共查询到20条相似文献,搜索用时 15 毫秒
2.
The capabilities of a new class of immobilized ( im) metal ion chelate complexes (IMCCs), derived from 1,4,7‐triazacyclononane (tacn), bis(1,4,7‐triazacyclononyl) ethane (dtne) and bis(1,4,7‐triazacyclononyl)propane (dtnp) complexed with the borderline metal ions Cu 2+, Ni 2+, Zn 2+, Mn 2+, Co 2+, and Cr 3+, for the purification of proteins have been investigated. In particular, the binding behavior of a model protein, the C‐terminal hexahistidine tagged recombinant fusion protein Schistosoma japonicum glutathione S‐transferase‐ Saccharomyces cerevisiae mitochondrial ATP synthase δ‐subunit (GST‐δATPase‐His 6), with these new immobilized metal ion affinity chromatographic (IMAC) sorbents was compared to the properties of a conventional sorbent, derived from immobilized Ni(II)‐nitrilotriacetic acid ( im‐Ni 2+‐NTA). Investigations using the recombinant GST‐δATPase‐His 6 and recombinant S. japonicum glutathione S‐transferase (GST) lacking a hexahistidine tag have confirmed that the C‐terminal tag hexahistidine residues were required for the binding process to occur with these IMAC systems. The results also confirm that recombinant fusion proteins such as GST‐δATPase‐His 6 can be isolated in high purity with these IMAC systems. Moreover, these new macrocyclic systems manifest different selectivity features as a function of pH or ionic strength when compared to the conventional, unconstrained iminodiacetic acid (IDA) or NTA chelating ligands, complexed with borderline metal ions such as Cu 2+ or Ni 2+, as IMAC systems. Biotechnol. Bioeng. 2009;103: 747–756. © 2009 Wiley Periodicals, Inc. 相似文献
3.
In aqueous alkaline Zn batteries (AZBs), the Co 3+/Co 4+ redox pair offers a higher voltage plateau than its Co 2+/Co 3+ counterpart. However, related studies are scarce, due to two challenges: the Co 3+/Co 4+ redox pair is more difficult to activate than Co 2+/Co 3+; once activated, the Co 3+/Co 4+ redox pair is unstable, owing to the rapid reduction of surplus Co 3+ to Co 2+. Herein, CoSe 2?x is employed as a cathode material in AZBs. Electrochemical analysis recognizes the principal contributions of the Co 3+/Co 4+ redox pair to the capacity and voltage plateau. Mechanistic studies reveal that CoSe 2?x initially undergoes a phase transformation to derived Co xO ySe z, which has not been observed in other Zn//cobalt oxide batteries. The Se doping effect is conducive to sustaining abundant and stable Co 3+ species in Co xO ySe z. As a result, the battery achieves a 10 000‐cycle ultralong lifespan with 0.02% cycle ?1 capacity decay, a 1.9‐V voltage plateau, and an immense areal specific capacity compared to its low‐valence oxide counterparts. When used in a quasi‐solid‐state electrolyte, as‐assembled AZB delivers 4200 cycles and excellent tailorability, a promising result for wearable applications. The presented effective strategy for obtaining long‐cyclability cathodes via a phase transformation‐induced heteroatom doping effect may promote high‐valence metal species mediation toward highly stable electrodes. 相似文献
4.
The difficulty in finding positive electrode materials for sodium‐ion (Na‐ion) batteries with a large specific energy has slowed down their commercialization. Layered transition metal (M) oxides Na xMO 2 with a two‐layer oxygen stacking (P2, 0.6 ≤ x ≤ 0.75), are promising candidates. However, the high average metal oxidation state needed during synthesis means that P2 Na xMO 2 cathodes often require the introduction of high‐valent cations (Mn 4+, Ti 4+, Sn 5+, or Te 6+), limiting the cathode's performance. Using a combination of first‐principles calculations and experiments, the feasibility of P2 cathodes containing only electrochemically active nickel and cobalt cations is investigated. It is found that P2 Na xNi yCo 1–yO 2 materials with x = 0.66, 0.75, and 0 ≤ y ≤ 0.33 are either thermodynamically stable or metastable yet close to the convex hull at typical P2 synthesis temperatures (≈1000 K). It is demonstrated that a novel P2 compound with y = 0.22 and both Ni 3+/4+ and Co 3+/4+ can be successfully synthesized. It is studied electrochemically and structurally, using in situ and ex situ X‐ray diffraction. It is demonstrated that the chemical space of P2 layered compounds is not fully explored yet and that ab initio phase diagrams allow the determination of new high‐specific energy positive electrodes to be targeted experimentally. 相似文献
6.
Bacterial chromosomes have genes for transport proteins for inorganic nutrient cations and oxyanions, such as NH 4
+, K +, Mg 2+, Co 2+, Fe 3+, Mn 2+, Zn 2+ and other trace cations, PO 4
3-, SO 4
2- and less abundant oxyanions. Together these account for perhaps a few hundred genes in many bacteria. Bacterial plasmids
encode resistance systems for toxic metal and metalloid ions including Ag + AsO 2
-, AsO 4
3-, Cd 2+, Co 2+, CrO 4
2−, Cu 2+, Hg 2+, Ni 2+, Pb 2+, TeO 3
2−, TI + and Zn 2+. Most resistance systems function by energy-dependent efflux of toxic ions. A few involve enzymatic (mostly redox) transformations.
Some of the efflux resistance systems are ATPases and others are chemiosmotic ion/proton exchangers. The Cd 2+-resistance cation pump of Gram-positive bacteria is membrane P-type ATPase, which has been labeled with 32P from [γ- 32P]ATP and drives ATP-dependent Cd 2+ (and Zn 2+) transport by membrane vesicles. The genes defective in the human hereditary diseases of copper metabolism, Menkes syndrome
and Wilson’s disease, encode P-type ATPases that are similar to bacterial cadmium ATPases. The arsenic resistance system transports
arsenite [As(III)], alternatively with the ArsB polypeptide functioning as a chemiosmotic efflux transporter or with two polypeptides,
ArsB and ArsA, functioning as an ATPase. The third protein of the arsenic resistance system is an enzyme that reduces intracellular
arsenate [As(V)] to arsenite [As(III)], the substrate of the efflux system. In Gram-negative cells, a three polypeptide complex
functions as a chemiosmotic cation/protein exchanger to efflux Cd 2+, Zn 2+ and Co 2+. This pump consists of an inner membrane (CzcA), an outer membrane (CzcC) and a membrane-spanning (CzcB) protein that function
together.
Received 08 August 1997/ Accepted in revised form 01 November 1997 相似文献
7.
Essentially all bacteria have genes for toxic metal ion resistances and these include those for Ag+, AsO
−2
, AsO
3−4
, Cd2+, Co2+, CrO
2−4
, Cu2+, Hg2+, Ni2+, Pb2+, TeO
2−3
, Tl+ and Zn2+. The largest group of resistance systems functions by energy-dependent efflux of toxic ions. Fewer involve enzymatic transformations (oxidation, reduction, methylation, and demethylation) or metal-binding proteins (for example, metallothionein SmtA, chaperone CopZ and periplasmic silver binding protein SilE). Some of the efflux resistance systems are ATPases and others are chemiosmotic ion/proton exchangers. For example, Cd2+-efflux pumps of bacteria are either inner membrane P-type ATPases or three polypeptide RND chemiosmotic complexes consisting of an inner membrane pump, a periplasmic-bridging protein and an outer membrane channel. In addition to the best studied three-polypeptide chemiosmotic system, Czc (Cd2+, Zn2+, and Co2), others are known that efflux Ag+, Cu+, Ni2+, and Zn2+. Resistance to inorganic mercury, Hg2+ (and to organomercurials, such as CH3Hg+ and phenylmercury) involve a series of metal-binding and membrane transport proteins as well as the enzymes mercuric reductase and organomercurial lyase, which overall convert more toxic to less toxic forms. Arsenic resistance and metabolizing systems occur in three patterns, the widely-found ars operon that is present in most bacterial genomes and many plasmids, the more recently recognized arr genes for the periplasmic arsenate reductase that functions in anaerobic respiration as a terminal electron acceptor, and the aso genes for the periplasmic arsenite oxidase that functions as an initial electron donor in aerobic resistance to arsenite. 相似文献
9.
Bacterial plasmids encode resistance systems for toxic metal ions, including Ag +, AsO 2-, AsO 43-, Cd 2+, Co 2+, CrO 42-, Cu 2+ Hg 2+, Ni 2+, Pb 2+, Sb 3+, TeO 32-, Tl + and Zn 2+. The function of most resistance systems is based on the energy-dependent efflux of toxic ions. Some of the efflux systems are ATPases and others are chemiosmotic cation/proton antiporters. The Cd 2+-resistance ATPase of Gram-positive bacteria (CadA) is membrane cation pump homologous with other bacterial, animal and plant P-type ATPases. CadA has been labeled with 32P from [ α- 32p]ATP and drives ATP-dependent Cd 2+ (and Zn 2+) uptake by inside-out membrane vesicles (equivalent to efflux from whole cells). Recently, isolated genes defective in the human hereditary diseases of copper metabolism, namely Menkes syndrome and Wilson's disease, encode P-type ATPases that are more similar to bacterial CadA than to other ATPases from eukaryotes. The arsenic resistance efflux system transports arsenite [As(III)], alternatively using either a double-polypeptide (ArsA and ArsB) ATPase or a single-polypeptide (ArsB) functioning as a chemiosmotic transporter. The third gene in the arsenic resistance system, arsC, encodes an enzyme that converts intracellular arsenate [As(V)] to arsenite [As(III)], the substrate of the efflux system. The triple-polypeptide Czc (Cd 2+, Zn 2+ and Co 2+) chemiosmotic efflux pump consists of inner membrane (CzcA), outer membrane (CzcC) and membrane-spanning (CzcB) proteins that together transport cations from the cytoplasm across the periplasmic space to the outside of the cell. 相似文献
10.
The toxicity of heavy metals on photosystem 2 photochemistry, was investigated by monitoring Hill activity, fluorescence, and thermoluminescence properties of photosystem 2 (PS 2) in pea ( Pisum sativum L. cv. Bombay) chloroplasts. In Co 2+-, Ni 2+- or Zn 2+-treated chloroplasts 2,6-dichlorophenolindophenol-Hill activity was markedly inhibited. Addition of hydroxylamine which donates electrons close to PS 2 reaction center did not restore the PS 2 activity. Co 2+-, Ni 2+ or Zn 2+ also inhibited PS 2 activity supported by hydroxylamine in tris (hydroxymethyl)aminomethane (Tris)-inactivated chloroplasts. These observations were confirmed by fluorescence transient measurements. This implies that the metal ions inhibit either the reaction center or the components of PS 2 acceptor side. Flash-induced thermoluminescence studies revealed that the S 2Q ?A charge recombination was insensitive to metal ion addition. The S 2Q ?B charge recombination, however, was inhibited with increase in the level of Co 2+, Ni 2+ or Zn 2+. The observed sensitivity of S 2?B charge recombination in comparison to the stability of S 2Q ?A recombination suggests that the metal ions inhibit at the level of secondary quinone electron acceptor. Q B. We suggest that Co 2+, Ni 2+ or Zn 2+ do not block the electron flow between the primary and secondary quinone electron acceptor, but possibly, directly modify Q B site, leading to the loss of PS 2 activity. 相似文献
11.
The dimeric Cu–Zn superoxide dismutase (SOD1) is a particularly interesting system for biological inorganic chemical studies because substitutions of the native Cu and/or Zn ions by a nonnative metal ion cause minimal structural changes and result in high enzymatic activity for those derivatives with Cu remaining in the Cu site. The pioneering NMR studies of the magnetically coupled derivative Cu 2Co 2SOD1 by Ivano Bertini and coworkers are of particular importance in this regard. In addition to Co 2+, Ni 2+ is a versatile metal ion for substitution into SOD1, showing very little disturbance of the structure in Cu 2Ni 2SOD1 and acting as a very good mimic of the native Cu ion in Ni 2Zn 2SOD1. The NMR studies presented here were inspired by and are indebted to Ivano Bertini’s paramagnetic NMR pursuits of metalloproteins. We report Ni 2+ binding to apo wild-type SOD1 and a time-dependent Ni 2+ migration from the Zn site to the Cu site, and the preparation and characterization of Ni 2Ni 2SOD1, which shows coordination properties similar to those of Cu 2Cu 2SOD1, namely, an anion-binding property different from that of the wild type and a possibly broken bridging His. Mutations in the human SOD1 gene can cause familial amyotrophic lateral sclerosis (ALS), and mutant SOD1 proteins with significantly altered metal-binding behaviors are implicated in causing the disease. We conclude by discussing the effects of the ALS mutations on the remarkable stabilities and metal-binding properties of wild-type SOD1 proteins and the implications concerning the causes of SOD1-linked ALS. 相似文献
12.
Dihydroorotase (DHO; EC 3.5.2.3) is an essential metalloenzyme in the biosynthesis of pyrimidine nucleotides. Here, we identified
and characterized DHO from the pathogenic bacterium Klebsiella pneumoniae ( Kp). The activity of KpDHO toward l-dihydroorotate was observed with K
m = 0.04 mM and V
max = 8.87 μmol/(mg min). Supplementing the standard growth medium with Co 2+, Mn 2+, Mg 2+, or Ni 2+ increased enzyme activity. The catalytic activity of KpDHO was inhibited with Co 2+, Zn 2+, Mn 2+, Cd 2+, Ni 2+, and phosphate ions. Substituting the putative metal binding residues His17, His19, Lys103, His140, His178, and Asp251 with
Ala completely abolished KpDHO activity. However, the activity of the mutant D251E was fourfold higher than that of the wild-type protein. On the basis
of these biochemical and mutational analyses, KpDHO (KPN01074) was identified as type II DHO. 相似文献
13.
Background. Helicobacter pylori produces Hpn, a 60-amino acid, histidine-rich protein that avidly binds nickel and zinc ions, and NixA, a high-affinity nickel transporter in the cytoplasmic membrane. We tested the hypothesis that Hpn and NixA govern susceptibility to metal ions in H. pylori. Materials and Methods. Hpn-negative mutants of four H. pylori strains were constructed by standard allelic exchange techniques to yield isogenic Hpn +/Hpn-deficient pairs. A metal concentration that inhibited growth by 50% (IC 50) was calculated for Ni 2+, Zn 2+, Cu 2+, and Co 2+ by comparing OD 600 of cultures in metal-supplemented and control media. Results. Among all four pairs of isogenic strains, the tolerance for Ni 2+ was reduced significantly ( p < .001) in the Hpn mutants; the mean IC 50 value for wild-type strains was 1.9 mM; for the mutant, it was 0.8 mM. In contrast, growth inhibition by Zn 2+ was identical within the fours pairs, as was Cu 2+ and Co 2+ tolerance in one pair tested. We also found that deletion of the hpn gene increases susceptibility to therapeutic forms of bismuth by testing a mutant and wild-type pair with ranitidine bismuth citrate, bismuth citrate, and four antibiotics. Minimal inhibitory concentrations of ranitidine bismuth citrate dropped from 9.2 to 2.3 μg/ml, and those of bismuth citrate dropped from 7.4 to 3.2 μg/ml ( p < .05 for both comparisons), while susceptibility to the antibiotics was unaffected. Disruption of the nixA gene encoding the specific Ni 2+ transport protein of H. pylori did not change susceptibility to bismuth. Conclusion. We concluded that bacteria lacking Hpn, cultured in vitro, are more susceptible than is the wild type to bismuth and Ni 2+. 相似文献
14.
Human serum butyrylcholinesterase (BChE) has been converted into a stable but less active desensitized form when heated at
45°C for 24 h. The desensitized BChE follows Michaelis-Menten kinetics, whereas native enzyme exhibits slightly negative cooperativity
with respect to butyrylthiocholine binding. In this study, we investigated the effects of Ni 2+, Co 2+, and Mn 2+ on the desensitized BChE. It is found that all three ions were noncompetitive inhibitors of the desensitized BChE, and K
i
values have been determined as 7.816±1.060 m M, 48.722±4.635 m M, and 84.795±5.249 m M for Ni 2+, Co 2+, and Mn 2+, respectively. In our previous study, these ions were linear mixed-type inhibitors of the native BChE. This finding confirms
that desensitized BChE changes to a different conformation than native BChE. From the comparison of K
i
values of the trace elements, it can be said that Ni 2+ is a more effective inhibitor of the desensitized BChE than Co 2+ and Mn 2+. 相似文献
15.
Summary Studying metal ion resistances gives us important insights into environmental processes and provides an understanding of basic living processes. This review concentrates on bacterial efflux systems for inorganic metal cations and anions, which have generally been found as resistance systems from bacteria isolated from metal-polluted environments. The protein products of the genes involved are sometimes prototypes of new families of proteins or of important new branches of known families. Sometimes, a group of related proteins (and presumedly the underlying physiological function) has still to be defined. For example, the efflux of the inorganic metal anion arsenite is mediated by a membrane protein which functions alone in Gram-positive bacteria, but which requires an additional ATPase subunit in some Gram-negative bacteria. Resistance to Cd 2+ and Zn 2+ in Gram-positive bacteria is the result of a P-type efflux ATPase which is related to the copper transport P-type ATPases of bacteria and humans (defective in the human hereditary diseases Menkes' syndrome and Wilson's disease). In contrast, resistance to Zn 2+, Ni 2+, Co 2+ and Cd 2+ in Gram-negative bacteria is based on the action of proton-cation antiporters, members of a newly-recognized protein family that has been implicated in diverse functions such as metal resistance/nodulation of legumes/cell division (therefore, the family is called RND). Another new protein family, named CDF for cation diffusion facilitator has as prototype the protein CzcD, which is a regulatory component of a cobalt-zinc-cadmium resistance determinant in the Gram-negative bacterium Alcaligenes eutrophus. A family for the ChrA chromate resistance system in Gram-negative bacteria has still to be defined. 相似文献
16.
Summary Mycelial biomass of wild type and a Co 2+-resistant N.crassa (cor) was used to remove Co 2+ from aqueous media. Mycelia obtained from growth in nitrate N-medium (NaNO 3) was more effective than ammonium N-medium (NH 4NO 3), in removing Co 2+. Co 2+-resistant N.crassa cor was more efficient than wild type in removing Co 2+ from medium containing higher concentrations (500 mg/L). Metal removal was linear up to 12 h at which 35–60% Co 2+ is depleted from medium, reaching near saturation by 24 h (90% removal). Co 2+ removal was as efficient even from pure solutions and sodium azide inhibited the process up to 60%. Cell walls prepared from nitrate N-medium grown mycelia bound 3–5 fold more Co 2+ when compared to ammonium N-medium. The importance of bioaccumulation and biosorption in bioremediating toxic metal ions from effluents is discussed. 相似文献
17.
Cobalt‐free layered lithium‐rich nickel manganese oxides, Li[Li xNi yMn 1?x?y]O 2 (LLNMO), are promising positive electrode materials for lithium rechargeable batteries because of their high energy density and low materials cost. However, substantial voltage decay is inevitable upon electrochemical cycling, which makes this class of materials less practical. It has been proposed that undesirable voltage decay is linked to irreversible structural rearrangement involving irreversible oxygen loss and cation migration. Herein, the authors demonstrate that the voltage decay of the electrode is correlated to Mn 4+/Mn 3+ redox activation and subsequent cation disordering, which can be remarkably suppressed via simple compositional tuning to induce the formation of Ni 3+ in the pristine material. By implementing our new strategy, the Mn 4+/Mn 3+ reduction is subdued by an alternative redox reaction involving the use of pristine Ni 3+ as a redox buffer, which has been designed to be widened from Ni 3+/Ni 4+ to Ni 2+/Ni 4+, without compensation for the capacity in principle. Negligible change in the voltage profile of modified LLNMO is observed upon extended cycling, and manganese migration into the lithium layer is significantly suppressed. Based on these findings, we propose a general strategy to suppress the voltage decay of Mn‐containing lithium‐rich oxides to achieve long‐lasting high energy density from this class of materials. 相似文献
18.
Intracellular pH (pH i) is a crucial parameter in cellular physiology but its mechanisms of homeostasis are only partially understood. To uncover novel roles and participants of the pH i regulatory system, we have screened an Arabidopsis mutant collection for resistance of seed germination to intracellular acidification induced by weak organic acids (acetic, propionic, sorbic). The phenotypes of one identified mutant, weak acid‐tolerant 1‐1D ( wat1‐1D) are due to the expression of a truncated form of AP‐3 β‐adaptin (encoded by the PAT2 gene) that behaves as a as dominant‐negative. During acetic acid treatment the root epidermal cells of the mutant maintain a higher pH i and a more depolarized plasma membrane electrical potential than wild‐type cells. Additional phenotypes of wat1‐1D roots include increased rates of acetate efflux, K + uptake and H + efflux, the latter reflecting the in vivo activity of the plasma membrane H +‐ATPase. The in vitro activity of the enzyme was not increased but, as the H +‐ATPase is electrogenic, the increased ion permeability would allow a higher rate of H + efflux. The AP‐3 adaptor complex is involved in traffic from Golgi to vacuoles but its function in plants is not much known. The phenotypes of the wat1‐1D mutant can be explained if loss of function of the AP‐3 β‐adaptin causes activation of channels or transporters for organic anions (acetate) and for K + at the plasma membrane, perhaps through miss‐localization of tonoplast proteins. This suggests a role of this adaptin in trafficking of ion channels or transporters to the tonoplast. 相似文献
19.
Methyl jasmonate (MeJA) elicits stomatal closure in many plant species. Stomatal closure is accompanied by large ion fluxes across the plasma membrane (PM). Here, we recorded the transmembrane ion fluxes of H +, Ca 2+ and K + in guard cells of wild‐type (Col‐0) Arabidopsis, the CORONATINE INSENSITIVE1 ( COI1) mutant coi1‐1 and the PM H +‐ATPase mutants aha1‐6 and aha1‐7, using a non‐invasive micro‐test technique. We showed that MeJA induced transmembrane H + efflux, Ca 2+ influx and K + efflux across the PM of Col‐0 guard cells. However, this ion transport was abolished in coi1‐1 guard cells, suggesting that MeJA‐induced transmembrane ion flux requires COI1. Furthermore, the H + efflux and Ca 2+ influx in Col‐0 guard cells was impaired by vanadate pre‐treatment or PM H +‐ATPase mutation, suggesting that the rapid H + efflux mediated by PM H +‐ATPases could function upstream of the Ca 2+ flux. After the rapid H + efflux, the Col‐0 guard cells had a longer oscillation period than before MeJA treatment, indicating that the activity of the PM H +‐ATPase was reduced. Finally, the elevation of cytosolic Ca 2+ concentration and the depolarized PM drive the efflux of K + from the cell, resulting in loss of turgor and closure of the stomata. 相似文献
20.
Development of contact allergy requires cooperation of adaptive and innate immunity. Ni 2+ stimulates innate immunity via TLR4/MD2, the bacterial LPS receptor. This likely involves receptor dimerization, but direct proof is pending and it is unclear if related haptens share this mechanism. We reveal Co 2+ as second metal stimulating TLR4 and confirm necessity of H456/H458 therein. Experiments with a new TLR4 dimerization mutant established dimerization as a mechanism of metal‐ and LPS‐induced TLR4 activation. Yet, in interaction studies only LPS‐ but not metal‐induced dimerization required MD2. Consistently, soluble TLR4 expressed without MD2 inhibited metal‐ but not LPS‐induced responses, opening new therapeutic perspectives. 相似文献
|