Presence Of CoCl2 Research Articles

Synthesis and structures of copper(I) and cobalt(III) dimers with the dicyano-acetic acid methyl ester anion derived from TCNE

In the presence of CoCl2 · 6H2O or CuCl, the reaction of tetracyanoethylene and CH3OH provides a dicyano-acetic acid methyl ester anion (L1), which has been obtained as a bridged ligand in two compounds [(PPh3)2(NC)2CoIII(μ2-L12)CoIII(CN)2(PPh3)2] · (PPh3)(CH3OH) 1 and [(PPh3)2CuI(μ2-L12)CuI(PPh3)2] 2. The coordination geometry of the Co atom in 1 is distorted octahedral, and the Co atoms are μ2-bridged by two pairs of L. For compound 2, Cu is coordinated with two P atoms from PPh3 and two N atoms of L1, and two Cu atoms are linked by μ2-bridged L1.

Silicon-Mediated Synthesis of Selenoaldehydes and Selenoacylsilanes and Their Hetero Diels–Alder Reactions

Bis(trimethylsilyl)selenide (HMDSS) reacts efficiently with aldehydes in the presence of CoCl 2 .6H 2 O to afford selenoaldehydes, which are trapped as Diels–Alder adducts by different dienes. The reaction can be applied to acylsilanes, to afford selenoacylsilanes, isolated as their cycloadducts.

CoCl2 inhibits neural differentiation of retinoic acid-treated embryoid bodies

The effects of CoCl(2) on retinoic acid (RA)-treated embryoid bodies (EBs) were investigated. Four-day EBs were treated with 5x10(-6) M of RA for 4 d, then subjected to attached culturing for 7 d in the presence of CoCl(2) at 0, 20, and 100 microM. Differentiation into MAP2- and GFAP-immunopositive cells was inhibited by CoCl(2) in a dose-dependent manner. Next, RA-treated EBs were dissociated into single cells and cultured for 7 d at an initial cell density of 1x10(3)/cm(2). The number of cells increased in a CoCl(2)-dose dependent fashion. In cultures with 100 microM of CoCl(2), more than 90% of the cells were immunopositive for nestin and nestin-immunopositive cells formed clusters, while there were few cells immunopositive for MAP2 or GFAP. These results suggest that CoCl(2) inhibits neural differentiation of RA-treated EB cells and promotes the proliferation of nestin-immunopositive cells, i.e., embryonic stem (ES)-derived neural stem-like cells.

Chemistry of tetracyanoethylene (TCNE): From TCNE to dicyanomethylacetate

In the presence of CoCl 2 · 6H 2O, the reaction of TCNE (tetracyanoethylene) with CH 3OH forms a dicyanomethylacetate molecule, which has been obtained as one solvent molecule in one new compound {[Co(bpy) 2CN 2][(NC) 2C–CO 2CH 3]} · 2H 2O ( 1). It was characterized by IR spectra, UV–Vis spectra, and cyclic voltammogram. Its structure was determined by X-ray crystallography: 1 crystallizes in P2(1)/ n with a = 13.3368(17), b = 12.5299(16), c = 16.074(2) Å, α = 90, β = 94.6320(10), γ = 90°, and Z = 2.

Carcinogen adsorbent prepared from DNA complex by gamma-ray irradiation

The effects of gamma-ray irradiation on aqueous solutions of chub mackerel chromatin, salmon milt DNA with CoCl2, mixtures of DNA with Type A gelatin, bovine serum albumin (BSA), CM-chitosan, carboxymethyl cellulose (CMC) and Catinal (hydroxyethyl-cellulose, O-[2-hydroxy-3-(trimethyl ammonio)-propyl], chloride) and DNA in the presence of polyfunctional monomers with the aim to insolubilize DNA for preparing a novel carcinogen adsorbent have been studied. Among those, precipitates or inhomogeneous gel consisting of cross-linked DNA were prepared from the samples of aqueous DNA in the presence of CoCl2 at low irradiation dose, around 10 Gy, and bulk homogeneous gels were successfully prepared from aqueous mixtures of DNA with gelatin, BSA, CMC and Catinal in a limited range of irradiation doses. Gel fraction and swelling ratio of the gels were measured. Adsorption of a carcinogen, acridine orange, was also examined for the gels. From the experimental results, the optimum conditions for preparing insolubilized homogeneous DNA gels were determined.

A facile and efficient synthesis of some (6 E)-hydroximino-4-en-3-one steroids, steroidal oximes from Cinachyrella spp. sponges

Using β-sitosterol as a starting material, (6 E)-hydroximino-24-ethylcholest-4-en-3-one ( 1), a natural steroidal oxime from Cinachyrella alloclada and C. apion, was synthesized in four steps with a high overall yield. First, β-sitosterol ( 5a) is transformed into the corresponding 24-ethylcholest-4-en-3,6-dione ( 6a) via oxidation with pyridinium chlorochromate (PCC). Selective reduction of 6a by NaBH 4 in the presence of CoCl 2 gives 24-ethylcholest- 4-en-3β-ol-6-one ( 7a). The reaction of 7a with hydroxylamine hydrochloride offers the oxime 8a and the oxidation of 8a by Jones reagent gives the target steroid 1. (6 E)-Hydroximinocholest-4-en-3-one ( 2) and (6 E)-hydroximino-24-ethylcholest-4,22-dien-3-one ( 4) were synthesized by a similar method. The cytotoxicity of the synthesized compounds against sk-Hep-1 (human liver carcinoma cell line), H-292 (human lung carcinoma cell line), PC-3 (human prostate carcinoma cell line) and Hey-1B (human ovarian carcinoma cell line) cells were investigated. The presence of a cholesterol-type side chain appears to be necessary for the biological activity.

Melatonin modulates the expression of VEGF and HIF‐1α induced by CoCl2 in cultured cancer cells

Melatonin is an important natural oncostatic agent. At present there are no data available as to its possible influence on tumor angiogenesis, which is a major biological mechanism responsible for tumor growth and dissemination. It is well known that vascular endothelial growth factor (VEGF) is crucial to a solid tumor's higher vascularization and development. To investigate the possible influence of melatonin on angiogenesis, we studied the effect of melatonin on endogenous VEGF expression in three human cancer cell lines (PANC-1, HeLa and A549 cells). In this study, we report that physiologic concentrations of melatonin have no obvious impact on the VEGF expression, whereas pharmacologic concentrations of melatonin suppress the VEGF mRNA and protein levels induced by hypoxia mimetic cobalt chloride (CoCl(2)). Melatonin also decreases hypoxia-inducible factor (HIF)-1alpha protein levels, suggesting a role for transcription factor HIF-1 in the suppression of VEGF expression. The effect of pharmacologic concentrations of melatonin on VEGF and HIF-1alpha under normoxia is uncertain, which indicates that the regulatory mechanisms of VEGF in the absence or presence of CoCl(2) are different and other or additional transcription factors may be involved. Taken together, our data show that melatonin in high concentrations markedly reduces the expression of endogenous VEGF and HIF-1alpha induced by CoCl(2) in cultured cancer cells.

Cobalt chloride, a hypoxia‐mimicking agent, targets sterol synthesis in the pathogenic fungus Cryptococcus neoformans

We investigated the effects of the hypoxia-mimetic CoCl2 in the pathogenic fungus Cryptococcus neoformans and demonstrated that CoCl2 leads to defects in several enzymatic steps in ergosterol biosynthesis. Sterol defects were amplified in cells lacking components of the Sre1p-mediated oxygen-sensing pathway. Consequently, Sre1p and its binding partner Scp1p were essential for growth in the presence of CoCl2. Interestingly, high copies of a single gene involved in ergosterol biosynthesis, ERG25, rescued this growth defect. We show that the inhibitory effect of CoCl2 on scp1Delta and sre1Delta cells likely resulted from either an accumulation of non-viable methylated sterols or a decrease in the amount of ergosterol. Similar findings were also observed in the ascomycetous yeast, Schizosaccharomyces pombe, suggesting that the effects of CoCl2 on the Sre1p-mediated response are conserved in fungi. In addition, gene expression analysis revealed limited overlap between Sre1p-dependant gene activation in the presence of CoCl2 and low oxygen. The majority of genes similarly affected by both CoCl2 and low oxygen were involved in ergosterol synthesis and in iron/copper transport. This article identifies the Sre1p pathway as a common mechanism by which yeast cells sense and adapt to changes in both CoCl2 concentrations and oxygen levels.

Intersectin-1s Regulates the Mitochondrial Apoptotic Pathway in Endothelial Cells

Intersectins (ITSNs) are multidomain adaptor proteins implicated in endocytosis, regulation of actin polymerization, and Ras/MAPK signaling. We have previously shown that ITSN-1s is required for caveolae fission and internalization in endothelial cells (ECs). In the present study, using small interfering RNA to knock down ITSN-1s protein expression, we demonstrate a novel role of ITSN-1s as a key antiapoptotic protein. Knockdown of ITSN-1s in ECs activated the mitochondrial pathway of apoptosis as determined by genomic DNA fragmentation, extensive mitochondrial fission, activation of the proapoptotic proteins BAK and BAX, and cytochrome c efflux from mitochondria. ITSN-1 knockdown acts as a proapoptotic signal that causes mitochondrial outer membrane permeabilization, dissipation of the mitochondrial membrane potential, and generation of reactive oxygen species. These effects were secondary to decreased activation of Erk1/2 and its direct activator MEK. Bcl-X(L) overexpression prevented BAX activation and the apoptotic ECs death induced by suppression of ITSN-1s. Our findings demonstrate a novel role of ITSN-1s as a negative regulator of the mitochondrial pathway-dependent apoptosis secondary to activation of the Erk1/2 survival signaling pathway.

Mesocarbon microbeads heat-treated at low temperature in presence of CoCl 2 as the anode material of a Li-ion battery

Anode materials for Li-ion secondary batteries were prepared by treating mesocarbon microbeads (MCMBs) in presence of CoCl2 at a temperature below 1000℃. They were characterized by Raman spectroscopy and X-ray diffraction. Results indicated that the heat treated samples belonged to low temperature carbons, but micro-crystals on the surface of the treated MCMBs became ordered. The reversible discharge capacity of the MCMBs was significantly improved, the coulombic efficiency was increased from 52.2% to 86.7%, and the cycling performance became better. These improvements were ascribed to the ordered structure on the surface of the treated samples that tended to prevent the electrolyte molecules from penetrating into the inside of the MCMBs, and as a result, reduced the irreversible electrochemical reactions.

Synthesis, structure and DNA binding studies of a mononuclear cobalt(III) complex with a NNO donor Schiff base derived from 4-methyl-2,6-dibenzoylphenol and ethane-1,2-diamine

The mononuclear cationic cobalt(III) complex 1 [Co(L) 2] + [where HL is H 2N(CH 2) 2NC(Ph)C 6H 2(Me)(OH)COPh] has been obtained by the condensation of 4-methyl-2,6-dibenzoylphenol and ethane-1,2-diamine in the presence of CoCl 2 · 6H 2O and isolated as the chloride solvate { 1 · Cl · 2H 2O · EtOH}. The water and ethanol do not form part of the cobalt(III) pseudo-octahedral [Co(L) 2] + coordination sphere, which is cis-CoN 4O 2 with the NNO-ligands mer. Compound 1 has been characterised by mass spectrometry, IR, electronic, 1H and 13C NMR spectroscopy, conductivity measurements, elemental analysis, TGA, cyclic voltammetry and an X-ray structural determination. The average Co–N and Co–O distances are, respectively, 1.929(4) and 1.882(3) Å. The N⋯N intraligand bite distance is 2.73(4) Å and the N–Co–N and O–Co–O angles are, respectively, 86.2(15)° and 93.3(13)°. Cyclic voltammetric studies of complex 1 indicate an irreversible cathodic peak ( E pc, ca. −0.61 V) corresponding to the reduction of cobalt(III) to cobalt(II). Absorption titration experiments gave a binding constant for DNA interaction of 1.4 × 10 4 M −1 and a binding site size 0.16 base pairs.

In vitro cytotoxicity of a theaflavin mixture from black tea to malignant, immortalized, and normal cells from the human oral cavity

The growth inhibitory effects of a theaflavin mixture from black tea were more pronounced to malignant (CAL27; HSC-2; HSG1) and immortalized (S-G; GT1) cells than to normal (HGF-2) cells from the human oral cavity. Studies with malignant carcinoma CAL27 cells and immortalized GT1 fibroblasts showed that cytotoxicity of the theaflavin mixture was enhanced as the exposure time was increased, with the tumor CAL27 cells more sensitive than the GT1 cells. Hydrogen peroxide (H 2O 2) was detected in cell culture medium amended with the theaflavin mixture. The level of H 2O 2 in cell culture medium amended with the theaflavin mixture was lessened in the presence of catalase and CoCl 2; the level of authentic H 2O 2 was also lessened in the presence of CoCl 2, suggesting that Co 2+ led to the rapid catalytic decomposition of H 2O 2. The cytotoxicity of the theaflavin mixture was due, in part, to the generation in the cell culture medium of H 2O 2, which lessened the intracellular levels of glutathione in the CAL27 cells and, to a lesser extent, in the GT1 cells. For both cell types, coexposures of the theaflavin mixture with catalase or CoCl 2 afforded protection.

Hypoxia-inducible Factor-1-dependent Overexpression of Myeloid Cell Factor-1 Protects Hypoxic Cells against tert-Butyl Hydroperoxide-induced Apoptosis

Increased levels of Mcl-1 (myeloid cell factor-1) have been reported in several cancers, suggesting an important role played by Mcl-1 in cancer cell survival. Mcl-1 is an anti-apoptotic protein shown to delay or block apoptosis. In this work, using semiquantitative immunofluorescence, real-time PCR, and RNase protection assay, an increase in Mcl-1 expression was detected in hepatoma HepG2 cells incubated under hypoxia or in the presence of cobalt chloride. Through analysis of the Mcl-1 promoter sequence, a putative HIF-1 (hypoxiainducible factor-1) binding site was identified. A Mcl-1 promoter fragment containing this hypoxia-responsive element was able to bind HIF-1 in vitro. It also induced hypoxia-dependent transcription of a luciferase reporter gene, which was suppressed by anti-HIF-1alpha short interfering RNA. Finally, overexpression of Mcl-1 protected HepG2 cells against apoptosis induced by tert-butyl hydroperoxide as shown by inhibition of caspase-3 activation and DNA fragmentation. All these data suggest a potential anti-apoptotic role of HIF-1 that could protect cells against apoptosis under hypoxia by overexpression of the Mcl-1 protein.

Synthesis of Polymeric Calix[4]arene Dinitrile and Diamino‐Derivatives: Exploration of Their Extraction Properties Towards Dichromate Anion

The article describes the syntheses and extraction properties of new alkylnitrile and alkylamino substituted calix[4]arene based copolymers. These compounds have been synthesized via nucleophilic substitution reactions involving 5,11,17,23‐tetra‐tert‐butyl‐25,27‐bis(cyanomethoxy)‐26,28‐dihydroxycalix[4]arene (3), or 25,27‐bis(cyanomethoxy)‐26,28‐dihydroxycalix[4]arene (4) with 1,5‐dibromopentane and bisphenol‐A, followed by their reduction with sodium borohydride in the presence of CoCl2 · 6H2O. In addition an oligomer containing pendant calix[4]arene units with nitrile functionalities on its lower rim has been synthesized via nucleophilic reaction involving 5,11,17,23‐tetra‐tert‐butyl‐25,27‐bis(cyanomethoxy)‐26,28‐dihydroxycalix[4]arene 3 with p‐dibromoxylene. The extraction properties of polymers 5–9 toward the HCr2O7 − anion are also reported. Due to the higher oxidative stability of nitrile groups, polymers 5–7 have been developed as good extractants for transferring the HCr2O7 − anion from an aqueous into a dichloromethane phase.

Cobalt‐Catalyzed Allylic Substitution Reaction of Allylic Ethers with Phenyl and Trimethylsilylmethyl Grignard Reagents.

Treatment of cinnamyl methyl ether with phenylmagnesium bromide in ether in the presence of CoCl 2 [1,5-bis(diphenylphosphino)pentane] affords 1,3-diphenylpropene in good yield. Similar allylic substitution reaction with trimethylsilylmethylmagnesium chloride proceeded smoothly to yield homoallylsilanes. α,β-Unsaturated aldehyde acetal also underwent allylic substitution.

Mediation of the in vitro cytotoxicity of green and black tea polyphenols by cobalt chloride

The effects of Co 2+ (as CoCl 2) on the cytotoxicity of green tea polyphenol (GTP) and black tea polyphenol (BTP) extracts towards proliferation of immortalized human gingival epithelial-like S-G cells were studied. The 24 h potencies of GTP and BTP extracts, as determined with the neutral red (NR) cell viability assay, were greatly reduced in the presence of 250, but not of 50, μM Co 2+ . The cytotoxicities of the GTP and BTP extracts were due, in part, to their generation of hydrogen peroxide (H 2O 2) in the cell culture medium (DMEM). Progressively increasing the concentration of Co 2+ in the tea polyphenol-amended cell culture medium resulted in a lowering of the level of H 2O 2. The cytotoxicity of freshly added H 2O 2 to S-G cells was abolished in the presence of 250 μM Co 2+ and the level of freshly added H 2O 2 to cell culture medium was progressively lowered as the concentration of Co 2+ was increased. Apparently, under the conditions of these studies, the decreases in the cytotoxicity of GTP and BTP extracts in the presence of CoCl 2 were due to the rapid catalytic decomposition by Co 2+ of the H 2O 2 generated in the tea polyphenol-amended cell culture medium.

Involvement of mitochondrial- and Fas-mediated dual mechanism in CoCl 2-induced apoptosis of rat PC12 cells

Hypoxic/ischemic condition induces neuronal apoptotic events, which consequently lead to neuronal cell death. However, its specific mechanistic pathways remain obscure. Cobalt chloride (CoCl 2) could mimic the hypoxic condition including the production of reactive oxygen species (ROS). In this report, we investigated the signal pathway of CoCl 2-induced apoptosis in PC12 cells. The main mechanism for these apoptosis appeared to be mitochondria-mediated pathway accompanied with loss of the mitochondrial transmembrane potential (ΔΨm) followed by cytochrome c release from the mitochondria into the cytosol, resulting in the activation of caspase-9 and caspase-3. Also, upregulation of pro-apoptotic protein Bax, and downregulation of anti-apoptotic protein Bcl-2 by presence of CoCl 2 appeared significantly and it might result in activating mitochondria-mediated apoptosis. We showed that expression of Fas and Fas ligand was upregulated and caspase-8 was significantly activated in CoCl 2-induced apoptotic cells. In addition, ZB4, an antagonistic Fas-antibody, inhibited the activation of caspase-8 by CoCl 2, indicating that Fas receptor was involved in this pathway. These results demonstrate that CoCl 2 induce apoptosis in PC12 cells via different dual apoptosis pathway through death receptor as well as mitochondria.

Induction of glucose transporter 1 expression through hypoxia-inducible factor 1α under hypoxic conditions in trophoblast-derived cells

Glucose transporter 1 (GLUT1) plays an important role in the transport of glucose in the placenta. During early pregnancy, placentation occurs in a relatively hypoxic environment that is essential for appropriate embryonic development, and GLUT1 expression is enhanced in response to oxygen deficiency in the placenta. Hypoxia-inducible factor-1 (HIF-1)alpha is involved in the induction of GLUT1 expression in other cells. The present study was designed to test whether HIF-1alpha is involved in hypoxia-induced activation of GLUT1 expression using trophoblast-derived human BeWo and rat Rcho-1 cells as models. GLUT1 mRNA and protein expression were elevated under 5% O2 or in the presence of cobalt chloride, which has been shown to mimic hypoxia. Using rat GLUT1 (rGLUT1) promoter-luciferase constructs, we showed that this up-regulation was mediated at the transcriptional level. Deletion mutant analysis of the rGLUT1 promoter indicated that a 184 bp hypoxia-responsive element (HRE) of the promoter was essential to increase GLUT1 reporter gene expression in response to low-oxygen conditions. BeWo and Rcho-1 cells cultured under 5% O2 or with CoCl2 showed increased expression of HIF-1alpha protein compared with those cultured under 20% O2. To test whether this factor is directly involved in hypoxia-induced GLUT1 promoter activation, BeWo and Rcho-1 cells were transiently transfected with an HIF-1alpha expression vector. Exogeneous HIF-1alpha markedly increased the GLUT1 promoter activity from constructs containing the HRE site, while the GLUT1 promoter constructs lacking the HRE site were not activated by exogenous HIF-1alpha These data demonstrate that GLUT1 is up-regulated under 5% O2 or in the presence of CoCl2 in the placental cell lines through HIF-1alpha interaction with a consensus HRE site of the GLUT1 promoter.

Study of l-aminoacylase deactivation in an ultrafiltration membrane reactor

The behaviour of an ultrafiltration membrane reactor (UFMR) (60 cm 3 of reactor volume) for the optical resolution of dl-butyrine catalysed by l-aminoacylase was studied, and the influence of substrate concentration (15–25 mmol dm −3 in N-acetyl- l-butyrine), temperature (30–50 °C) and the presence of CoCl 2 (0.5 mmol dm −3) on enzyme deactivation was analysed. Adsorption studies with polysulphone and regenerated cellulose membranes (30 cm 2 of filtration surface), as well as deactivation studies in the reaction conditions, were carried out to determine the causes of deactivation. A single-step deactivation scheme is proposed, and it was shown that this first-order model adequately describes enzyme deactivation. The dependence of K d on the enzyme concentration points to the enzyme deactivation, which is mainly caused by the adsorption phenomena on the membrane surface.

Cobalt-Catalyzed Allylic Substitution Reaction of Allylic Ethers with Phenyl and Trimethylsilylmethyl Grignard Reagents

Abstract Treatment of cinnamyl methyl ether with phenylmagnesium bromide in ether in the presence of CoCl2[1,5-bis(diphenylphosphino)pentane] affords 1,3-diphenylpropene in good yield. Similar allylic substitution reaction with trimethylsilylmethylmagnesium chloride proceeded smoothly to yield homoallylsilanes. α,β-Unsaturated aldehyde acetal also underwent allylic substitution.