Browsing by Subject "zinc"
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Item Copper and zinc balance in exercising horses fed two forms of mineral supplements(2009-05-15) Wagner, Elizabeth LynnThis study was undertaken to compare the absorption and retention of copper and zinc when supplemented to exercising horses in the form of sulfate or organic-chelate mineral supplements. Nine mature horses were used in a modified-switchback designed experiment consisting of seven 28-d periods. Horses were fed a diet consisting of 50% coastal Bermudagrass and 50% concentrate. All diets were balanced to meet the energy, protein, calcium and phosphorus requirements for horses performing moderate to intense exercise. Copper and zinc supplementation varied by period. During mineral depletion and repletion periods, horses respectively consumed diets with no supplemental mineral or Cu and Zn supplemented in the sulfate form to provide 100% of NRC (1989) values. In periods 4 and 7, horses were fed diets designed to provide 90% of NRC (1989) values for Cu and Zn supplied in the sulfate or organic-chelate forms. Horses were subjected to a standard exercise test on d 23 of periods 4 and 7 followed by a 4-d total fecal and urine collection. Blood samples were drawn every 28-d for determination of plasma Cu, Zn and ceruloplasmin concentration, and white blood cell counts and Cu,Zn-superoxide dismutase activity were evaluated in periods 4 and 7. Copper and zinc balance was determined from feed, fecal, urine and water samples obtained during the total collections in periods 4 and 7. Copper and Zn intake and fecal excretion were greater (P<0.05) for horses consuming the organic-chelate supplemented diet. Apparent Cu absorption as a percent of intake and retention as a percent of intake were also greater for this group. Plasma Cu, Zn and ceruloplasmin concentration was not different for horses consuming the two mineral supplement forms. White blood cell counts and superoxide dismutase activity were not affected by diet treatment. Formulation error and suspected sample contamination made it difficult to compare absorption and retention of Cu and Zn, but the use of a controlled repletion-depletion diet sequence appeared to be an effective experimental design component.Item Effects of zinc on Salmonella in the layer house environments and laying hens, and the ability of zinc to induce molt in laying hens(Texas A&M University, 2005-02-17) Park, ShinyoungThere is increasing interest in developing methods to detect and identify Salmonella, to eliminate or reduce the risk of contamination of shell eggs, and to retain the economic advantages of induced molting without increasing the risk of Salmonella enteritidis infection. S. enteritidis and S. typhimurium are the most common serotypes among 2449 known serotypes of the Salmonella, and are the causes of most egg- related foodborne salmonellosis in humans in the U. S. These two species are also responsible for environmental contamination and the incidence of infections. Therefore, this study was conducted in three phases consisting of ten in vivo and in vitro experiments. This study investigated the effects of zinc on Salmonella growth and survivability in poultry environments, and its ability to induce a molt in single comb white leghorn hens. In part, the antibacterial properties of zinc may reduce environmental contamination in a poultry house by interrupting airborne routes. The first phase involved detecting airborne bacteria by aerosol sampling methods, and then screening any Salmonella mutant (s) that survived desiccation by transposon footprinting. The second phase examined, in vitro, the addition of zinc on the growth kinetics of Salmonella under aerobic or anaerobic conditions, the effects of combinating zinc and acidic conditions on the growth kinetics of Salmonella in vitro under aerobic or anaerobic conditions, and the effects of zinc amended feed on the survival of a dry inoculum of Salmonella. The third phase investigated the ability of zinc propionate, as an alternative salt form of zinc, to induce molt in laying hens, the influence of zinc acetate and zinc propionate on gastrointestinal tract fermentation, and susceptibility of laying hens to S. enteritidis during an induced molt, and the comparison of digestive microbial crop and cecal communities among molted hens fed by either zinc acetate or zinc propionate amended molting diets with hens undergoing feed withdrawal or full fed nonmolted hens using molecular-based denaturing gradient gel electrophoresis.Item Soil and Mold Influences on Fe and Zn Concentrations of Sorghum Grain in Mali, West Africa(2012-10-19) Verbree, CherylIron (Fe) and zinc (Zn) deficiencies affect an estimated 3 billion people worldwide and are linked with cognitive and physical impairments, maternal and child mortality rates, and decreased adult work activity. To combat this "hidden" hunger, plant breeders in Mali are working to increase sorghum grain Fe and Zn concentrations. The objective of this study was to investigate soil and mold influences that affect Fe and Zn uptake and accumulation in sorghum grain. In southern Mali, soils from participatory sorghum variety trials and areas of different parent material and proximity to Shea (Vitellaria paradoxa) trees were analyzed for diethylenetriaminepentaacetic acid (DTPA)-extractable Zn and related soil properties, and sorghum grain was analyzed for Zn concentration. An inoculation trial was also performed at College Station, TX to determine if sorghum grain infected by the mold Curvularia lunata significantly increased grain Fe concentrations. DTPA-extractable Zn concentration was highly variable with high concentrations found in soils under Shea tree canopies with high pH and organic carbon and derived from mafic, high Zn-content parent material. However, these high concentrations did not significantly affect grain Zn concentrations in sorghum grown outside of the canopy. Groundnut grown underneath the canopy is likely to be affected and warrants further investigation. In many cases, soil DTPA-extractable Zn concentrations were at deficient levels, thus hampering its correlation to sorghum grain Zn concentration and potentially limiting the expression of genetic Zn biofortification. Knowledge of soil DTPA-extractable Zn concentrations or basic soil properties such as pH, organic carbon, and soil parent material may aid in the location of suitable available Zn fields and overall biofortification efforts. Grain Fe concentration was not significantly related to Curvularia lunata percent recovery or grain mold rating, but instead showed a relatively high variance by panicle, digestion batch, and grain subsample. Additional work is needed to address these sources of Fe variation so as to determine better if mold affects grain Fe concentrations.Item The Pro-Antioxidant Role of Zinc Supplementation in Cadmium-Treated Choroid Plexus(2014-05-06) Francis Stuart, Samantha D.Cadmium (Cd) is a toxic heavy metal with no known physiological function in higher order animals. Previous studies in primary cultures of neonatal rat choroid plexus (CP) epithelial cells indicated Cd induced oxidative stress and stimulated apical choline transport, and suggested zinc (Zn) supplementation might abate both oxidative stress and modulation of transport. The objective of this thesis was to elucidate how Zn, a nutritive mineral normally accumulated by CP, attenuated oxidative stress. I hypothesize that Zn, which can function as a pro-antioxidant, abates Cd-induced oxidative stress either by induction of metallothionein-1 (MT-1) or enhancement of glutathione (GSH) biochemistry. Thus, in primary cultures of neonatal rat CP epithelial cells, I characterized the effects of sub-micromolar Cd and efficacy of Zn supplementation to attenuate Cd-induced cellular and oxidative stress without or with manipulation of GSH synthesis. To characterize the Cd-induced stress response, CP epithelial cells were treated with 0 or 500 nM CdCl_(2) in serum-free medium (SFM) for 12 h; samples were collected at 3, 6, 9, and 12 h. Induction of heme oxygenase-1 (HO-1), heat-shock protein 70 (HSP70), and metallothionein-1 (MT-1) in Cd-treated cells was compared to time-matched controls by immunoblot and qRT-PCR analyses. Cd induced the catalytic and modifier subunits of glutamate-cysteine ligase (GCL), the rate-limiting enzyme in GSH synthesis. To elucidate the effects Zn supplementation in Cd-treated cells depleted of GSH, cells were supplemented for 48 h with 0 or 25 ?M ZnCl_(2) alone or with 100 ?M buthionine sulfoximine (BSO), an inhibitor of GCL, before treatment with 0 or 500 nM CdCl_(2) ? 100 ?M BSO ? 10?M ZnCl_(2) in SFM for 12 h. By luminescence assay, intracellular GSH and oxidized glutathione (GSSG) concentrations were measured. Cd increased intracellular GSH and GSSG, but markedly decreased GSH:GSSG ratio. Inhibition of GSH synthesis exacerbated Cd-induced stress. However, Zn supplementation attenuated the stress response irrespective of BSO treatment, as per decreased induction of HSP70. These data indicate that CP adapts to low-dose Cd by up-regulation of stress proteins and GSH synthesis. Zinc supplementation also may attenuate Cd-induced cellular and oxidative stress, but cytoprotection is independent of GSH status.Item Zinc ion homeostasis in cellular physiology and experimental models of traumatic brain injury(2009-03-06) Yuan Li; Jonathan B. Ward; Wolfgang Maret; Robert A. Colvin; Ping Wu; Karl E. Anderson; Douglas S. DeWittA major yet unsolved quest in treating traumatic brain injury (TBI) is the understanding of the secondary cellular injury that contributes to cell death. Whether zinc ions are toxic or protective in TBI is controversial. As an essential human micronutrient, zinc is needed for the structure and function of at least 3,000 proteins, and thus affects almost any aspect of cellular function. Although extremely low, intracellular zinc ion concentrations, [Zn2+]i, are tightly controlled to ensure optimal physiology and to avoid toxicity. Furthermore, zinc ions are now believed to be signaling ions, especially in neuronal systems. This dissertation addresses the dynamics of [Zn2+]i and quantitatively defines its safe range in particular cell types. [Zn2+]i was measured to be pico- to nanomolar in undifferentiated and differentiated rat pheochromocytoma (PC12) cells and in rat glioma (C6) cells. When PC12 cells proliferate, [Zn2+]i undergoes precisely controlled fluctuations with two peaks within one cell cycle. These results demonstrate that the already established requirement for zinc in the cell cycle and in differentiation relates to the availability of zinc ions. In a mechanical model of cellular injury, namely rapid stretch injury (RSI), nitric oxide induces an increase in [Zn2+]i that subsequently may protect cells by repressing the generation of ROS. A peak at one hour was followed by decreased [Zn2+]i. In PC12 cells, [Zn2+]i dropped below its normal level, indicating that these cells were in a state of ¡°zinc ion deficiency¡± hours after RSI. In an in vivo model of neural injury, namely fluid percussion TBI of rats, changes of [Zn2+]i were indirectly demonstrated by measuring the levels and states of the zinc-binding protein, metallothionein/thionein, in the hippocampus and the cortex. These results demonstrate that [Zn2+]i as well as zinc buffering dynamically fluctuate to adapt to the requirements of cellular functions, even when [Zn2+]i is extremely low inside the cell. They suggest that toxicity occurs when [Zn2+]i falls outside the safety thresholds. Therefore, when, where, how much and in which form zinc is present determine whether chelation or supplementation is an option for treatment. These new concepts provide new leads for developing strategies to treat TBI.Item Zinc-mediated cell death in the hippocampus following experimental traumatic brain injury(2008-07-15) Bridget Eva Hawkins; Wolfgang Maret, Ph.D.; Kelly Dineley, Ph.D.; Helen Hellmich, Ph.D.; Claudia Robertson, M.D.Traumatic brain injury (TBI) is a leading cause of morbidity and mortality of Americans both in the 15-25 age range and in the elderly population. Hippocampal neuronal damage is a key feature of experimental fluid percussion traumatic brain injury in rodents. However, the mechanisms contributing to the susceptibility to neuronal injury in this region are largely unknown. Since free ionic zinc (Zn2+) was shown to be toxic to neurons in vitro, I sought to examine the effects of Zn2+ on neuronal injury following TBI. To study this problem, I characterized a model of Zn2+-induced injury in an attempt to isolate zinc’s effect on cell death, in vivo. I also adapted a fluorimetric method to measure the amount of extracellular Zn2+ present following TBI, using microdialysis techniques. To date, the measurement of free ionic Zn2+ release in vivo after trauma has not been shown. I demonstrate that the amount of Zn2+ found in the extracellular fluid of TBI rats was below the range that causes neuronal injury and was not different than the amount of Zn2+ found in sham operated rats. Results of my experiments do not support the idea that presynaptic release of Zn2+ causes injury to surrounding neurons.