Ability Of Zn Research Articles

Psoralen synergies with zinc implants to promote bone repair by regulating ZIP4 in rats with bone defect

BackgroundThe regulation of dose-dependent biological effects induced by biodegradation is a challenge for the production of biodegradable bone-substitute materials, especially biodegradable zinc (Zn) -based materials. Cytotoxicity caused by excess local Zn ions (Zn2+) from degradation is one of the factors limiting the wide application of Zn implants. Given that previous studies have revealed that delayed degradation of Zn materials by surface modification does not reduce cytotoxicity; in the present study, we explore whether preventing the entry of excess Zn2+ into cells may can reduce local Zn toxicity by applying Psoralen (PRL) to Zn implants and assessing its ability to regulate intracellular Zn2+ concentrations.MethodsThe effects of different concentrations of Zn2+ on cellular activity and cytotoxicity were investigated; briefly, we identified natural compounds that regulate Zn transporters, thereby regulating the concentrations of intracellular Zn2+, and applied them to Zn materials. Of these materials, PRL, a natural, tricyclic, coumarin-like aromatic compound that promotes the proliferation and differentiation of osteoblasts and enhances osteogenic activity, was loaded onto the surface of a Zn material using peptides and chitosan (CS), and the surface characteristics, electrochemical properties, and activity of the modified Zn material were evaluated. In addition, the ability of Zn + CS/pPRL implants to promote bone formation and accelerate large-scale bone defect repairs was assessed both in vitro and in vivo.ResultsWe determined that 180 µM Zn2+ significantly induced pre-osteoblast cytotoxicity, and a 23-fold increase in Zrt- and Irt-like protein 4 (ZIP4) expression. We also found that PRL dynamically regulates the expression of ZIP4 in response to Zn2+ concentration. To address the problem of cytotoxicity caused by excessive Zn2+ in local Zn implants, PRL was loaded onto the surface of Zn implants in vivo using peptides and CS, which dynamically regulated ZIP4 levels, maintained the balance of intracellular Zn2+ concentrations, and enhanced the osteogenic activity of Zn implants.ConclusionsThis study reveals the importance of Zn2+ concentration when using Zn materials to promote bone formation and introduces a natural active ingredient, PRL, that can regulate intracellular Zn2+ levels, and thus may be clinically applicable to Zn implants for the treatment of critical bone defects.Graphical

Zinc(II) Carboxylate Coordination Polymers with Versatile Applications.

This review considers the applications of Zn(II) carboxylate-based coordination polymers (Zn-CBCPs), such as sensors, catalysts, species with potential in infections and cancers treatment, as well as storage and drug-carrier materials. The nature of organic luminophores, especially both the rigid carboxylate and the ancillary N-donor bridging ligand, together with the alignment in Zn-CBCPs and their intermolecular interaction modulate the luminescence properties and allow the sensing of a variety of inorganic and organic pollutants. The ability of Zn(II) to act as a good Lewis acid allowed the involvement of Zn-CBCPs either in dye elimination from wastewater through photocatalysis or in pathogenic microorganism or tumor inhibition. In addition, the pores developed inside of the network provided the possibility for some species to store gaseous or liquid molecules, as well as to deliver some drugs for improved treatment.

(Invited) All Electrochemical Synthesis of Nanoporous Cu Films for the Purposes of Fine Pitch and Low Temperature Interconnection in 3D Packaging

Nanoporous Cu (np-Cu) films can be employed in the electronic packaging as materials facilitating chip-to-substrate interconnections, which is realized by Cu-on-Cu bonding. Unlike their bulk counterparts, np metals feature unique interconnected pore-ligament structure with a length scale in the range of single-to-tens of nanometers. This results in a high surface area-to-volume ratio accompanied with a substantially lower melting temperature. Research has been done in the field to experiment with Cu-on-Cu interconnects realized by np-Cu precursor films (1). While the initial results are undoubtedly promising, difficulties haver been met with sufficiently lowering the sintering / soldering temperature below 380-400oC. A way to address these shortcomings is to develop of approaches to sintering at much lower temperatures by introducing Sn into the np-Cu structures either directly or by coating then followed by processing to produce at lower sintering temperature Cu-Sn bonds with low resistivity and a greater current carrying capability than bare np-Cu. The foundation of this study relies on the development of fine structured np-Cu films with an open and uniform interconnected network of ultra-fine ligaments and pores of size preferably in the single digit nanometer range.The present report is focused on the development of a two-step all-electrochemical approach for the synthesis of the targeted np-Cu structures including (i) a controlled electrodeposition of Cu-based precursor alloy with a less-noble counterpart that is then (ii) selectively removed (de-alloyed) by anodization at appropriate potential to leave behind the desired “spongy” np-Cu structure (2). Therefore, the first part of this report introduces and discusses the development of protocols for flat and uniform deposition of Cu-Zn and Cu-Mn alloys that could both serve as precursors of the synthetically targeted np-Cu films. The choice of said alloy systems is motivated by the ability of Zn and Mn to form single-phase alloys or intermetallic compounds with Cu thus ensuring the ultra-fine length scale of the eventually synthesized np Cu structure. The alloy deposition routines included use of a pyrophosphate (P2O7 4-) plating bath for Cu-Zn alloys which were shown to have high stability and optimizable for the plating of smooth and fine-grained brass deposits (3). Also, ammonium sulfate with excess of ammonia as complexing agent, was employed in the optimization activity aimed at the deposition of continuous and relatively smooth Cu-Mn deposits (4). The report discusses the optimization of plating parameters and conditions along with the subsequent structural and compositional characterization of the accordingly deposited precursor alloys with 60 at % and higher representation of the less noble constituent.Next, the electrochemical de-alloying of as-deposited CuxZn(1-x) and CuxMn(1-x) precursor alloys on a gold substrate is introduced and discussed. Alike with the first part of the report, the emphasis is on the optimization routines that looked at the effect of de-alloying scan rate, de-alloying at different constant potentials, de-alloying bath, and precursor alloy composition on the morphology and composition of the resulting np-Cu. A valuable part of the report is the demonstration of how the implementation of best combinations of optimized parameters and conditions leads to the synthesis of interconnected pore-ligament thin film networks of np-Cu structures with average ligament sizes in the range of 15-30 nm. In conclusion, the discussion takes direction towards ideas and perspectives for improvement of the uniformity and further refinement of the pore ligament length scale. Finally, consideration is also given to the intended approaches to introduce Sn on or into the accordingly synthesized np-Cu films and eventually convert them to np-Cu-Sn alloy ready for sintering/soldering at low temperatures.

Ameliorating effect of zinc and manure application on the growth of Macrophomina phaseolina (Tassi) goid infected genotypes of Arachis hypogea L.

Peanut [Arachis hypogea (L.)] is a valuable legume crop that is widely cultivated in Northern Nigeria. The yield of this crop is affected by root rot disease caused by the fungal pathogen (Macrophomina phaseolina). This study was carried out to assess the efficacy of Zinc (Zn) (1.76, 3.59, 4.71 and 6 mg kg−1) and Manure [M (2% and 4%)] in a complex interaction to manage the disease and improve yield. Two genotypes of peanut were selected for this study on the basis of their susceptibility to M. phaseolina (severely infected UGA 2) and (moderately infected ICGV 86015). The results showed that M. phaseolina suppressed the plant defense action through the activities of malionaldehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and peroxidase (POD) thereby hindering identification of the pathogen elicitor. It was observed that manure enhanced the microbial activity and physicochemical properties of soil, which induced plant defense and antimicrobial protein against reactive oxygen species (ROS) thereby reducing the susceptibility of the pathogen to the peanut plant. The co-factor ability of Zn enhanced the activities of antioxidant enzymes to scavenge ROS molecules in the pathogen stressed cells, improve photosynthetic efficiency and prevent the plant from death. Therefore, this study has revealed that Zn and manure inhibits the multiplication of M. phaseolina in the peanut seedlings.

Zinc Selectively Blocks Neurosteroid-Sensitive Extrasynaptic δGABAA Receptors in the Hippocampus.

Zinc (Zn(2+)) is an essential cofactor in mammalian cells and neurons. Zn(2+) is released from synaptic vesicles of certain nerve terminals in the hippocampus during neuronal activity. Zn(2+) has been shown to inhibit synaptic GABAA receptors and alter the hippocampal network excitability. However, the ability of Zn(2+) to block extrasynaptic receptors remains unclear. Endogenous neurosteroids, such as allopregnanolone (AP), regulate neuronal excitability by allosteric activation of synaptic and extrasynaptic GABAA receptors. Neurosteroids activate extrasynaptic δGABAA receptor-mediated tonic inhibition in dentate gyrus granule cells (DGGCs), thereby contributing to the regulation of downstream circuit excitability. Here we report a novel inhibitory role of Zn(2+) at neurosteroid-sensitive, extrasynaptic δGABAA receptors by electrophysiological recordings in DGGCs from adult mice. Zn(2+) displayed a concentration-dependent, reversible noncompetitive blockade of AP-sensitive tonic current in DGGCs (IC50, 16 μm). Tonic current was fully blocked by Zn(2+), akin to the GABAA receptor antagonist gabazine. Zn(2+) inhibition of tonic current was lacking in DGGCs from δ-subunit knock-out mice. Moreover, AP-activated synaptic receptor-mediated phasic currents were not affected by Zn(2+) Finally, intrahippocampal infusion of Zn(2+) elicited rapid epileptiform activity and significantly blocked the antiseizure activity of AP in the kindling model of epilepsy. Thus, Zn(2+) inhibition of neurosteroid-sensitive, extrasynaptic GABAA receptors in the hippocampus has direct implications in many brain hyperexcitability conditions, such as seizures, epileptogenesis, and epilepsy. Zn(2+) interactions may aid to further understand the physiology of extrasynaptic GABAA receptors. Zn(2+) is most abundant in the synaptic vesicles of hippocampal mossy fibers. Zn(2+) release occurs with neuronal excitation, including seizure events, and exerts powerful excitability effects in the hippocampus circuits. Zn(2+) inhibits synaptic GABAA receptors, but its interaction is less well appreciated at the extrasynaptic receptors, which respond sensitively to endogenous neurosteroids. Here, we describe selective functional blockade by Zn(2+) of neurosteroid-sensitive, extrasynaptic GABAA receptors in the mouse hippocampus dentate gyrus, a key region associated with epilepsy and memory disorders. By demonstrating that extracellular Zn(2+) prevents neurosteroid augmentation of tonic current and protection against limbic seizures, our findings provide novel implications of this potential antagonistic interaction in a variety of neurological conditions.

Effects of Added Zinc on Skeletal Muscle Morphometrics and Gene Expression of Finishing Pigs Fed Ractopamine-HCL

ABSTRACTFinishing pigs (n = 320) were used in a 35-day study to determine the effects of ractopamine-HCl (RAC) and supplemental Zinc (Zn) level on loin eye area (LEA) and gene expression. Pens were randomly allotted to the following treatments for the final 35 days on feed: a corn-soybean meal diet (CON), a diet with 10 ppm RAC (RAC+), and RAC diet plus added Zn at 75, 150, or 225 ppm. Sixteen pigs per treatment were randomly selected for collection of serial muscle biopsies and carcass data on day 0, 8, 18, and 32 of the treatment phase. Compared to CON carcasses, RAC+ carcasses had 12.6% larger (P = 0.03) LEA. Carcasses from RAC diets with added Zn had a tendency for increased (quadratic, P < 0.10) LEA compared to the RAC+ carcasses. Compared to RAC+ pigs, relative expression of IGF1 decreased with increasing levels of Zn on day 8 and 18 of treatment, but expression levels were similar on day 32 due to Zn treatments increasing in expression while the RAC+ treatment decreased (Zn quadratic × day quadratic, P = 0.04). A similar trend was detected for the expression of β1-receptor where expression levels in the RAC+ pigs were greater than Zn supplemented pigs on day 8 and 18 of the experiment, but the magnitude of difference between the treatments was reduced on day 32 due to a decrease in expression by RAC+ pigs and an increase in expression by the Zn pigs (Zn quadratic × day quadratic, P = 0.01). The ability of Zn to prolong the expression of these two genes may be responsible for the tendency of Zn to increase LEA in RAC supplemented pigs.

Influence of magnesium content on the corrosion resistance of the cut-edges of Zn–Mg-coated steel

The ability of Zn–Mg coatings (with magnesium content between 5.8 and 15.5wt.%) to protect steel sheets has been evaluated with local electrochemical techniques (scanning vibrating electrode technique, microcapillary electrochemical cell) and rotating disk electrode, and compared with the corrosion protection afforded by a pure zinc coating. From immersion tests of coated steel cut-edges, it is observed that alloying zinc with magnesium leads to a decrease of the galvanic current between the coating and the steel surface, and to an improvement of the steel corrosion resistance after a drying period, due to the presence of magnesium in the corrosion products.

Allosteric regulation of the ligand-binding ability of Zn–porphyrin by metal complexation

Abstract Zn–porphyrin with bipyridyl units at the ends of a conjugated chain, in addition to two alkyl side chains, was prepared as an artificial allosteric system. The axial ligand-binding ability of the compound was considerably reduced by the formation of a Fe(bpy) 3 -type complex. The degree of the allosteric suppression strongly depended on both alkyl chain length and the steric demand of the pyridyl ligand.

On the acid–base properties of Zn–Mg–Al mixed oxides

The influence of Zn 2+ cation substitution in Mg–Al mixed oxides is explored in the Zn 2+ concentration range from 20 to 60 mol%. The mixed oxides are derived by calcination of layered double hydroxide precursors. Structural analyses by XRD and 27Al MAS NMR show that Al 3+, Mg 2+ and Zn 2+ cations are well dispersed among the oxide phases. The acid site concentration increases with increasing zinc content, while the concentration of basic sites decreases compared to Zn 2+ free mixed oxides. Acetone is the primary reaction product of propan-2-ol elimination with all zinc containing oxides. This suggests that the high activity for dehydrogenation of propan-2-ol is related to the pronounced hydride abstraction ability of Zn 2+ cations and not to an enhanced strength or concentration of basic sites.

Thermal and spectral analyses of complexes of zinc(II)tetra-tertbutylphthalocyanine with amines

Spectral and thermochemical studies of complexes of zinc(II)tetra-tertbutylphthalocyanine (Zn(t-Bu)4Pc) with some amines have been carried out. Spectral effects of the complex formation of the metallophthalocyanine with amines have been established. It has been found that an ability of Zn(t-Bu)4Pc to coordinate amines depends on both their nature and conditions of preparation. Similarity of the crystal structures of biligand and monoligand of Zn(t-Bu)4Pc complexes to individual β- and α-polymorphs of Zn(t-Bu)4Pc, respectively is proved by IR spectroscopy and X-ray diffraction method.

Modulation of Energy Metabolism in C6 Glioma Cells as Possible Mechanism Contributing to Zinc Neurotoxicity

Elevated tissue levels of zinc (Zn) have been associated with neurodegenerative diseases such as global ischemia, seizure, and Alzheimer's. The mechanism of action of Zn in causing neuronal injury is not clear. One of the possible mechanisms is the ability of Zn to alter cellular energy metabolism. Using the C6 glioma cell as a model, the present study aimed to determined the effects of increasing concentrations of Zn on cellular energy states, as defined by the levels of adenosine 5'-triphosphate (ATP), adenosine 5'-diphosphate (ADP), and adenosine 5'-monophosphate (AMP), the total adenosine nucleotides (TAN) (TAN = ATP + ADP + AMP), and the energy charge potential (ECP = [ATP + 0.5 ADP]/TAN). Uptake of Zn was visualized by the appearance of N-(6-methoxy-8-quinolyl)-p-toluene sulfonamide (TSQ)-stained fluorescent granules after a 3-h exposure to Zn in the medium. At [Zn] = 1 mM, cells appeared apoptotic. Levels of ATP and TAN decreased as the level of Zn increased. The change mirrors the increase in cell death as determined by the trypan blue exclusion test. However, when the ratio of ATP:ADP:AMP within the TAN was calculated, the percentage of ATP in the TAN increased significantly, while that of AMP decreased. The change in the relative AMP level mirrored the change in cell viability as measured by the MTT assay, which indicated a decreased in mitochondrial activity. Cellular ECP increased significantly from 0.85 ± 0.007 to 0.92 ± 0.04. The elevated ECP and relative ATP level, together with a significant decrease in the relative AMP level, are all indicators of inhibition of cellular metabolism. These results support the notion that acute exposure of C6 glioma cells to a high concentration of Zn might initially result in a decrease in relative AMP and an inhibition of mitochondrial activity. However, the ultimate toxic action of Zn on the C6 glioma cells appears to be due to a gradual inhibition of energy utilization, leading to cell shrinkage and apoptosis.

Zinc Inhibition of cAMP Signaling

Zn(2+) is required as either a catalytic or structural component for a large number of enzymes and thus contributes to a variety of important biological processes. We report here that low micromolar concentrations of Zn(2+) inhibited hormone- or forskolin-stimulated cAMP production in N18TG2 neuroblastoma cells. Similarly, low concentrations inhibited hormone- and forskolin-stimulated adenylyl cyclase (AC) activity in membrane preparations and did so primarily by altering the V(max) of the enzyme. Zn(2+) also inhibited recombinant isoforms, indicating that this reflects a direct interaction with the enzyme. The IC(50) for Zn(2+) inhibition was approximately 1-2 microm with a Hill coefficient of 1.33. The dose-response curve for Zn(2+) inhibition was identical for AC1, AC5, and AC6 as well as for the C441R mutant of AC5 whose defect appears to be in one of the catalytic metal binding sites. However, AC2 displayed a distinct dose-response curve. These data in combination with the findings that Zn(2+) inhibition was not competitive with Mg(2+) or Mg(2+)/ATP suggest that the inhibitory Zn(2+) binding site is distinct from the metal binding sites involved in catalysis. The prestimulated enzyme was found to be less susceptible to Zn(2+) inhibition, suggesting that the ability of Zn(2+) to inhibit AC could be significantly influenced by the coincidence timing of the input signals to the enzyme.

The Protective Effect of ZnCl 2 Pretreatment on the Development of Postanoxic Neuronal Damage in Organotypic Rat Hippocampal Cultures

Zinc is one of the trace elements playing an important role in many fundamental biological processes. However, it is also one of the possible etiological agents involved in nerve cell damage in certain human neurodegenerative disorders. The precise mechanism of neuroprotective ability of Zn against neurotoxicity evidenced in various pathological conditions remains unclear, especially concerning the intrinsic potential toxicity of this metal. This ultrastructural study was undertaken to determine the effect of zinc on the evolution of anoxia-induced neuronal injury in the organotypic cultures of rat hippocampus. The in vitro model of oxygen deprivation was produced by maintaining the cultures in a pure nitrogen atmosphere in flask adapted for permanent gas flow for 20 min. The selected cultures were pretreated with micromolar concentration of ZnCl 2 (25-500 µM) at 30 min prior anoxia. The ultrastructural findings documented that Zn exhibited dose-dependent ability to reduce anoxia-induced neuronal changes in hippocampal neurons in vitro. Zn at a concentration of 100 µM was able to significantly protect the hippocampal formation against the development of late apoptotic changes, whereas the early necrotic anoxia-induced neuronal injury was not so efficiently reduced.

Construction of a High Affinity Zinc Binding Site in the Metabotropic Glutamate Receptor mGluR1: NONCOMPETITIVE ANTAGONISM ORIGINATING FROM THE AMINO-TERMINAL DOMAIN OF A FAMILY C G-PROTEIN-COUPLED RECEPTOR

The metabotropic glutamate receptors (mGluRs) belong to family C of the G-protein-coupled receptor (GPCR) superfamily. The receptors are characterized by having unusually long amino-terminal domains (ATDs), to which agonist binding has been shown to take place. Previously, we have constructed a molecular model of the ATD of mGluR1 based on a weak amino acid sequence similarity with a bacterial periplasmic binding protein. The ATD consists of two globular lobes, which are speculated to contract from an "open" to a "closed" conformation following agonist binding. In the present study, we have created a Zn(2+) binding site in mGluR1b by mutating the residue Lys(260) to a histidine. Zinc acts as a noncompetitive antagonist of agonist-induced IP accumulation on the K260H mutant with an IC(50) value of 2 microm. Alanine mutations of three potential "zinc coligands" in proximity to the introduced histidine in K260H knock out the ability of Zn(2+) to antagonize the agonist-induced response. Zn(2+) binding to K260H does not appear to affect the dimerization of the receptor. Instead, we propose that binding of zinc has introduced a structural constraint in the ATD lobe, preventing the formation of a "closed" conformation, and thus stabilizing a more or less inactive "open" form of the ATD. This study presents the first metal ion site constructed in a family C GPCR. Furthermore, it is the first time a metal ion site has been created in a region outside of the seven transmembrane regions of a GPCR and the loops connecting these. The findings offer valuable insight into the mechanism of ATD closure and family C receptor activation. Furthermore, the findings demonstrate that ATD regions other than those participating in agonist binding could be potential targets for new generations of ligands for this family of receptors.

Genetically Engineered Metal Ion Binding Sites on the Outside of a Channel's Transmembrane β-Barrel

We are exploring the ability of genetically engineered versions of the Staphylococcus aureus α-hemolysin ( αHL) ion channel to serve as rationally designed sensor components for analytes including divalent cations. We show here that neither the hemolytic activity nor the single channel current of wild-type αHL was affected by [Zn(II)] ≤ 1 mM. Binding sites for the divalent cations were formed by altering the number and location of coordinating side chains, e.g., histidines and aspartic acids, between positions 126 and 134, inclusive. Several mutant αHLs exhibited Zn(II)-induced current noise that varied with Zn(II) concentration. At a fixed divalent cation concentration, the current fluctuation kinetics depended on the analyte type, e.g., Zn(II), Cu(II), Ni(II), and Co(II). We also show that the ability of Zn(II) to change the mutant channel current suggests that the pore's topology is β-sheet and that position 130 is near the turn at the trans mouth. Both conclusions are consistent with the crystal structure of WT- αHL oligomerized in detergent. Our results, in the context of the channel's crystal structure, suggest that conductance blockades were caused by Zn(II) binding to the outside surface of the pore. Thus, analyte-induced current blockades alone might not establish whether an analyte binding site is inside a pore.

Laboratory simulation of atmospheric corrosion by SO2—II. Electrochemical mass loss comparisons

Mass losses of zinc, steel and rolled Zn-55%Al alloy over the range 0–1 ppm [SO2], obtained by weighing, or calculated using atmospheric corrosion monitors, ACMs, from galvanic current, Ig, charge-transfer resistance, Rm, polarization resistance, Rp, or corrosion current, Ik have been compared. The ability of Zn and Zn-55%Al alloy coatings to protect steel under these conditions is discussed. Although similar trends in mass loss vs [SO2] are generally apparent for each of the methods of obtaining mass loss, there are differences in the magnitude of mass loss, which in some cases are substantial. The reasons for these differences are discussed in detail. One reason, that of partial short circuits between adjacent ACM plates in the presence of [SO2], thought due to electron-conducting corrosion products, leads to high values of calculated mass loss. Partial short circuits appear to occur at random and may or may not occur in apparently identical tests for ACM3 (Zn) and ACM8 (Fe) but not ACM4 (rolled Zn-55%Al). The effect of these partial short circuits can be modelled by inclusion of a corrosion product resistance, Rep, in parallel with Rt and Warburg impedance, Zω. The scope of the work with these ACMs is wider than previous work in the literature. This includes a modified method of manufacture; a more sophisticated method of measuring ACM corrosion currents; and a wider correlation of electrochemically calculated mass loss with weighed mass loss.

Degradation of thymopentin by human lymphocytes: evidence for aminopeptidase activity

Thymopentin (Arg-Lys-Asp-Val-Tyr) was shown to be degraded in vitro by human lymphocytes into two main fragments; the tetrapeptide Lys-Asp-Val-Tyr and the tripeptide Asp-Val-Tyr. Degradation products were identified by HPLC and amino-acid analysis. Analysis of the time-course of degradation revealed a ‘stepwise’ degradative event beginning at the N-terminal. The degradation of thymopentin after the first 10 min, as well as the formation of the tetrapeptide (5–30 min) were essentially curvilinear. Degradation of the tripeptide, was linear. Upon screening a panel of compounds that inhibit enzymatic activity, bestatin, amastatin and 1,10-phenanthroline were shown to be the most effective. Bestatin and amastatin caused an 85–90% inhibition of thymopentin degrading activity with IC 50 values of 7.1·10 −6 M and 4.5·10 −9 M, respectively. 1,10-Phenanthroline completely inhibited the degradative process with an IC 50 of 2·10 −4 M. When the tetrapeptide Lys-Asp-Val-Tyr was used as the starting substrate, similar IC 50 values were seen for amastatin, bestatin and 1,10-phenanthroline. The importance of divalent metal ions in the degradative event was demonstrated not only by the effect of 1,10-phenanthroline, but also by the ability of Zn 2+ and Co 2+ to reverse the inhibition of 1,10-phenanthroline (at its IC 50) to activities near control values (no inhibitor). These data strongly suggest that an aminopeptidase(s) is responsible for the degradative activity.

Mobilization of tissue cadmium in mice and calves and reversal of cadmium induced tissue damage in calves by zinc.

Earlier studies demonstrated that simultaneous dietary Zn supplementation to calves fed Cd, significantly decreased the accumulation of Cd in liver, kidney and muscle. However, studies are lacking in evaluating the effectiveness of zinc in reducing Cd-burden in animals with pre-existing tissue Cd-load, a situation encountered in chronic Cd intoxication. This study examined the effects of oral Zn (AnO) on tissue Cd levels in mice. N-acetylcysteine (NAC) and sodium sulfate (SS) were also used to evaluate the effects of providing organic and inorganic sources of sulfur on tissue Cd levels. Following demonstration of reduced Cd levels in tissues of mice receiving antidotal Zn, subsequent investigation was aimed at studying the reversal of Cd-induced changes by Zn. The authors also examined whether Cd-induced reduction in epididymal 5 ..cap alpha..-reductase activity could explain previously reported low levels of circulating dihydrotestosterone (DHT) following Cd treatment. The ability of Zn to reverse the inhibition of 5 ..cap alpha..-reductase activity by Cd was also examined.

Equilibrium and kinetic studies involving schiff base complexes

Abstract The species formed in aqueous solutions of Zinc(II), pyruvate (P−) and pyridoxamine phosphate (PMP) at equilibrium have been determined and their stability constants evaluated from pH titration data. Schiff base formation in the absence of Zn(II) was studied potentiometrically and spectrophotometrically, both methods giving evidence for only one form, H(P . PMP)3−. The binary complexes, Zn(PMP)i+2–3i, where i = 1, 2 and 3, were found and in addition, monoprotonated complexes were formed to a small extent. Seven ketimine complexes were characterized: Zn(P . PMP)H +i−2 i , i = 1, 2 and Zn(P . PMP) 2 H +i−6 i , i = 0−4. Complexing with Zn(II) increases the basicity of the ketimine pyridine nitrogen, over that in the free ketimine H(PMP . P)3−, an effect which has important consequences regarding the ability of Zn(II) to promote the rate of transamination under neutral conditions. Rate studies in the presence and absence of metal ion indicate that Zn(II) promotes transamination by stabilizing the Schiff bases toward hydrolysis, preserving the integrity of the activating pyridinium group to higher pH regions and providing more active base catalyzed paths.