zn as ZnO than for pigs fed the control diet or the diet containing 150 ppm Zn as Zn-PS. For Phase 2 and overall, ADG and G:F for pigs fed the diets containing 300 or 450 ppm of Zn as Zn-PS did not differ (P > or = 0.29) from pigs fed the diet containing ZnO. Pigs fed the diet containing ZnO also had a greater Phase 2 (P < or = 0.10) and overall (P < or = 0.05) ADG and G:F than pigs fed the control diet. There were no differences (P > or = 0.46) in ADFI for any planned comparison. There were linear increases (P < 0.001) in the Zn excreted (mg/d) with increasing dietary Zn-PS. Pigs fed the diet containing ZnO absorbed, retained, and excreted more Zn (P < 0.001) than pigs fed the control diet or any of the diets containing Zn-PS. In conclusion, Phase 2 and overall growth performance by pigs fed diets containing 300 or 450 ppm Zn as Zn-PS did not differ from that of pigs fed 2,000 ppm Zn as ZnO; however, feeding 300 ppm Zn as Zn-PS decreased Zn excretion by 76% compared with feeding 2,000 ppm Zn as ZnO.
Analysis of Variance↗
STUDIES IN METABOLISM OF ZINC. 2. SERUM ZINC LEVELS AND URINARY ZINC EXCRETIONS IN SOUTH AFRICAN BANTU KWASHIORKOR PATIENTS.
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Africa↗
[Effect of a highly dispersed zinc powder and of zinc sulphate on endogenous zinc and iron levels in animal organs and tissues].
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Animals↗
[Oral replacement with zinc aspartate and zinc carbonate in zinc deficiency in rats].
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Administration, Oral↗
Influence of zinc-ligand mixtures on serum zinc levels in rats.
The influence of various salts, chelates, and other complexes of zinc given by gavage on serum zinc levels in rats was studied. Serum zinc concentrations were determined over 6 hr after administration of zinc sulfate at doses of 5, 10, 20, 50, and 100 mg of zinc/kg. Serum zinc levels following doses of zinc salts and complexes were compared with those after zinc sulfate. Phytic acid, aminopolycarboxylic acids (including edetate disodium), and penicillamine significantly suppressed increases in serum zinc concentration. Some natural amino acid-zinc sulfate mixtures (those with lysine, cysteine, glycine, and histidine) produced greater levels than the equivalent dose of zinc sulfate alone. Several thiocarboxylic acids, such as mercaptoacetic acid and thiosalicylic acid, also increased serum zinc concentrations. These observations form a basis for attempted modification of zinc absorption in other species.
Animals↗
The effect of dietary zinc deficiency on the mossy fiber zinc content of the rat hippocampus. A microbeam PIXE study. Particle Induced X-Ray Emission.
The effect of dietary zinc deficiency on the mossy fiber zinc content of the rat hippocampus was investigated using PIXE (Particle Induced X-Ray Emission) spectroscopy. Using the proton microbeam (60 X 60 microns), 2 mm line-scans were made on hippocampal sections and the data were expressed as absolute zinc concentrations. Values of 55 and 136 ppm (dry weight) were found for the mean background zinc level and the maximum mossy fiber zinc level, respectively, in animals fed a control diet containing 50 ppm zinc. Treatment of these animals with dithizone caused about 50% reduction in the maximum mossy fiber zinc level. Feeding a zinc-deficient diet for 28 days did not cause a decrease in the mossy fiber zinc level, however, feeding the zinc-deficient diet for 90 days reduced the maximum mossy fiber zinc level by about 30%. The results are discussed in relation to the behavioral abnormalities that have been observed in zinc-deficient animals.
Animals↗
Stimulatory effect of zinc on deoxyribonucleic acid synthesis in bone growth of newborn rats: enhancement with zinc and insulin-like growth factor-I.
The effect of zinc on in vitro deoxyribonucleic acid (DNA) synthesis activity in the femoral-diaphyseal and metaphyseal tissues of newborn rats was investigated to determine a role of zinc in bone growth. In vitro DNA synthesis was assayed in a reaction mixture containing the 100 g centrifugation supernatant, which includes the nucleus of bone cells, of bone issue homogenate with incorporation of [3H]-deoxythymidine 5'-triphosphate (dTTP). DNA synthesis activity in the femoral-diaphyseal and metaphyseal tissues of newborn rats was significantly raised with increasing age (1-21 days) after birth. The presence of dipicolinate (10(-3) M), a chelator of zinc, in the reaction mixture caused a significant decrease in DNA synthesis activity in the diaphyseal and metaphyseal tissues of newborn rats at 7 and 14 days after birth. The addition of zinc sulfate (10(-6) - 10(-4) M) resulted in a significant increase in DNA synthesis activity in the diaphyseal and metaphyseal tissues. When the diaphyseal and metaphyseal tissues of newborn rats at 7 days after birth were cultured for 24 hours in a serum-free medium containing either vehicle, zinc sulfate (10(-4) M), insulin-like growth factor-I (IGF-I; 10(-8) M) or transforming growth factor-beta (TGF-beta; 10(-10) M), bone DNA synthesis activity was significantly elevated. Culture with both zinc and IGF-I enhanced additively bone DNA synthesis activity. Such an effect was not seen in the case of zinc and TGF-beta. The effect of zinc, IGF-I, or zinc plus IGF-I in increasing bone DNA synthesis activity was completely prevented by culture with PD98059 (10(-5) M), an inhibitor of mitogen-activated protein (MAP) kinase. Also, the effect of zinc, TGF-beta. or zinc plus TGF-beta in elevating bone DNA synthesis activity was significantly inhibited by culture with staurosporine (10(-6) M), an inhibitor of protein kinase C. The present study demonstrates that zinc, like bone growth factors, has a stimulatory effect on bone DNA synthesis in newborn rats.
Age Factors↗
Influence of dietary zinc on di(2-ethylhexyl)phthalate-induced testicular atrophy and zinc depletion in adult rats.
Groups of 48 adult male F344 rats were maintained on synthetic diets containing 20 ppm (normal), 2 ppm (low), or 200 ppm (high) zinc. After 1 week of acclimation to the various diets, groups of 12 rats from each dietary regimen were gavaged for 13 consecutive days with 0.0 (vehicle), 0.33, 1.0, or 3.0 g/kg di(2-ethylhexyl)phthalate (DEHP). These were selected as relatively nontoxic, mildly toxic, and moderately toxic doses for producing testicular injury in adult male rats. At termination on the 14th day, body weight gain was reduced by 3.0 g/kg DEHP dose in the normal and low-zinc diet groups but not in the high-zinc diet group. The low-zinc diet alone reduced body weight gain, independent of DEHP treatment. DEHP had no perceptible effects on the weights of testis, seminal vesicle, prostate, or epididymis from rats maintained on normal- or high-zinc diets, but reduced the weights of all of these organs from animals on the low-zinc diet in a dose-dependent manner. Lactate dehydrogenase activity, total and free sulfhydryl contents, and zinc concentrations in testes were also reduced, and testicular degeneration was induced by DEHP in the low-zinc diet groups. In contrast, dose-dependent liver enlargement and hypolipidemia (reduction of serum cholesterol and triglyceride concentrations) were produced by equivalent doses of DEHP in all of the three zinc groups. The selectively enhanced susceptibility of adult male F344 rats on a zinc deficient diet to the gonadotoxic effects of DEHP supports the hypothesis that testicular zinc depletion is causally related to the ensuing testicular and accessory sex organ atrophies. Other biological effects of DEHP (e.g., hypolipidemia, hepatomegaly) appear to occur independent of zinc homeostasis.
Animals↗
Comparative in vitro oxygen radical scavenging ability of zinc methionine and selected zinc salts and antioxidants.
1. The concentration-dependent scavenging abilities of zinc DL-methionine, zinc sulfate, zinc gluconate, zinc picolinate and selected free radical scavengers, including superoxide dismutase (SOD), catalase, mannitol, allopurinol and DL-methionine, were examined against biochemically generated superoxide anion, hydroxyl radical and hypochlorite radical plus hypochlorous acid, by chemiluminescence and cytochrome c reduction. 2. Zinc methionine was the most effective of the zinc compounds that were tested. Following incubations with superoxide anion, hydroxyl radical, and hypochlorite radical-generating systems, in the presence of 50 microM zinc DL-methionine approximately 38%, 47% and 28% inhibition in reactive oxygen species generation was observed, respectively, compared to control groups. 3. The protective abilities of various zinc salts, as well as selected free radical scavengers and antioxidants were also assessed on phorbol ester (TPA)-induced lactate dehydrogenase (LDH) release from cultured PC-12 cells. Preincubation showed better protection than coincubation. Approximately 45% and 50% inhibition in TPA-induced LDH leakage was observed following preincubation with 50 microM zinc DL-methionine and 50 microM vitamin E succinate, respectively. Zinc DL-methionine exhibited better protection against LDH leakage than any other zinc salt tested. 4. The results indicate that zinc DL-methionine can attenuate the biochemical consequences of oxygen free radicals, and is comparable to other well-known antioxidants and free radical scavengers in the in vitro system that was employed.
Animals↗
Zinc levels in maternal milk: the influence of nutritional status with respect to zinc during the third trimester of pregnancy.
OBJECTIVE: To study the relationship between nutritional status with respect to zinc during the third trimester of pregnancy and levels of the same mineral in transition milk (days 13 and 14 of lactation) and mature milk (day 40 of lactation). DESIGN: Longitudinal study. SUBJECTS: A group of 57 healthy, lactating mothers aged between 18 and 35 y (27 +/- 3.7) whose pregnancy and labour were attended by the Department of Obstetrics and Gynaecology of Cuenca INSALUD Hospital, Spain. INTERVENTIONS: Zinc intake during the third trimester was determined by recording the consumption of foods over a five day period and by registering zinc provided by dietary supplements. Zinc levels in maternal serum during this stage of pregnancy, and in transition and mature milk, were determined by atomic absorption spectroscopy. RESULTS: During pregnancy all subjects showed zinc intakes lower than those recommended. Only one pregnant subject took a supplement that provided extra zinc (1 mg/d). Subjects with an intake of lower than 50% of that recommended (L) (43.9%) showed significantly lower serum and mature milk zinc levels than did those with higher intakes (H) (56.1%) [12.0 +/- 1.5 mumol/L and 28.7 +/- 6.2 mumol/L compared to 13.3 +/- 2.6 mumol/L and 33.1 +/- 8.0 mumol/L respectively]. 56% of L subjects and 28.6% of H subjects showed serum zinc levels of less than 12.2 mumol/L. 8% of L subjects and no H subjects showed less than 11.5 mumol/L of zinc in maternal milk. CONCLUSIONS: The diet conditions maternal serum zinc levels during pregnancy and those of milk during lactation. Though all subjects showed intakes clearly below those recommended, low levels in serum or milk were much rarer. These results support the idea that there is a need to reset the limits of normality for serum and milk zinc levels. Further work in this area may confirm that the present recommended intakes of zinc be modified.
Adolescent↗
Active-site zinc ligands and activated H2O of zinc enzymes.
The x-ray crystallographic structures of 12 zinc enzymes have been chosen as standards of reference to identify the ligands to the catalytic and structural zinc atoms of other members of their respective enzyme families. Universally, H2O is a ligand and critical component of the catalytically active zinc sites. In addition, three protein side chains bind to the catalytic zinc atom, whereas four protein ligands bind to the structural zinc atom. The geometry and coordination number of zinc can vary greatly to accommodate particular ligands. Zinc forms complexes with nitrogen and oxygen just as readily as with sulfur, and this is reflected in catalytic zinc sites having a binding frequency of His much greater than Glu greater than Asp = Cys, three of which bind to the metal atom. The systematic spacing between the ligands is striking. For all catalytic zinc sites except the coenzyme-dependent alcohol dehydrogenase, the first two ligands are separated by a "short-spacer" consisting of 1 to 3 amino acids. These ligands are separated from the third ligand by a "long spacer" of approximately 20 to approximately 120 amino acids. The spacer enables formation of a primary bidentate zinc complex, whereas the long spacer contributes flexibility to the coordination sphere, which can poise the zinc for catalysis as well as bring other catalytic and substrate binding groups into apposition with the active site. The H2O is activated by ionization, polarization, or poised for displacement. Collectively, the data imply that the preferred mechanistic pathway for activating the water--e.g., zinc hydroxide or Lewis acid catalysis--will be determined by the identity of the other three ligands and their spacing.
Alcohol Dehydrogenase↗
Identification of a mutation in SLC30A2 (ZnT-2) in women with low milk zinc concentration that results in transient neonatal zinc deficiency.
Breast milk normally contains adequate zinc to meet infant requirements up to six months of age; however, transient neonatal zinc deficiency has been documented in exclusively breastfed infants of women with low milk zinc concentration. This condition is not corrected by maternal zinc supplementation, supporting the speculation that it results from an inherited genetic condition. We identified a family in which two exclusively breast-fed infants developed zinc deficiency that was associated with low milk zinc concentration in both women. Sequencing of genomic DNA detected a mis-sense mutation (Ade-->Gua) that substitutes a conserved histidine at amino acid 54 with arginine (H54R) in SLC30A2 (ZnT-2) that is present in both affected subjects and several other siblings. Gene knockdown of SLC30A2 in mammary epithelial cells reduced zinc secretion, illustrating the role of ZnT-2 in zinc secretion from this cell type. Expression of the H54R mutant in human embryonic kidney-293 cells resulted in reduced zinc secretion as a consequence of perinuclear, aggresomal accumulation, whereas co-expression of the H54R mutant and wild-type ZnT-2 did not abrogate increased zinc secretion in cells overexpressing wild-type ZnT-2 alone. Together, these data provide evidence that low milk zinc concentration in some women is a consequence of a genetic disorder resulting from a mutation in SLC30A2 and can result in neonatal zinc deficiency if unrecognized. Further studies are needed to evaluate the incidence and penetrance of this mutation in the human population.
Amino Acid Sequence↗
Zinc in growth and development and spectrum of human zinc deficiency.
Growth retardation is seen in experimental animals as a result of severe dietary restriction of several essential trace elements. However, in humans, the effect of zinc deficiency is most pronounced. Growth failure and hypogonadism in males, related to a deficiency of zinc, have been recognized in many developing countries. A mild deficiency of zinc, affecting growth and development in children and adolescents, has been reported from developed countries as well. Zinc deficiency in humans may manifest as severe, moderate, or mild. The manifestations of severe zinc deficiency include bullous pustular dermatitis, alopecia, diarrhea, emotional disorder, weight loss, intercurrent infections due to cell-mediated immune dysfunctions, hypogonadism in males, neurosensory disorders, and problems with healing of ulcers. This condition can be fatal. A moderate level of zinc deficiency has been reported in a variety of conditions. Clinical manifestations include growth retardation and male hypogonadism in adolescence, rough skin, poor appetite, mental lethargy, delayed wound healing, cell-mediated immune dysfunctions, and abnormal neurosensory changes. A mild level of zinc deficiency may manifest with decreased serum testosterone level and oligospermia in males, decreased lean body mass, hyper-ammonemia, neurosensory changes, anergy, decreased serum thymulin activity, and decreased IL-2 activity. Although the clinical aspects of severe and moderate levels of zinc deficiency are well known, the recognition of mild levels of zinc deficiency has been difficult. Currently plasmas zinc appears to be the most widely used parameter for assessment of human zinc status, and it is known to be decreased in cases of severe and moderate deficiency of zinc.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Zinc and nitrogen balance in adolescent females fed varying levels of zinc and soy protein.
Zinc and nitrogen balances were determined in 14 girls, 12.5 to 14.5 years of age, during a 30-day period. Diets were composed of ordinary foods and supplied 100% of the Recommended Daily Allowance for protein. The lunch menus were typical of those served in School Lunch Programs except that milk was omitted and calcium supplements were added. The dietary variables were the levels of zinc and the amount of defatted soy which replaced the meat in noon meals. The diets were: S0Z13.4 (13.4 mg zinc and no soy); S30Z13.4 (13.5 mg zinc and 30% of meat replaced by soy); and S30Z7.4 (7.4 mg zinc and 30% of meat replaced by soy). Subjects fed 7.4 mg zinc daily lost significantly (P less than 0.01) less zinc in their feces than the subjects fed the higher level of zinc during the 18-day collection period. Partial substitution of soy for meat in lunch menus did not affect fecal or urinary zinc or nitrogen losses. Mean retentions of zinc by subjects Diets S0Z13.4 nad S30Z7.4 were +0.53, +0.42 and -0.32 mg/day, respectively. Nitrogen retention was not significantly affected by zinc intake. However, nitrogen and zinc retentions were significantly correlated (r = 0.416, P less than 0.015).
Adolescent↗
Dietary zinc intake and zinc concentrations of plasma, erythrocytes, and breast milk in antepartum and postpartum lactating and nonlactating women: a longitudinal study.
The zinc status of a group of 23 lactating and 13 nonlactating women was assessed longitudinally from 37-wk gestation through 6 months postpartum. Dietary zinc intake was determined by chemical analysis of 3-day duplicate plate food composites. In addition, zinc concentrations were measured in plasma, erythrocytes, and breast milk. The mean dietary zinc intake of both groups of postpartum women as determined by direct analyses was 42% of the Recommended Dietary Allowances or less. The plasma and erythrocyte zinc concentrations were not significantly different between the lactating and nonlactating women. Plasma zinc concentration increased from the time of delivery to one month postpartum for both groups and did not significantly increase further through 6 months postpartum. Erythrocyte zinc decreased from delivery through 6 months postpartum for both groups. Breast milk zinc concentration decreased with the duration of lactation. The calculated zinc intake of infants from breast milk was less than 50% of the Recommended Dietary Allowances. There was no correlation of maternal dietary zinc intake or maternal plasma and erythrocyte zinc with the concentration of zinc in breast milk.
Adult↗