Effects of Ni(2+), Co(2+), and Mn(2+) on desensitized butyrylcholinesterase prepared from human serum

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 Ni²⁺, Co²⁺, and Mn²⁺ 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 mM, 48.722±4.635 mM, and 84.795±5.249 mM for Ni²⁺, Co²⁺, and Mn²⁺, 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 Ni²⁺ is a more effective inhibitor of the desensitized BChE than Co²⁺ and Mn²⁺.     

Nickel and cobalt phytoextraction by the hyperaccumulator Berkheya coddii: implications for polymetallic phytomining and phytoremediation

We investigated the potential of the South African high-biomass Ni hyperaccumulator Berkheya coddii to phytoextract Co and/or Ni from artificial metalliferous media. Plant accumulation of both metals from single-element substrates indicate that the plant/media metal concentration quotient (bioaccumulation coefficient) increases as total metal concentrations increase. Cobalt was readily taken up by B. coddii with and without the presence of Ni. Nickel uptake was, however, inhibited by the presence of an equal concentration of Co. Bioaccumulation coefficients of Ni and Co for the single element substrates (total metal concentration of 1000 micrograms g-1) were 100 and 50, respectively. Cobalt phytotoxicity was observed above a total Co concentration in plant growth media of 20 micrograms g-1. Elevated Co concentrations significantly decreased the biomass production of B. coddii without affecting the bioaccumulation coefficients. The mixed Ni-Co substrate produced bioaccumulation coefficients of 22 for both Ni and Co. Cobalt phytotoxicity in mixed Ni-Co substrate occurred above a total Co concentration of 15 micrograms g-1. When grown in the presence of both Ni and Co, the bioaccumulation coefficients of each metal were reduced, as compared to single-element substrate. This may indicate competition for binding sites in the root zone. The interference relationship between Ni and Co uptake demonstrated by B. coddii suggests a significant limitation to phytoextraction where both metals are present.     

Thin Film Co3O4/TiO2 Heterojunction Solar Cells

Co₃O₄ is investigated as a light absorber for all‐oxide thin‐film photovoltaic cells because of its nearly ideal optical bandgap of around 1.5 eV. Thin film TiO₂/Co₃O₄ heterojunctions are produced by spray pyrolysis of TiO₂ as a window layer, followed by pulsed laser deposition of Co₃O₄ as a light absorbing layer. The photovoltaic performance is investigated as a function of the Co₃O₄ deposition temperature and a direct correlation is found. The deposition temperature seems to affect both the crystallinity and the morphology of the absorber, which affects device performance. A maximum power of 22.7 μW cm^?2 is obtained at the highest deposition temperature (600 °C) with an open circuit photovoltage of 430 mV and a short circuit photocurrent density of 0.2 mA cm^?2. Performing deposition at 600 °C instead of room temperature improves power by an order of magnitude and reduces the tail states (Urbach edge energy). These phenomena can be explained by larger grains that grows at high temperature, as opposed to many nucleation events that occur at lower temperature.     

Hyperaccumulator Alyssum murale relies on a different metal storage mechanism for cobalt than for nickel

The nickel (Ni) hyperaccumulator Alyssum murale has been developed as a commercial crop for phytoremediation/phytomining Ni from metal-enriched soils. Here, metal co-tolerance, accumulation and localization were investigated for A. murale exposed to metal co-contaminants. A. murale was irrigated with Ni-enriched nutrient solutions containing basal or elevated concentrations of cobalt (Co) or zinc (Zn). Metal localization and elemental associations were investigated in situ with synchrotron X-ray microfluorescence (SXRF) and computed-microtomography (CMT). A. murale hyperaccumulated Ni and Co (> 1000 microg g(-1) dry weight) from mixed-metal systems. Zinc was not hyperaccumulated. Elevated Co or Zn concentrations did not alter Ni accumulation or localization. SXRF images showed uniform Ni distribution in leaves and preferential localization of Co near leaf tips/margins. CMT images revealed that leaf epidermal tissue was enriched with Ni but devoid of Co, that Co was localized in the apoplasm of leaf ground tissue and that Co was sequestered on leaf surfaces near the tips/margins. Cobalt-rich mineral precipitate(s) form on leaves of Co-treated A. murale. Specialized biochemical processes linked with Ni (hyper)tolerance in A. murale do not confer (hyper)tolerance to Co. A. murale relies on a different metal storage mechanism for Co (exocellular sequestration) than for Ni (vacuolar sequestration).     

The RcnRA (YohLM) system of <Emphasis Type="Italic">Escherichia coli</Emphasis>: A connection between nickel,cobalt and iron homeostasis

The transporter RcnA has previously been implicated in Ni(II) and Co(II) detoxification in E. coli probably through efflux. Here we demonstrate that the divergently described rcnA and rcnR gene products constitute a link between nickel, cobalt and iron homeostasis. Deletion of the rcnA gene resulted in increased cellular nickel, cobalt and iron concentrations. Expression of rcnA was induced by Ni(II) or Co(II). Overproduction of rcnR inhibited induction of rcnA by metal cations but RcnR did not bind to the rcnA promoter in vitro. When rcnR or fur, the gene of the global repressor of iron homeostasis, was deleted, expression of rcnA was also induced by iron. The promoter region of rcnA was positive in a Fur titration (FURTA) in vivo assay indicative of Fur binding. Thus, rcnA is part of the Fur regulon of E.␣coli. The implications of a connection between the homoeostasis of closely related transition metals are discussed.     

ROLE OF SERUM AND ION CHANNEL BLOCK ON GROWTH AND HORMONALLY‐INDUCED DIFFERENTIATION OF Spodoptera frugiperda (Sf21) INSECT CELLS

A neuronal morphological phenotype can be induced in cultured Spodoptera frugiperda insect cells (Sf21) by supplementing serum‐containing media with 20‐hydroxyecdysone (20‐HE) and/or insulin. In this study, the primary objectives were to determine any role of ion channels in mediating the morphological change in cells treated with 20‐HE and insulin, and whether serum was required to observe this effect. Results showed serum‐free media also induced growth of processes in Sf21 cells, but at a lower percentage than that found previously in cells bathed in serum‐containing media. Veratridine, a sodium channel activator, increased cell survival when applied in combination with 20‐HE to Sf21 cells, and the effect was blocked by tetrodotoxin (1 μM) a known sodium channel blocker. Cobalt, a calcium channel blocker, showed significant inhibition of cell process growth when applied in combination with both 20‐HE and 20‐HE plus veratridine. Cobalt also showed significant inhibition of cell process growth when applied in combination with insulin. Thus, some type of sodium channel, as well as a mechanism for transmembrane calcium ion movement, are apparently expressed in Sf21 cells and are involved in the differentiation process. These cell lines may be used in a wide variety of endeavors, including the screening of insecticides, as well as foster basic studies of neurodevelopment and ecdysone action.     

Induction of hypoxia inducible factor-1 attenuates metabolic insults induced by 3-nitropropionic acid in rat C6 glioma cells

Compromised mitochondrial function in neurons and glia has been observed in several neurodegenerative disorders, including Huntington's disease and Alzheimer's disease. Chemical/hypoxic preconditioning may afford protection against subsequently more severe oxidative damages. In this study, we tested whether induction of hypoxia inducible factor-1 (HIF-1) may exert cytoprotective effects against mitochondrial dysfunction caused by 3-nitropropionic acid (3-NP) in glial cells. Preconditioning of C6 astroglial cells with cobalt chloride, mimosine (MIM), and desferrioxamine (DFO), all of which known to activate HIF-1, significantly attenuated cytotoxicity induced by 3-NP, an irreversible inhibitor of mitochondrial complex II, and antimycin A, a mitochondrial complex III inhibitor. Application of cadmium chloride capable of neutralizing cobalt-induced HIF-1 activation, HIF-specific oligodeoxynucleotide (ODN) decoy, and antisense phosphorothioate ODN against HIF-1alpha abolished the protective effect mediated by preconditioning with cobalt chloride. Preloading of C6 cells with SN50, PD98059, or SB202190, the respective inhibitor of nuclear factor-kappaB (NF-kappaB), p44/p42 extracellular signal-regulated kinase (ERK), and p38 mitogen-activated protein kinase (MAPK), failed to affect the protection afforded by cobalt preconditioning. Taken together, these results suggest that HIF-1 induction secondary to preconditioning with cobalt chloride or iron chelators may mediate the protective effects against metabolic insult induced by the mitochondrial inhibitor 3-NP in C6 astroglial cells.     

Cobalt complexes with cinchonidine and quinidine: effect of C8/C9 stereochemistry and 6'-substitution on intermolecular interactions

The title compounds, (cinchonidinium)trichlorocobalt(II) [(C(19)H(23)ON(2))CoCl(3)] (CoCdn) and (quinidinium)trichlorocobalt(II) [(C(20)H(25)O(2)N(2))CoCl(3)] (CoQd), are zwitterions that differ in absolute configuration and conformation. In both complexes, the sp(3) nitrogen of quinuclidine is protonated, whereas the sp(2) nitrogen of quinoline is linked to the Co(II) atom, which coordinates three chlorine atoms in distorted tetrahedral geometry. The mutual orientations of the quinoline and quinuclidine moieties in CoCdn and CoQd differ significantly because of different hydrogen bonding involving the hydroxyl group. In both complexes, the quinuclidine NH groups and hydroxyl groups are hydrogen-bond donors to the chlorine atoms of Co(II) tetrahedra. In CoQd the hydrogen bonding leads to formation of a nine-membered ring consisting of Co, two chlorines, and a fragment of the quinidine molecule. A comparison of the crystal structures of four Cinchona alkaloid complexes with trichlorocobalt(II) shows that their space groups are determined by the absolute configuration of the alkaloid, whereas the hydrogen-bonding pattern is mainly affected by the substituent in the quinoline ring, i.e., by hydrogen or methoxyl group.     

Electronic spectral studies of dinuclear Cobalt(II) complexes with a phenol-based dinucleating ligand containing four methoxyethyl chelating arms

The electronic spectra of dinuclear cobalt(II) complexes [Co₂(bomp)(MeCO₂)₂]BPh₄ (1) and [Co₂(bomp)(PhCO₂)₂]BPh₄ (2) were studied [H(bomp): 2,6-bis[bis(2-methoxyethyl)aminomethyl]-4-methylphenol]; the spectral components obtained by Gaussian curve analysis were well simulated based on the angular overlap model using the aomx program. The first transition band ⁴T₁ → ⁴T₂(⁴F) of an octahedral high-spin cobalt(II) complex was found to be sensitive to the distortion around the cobalt(II) ion.