Simvastatin ameliorates synaptic plasticity impairment in chronic mild stress-induced depressed mice by modulating hippocampal NMDA receptor.

BACKGROUND: In our previous study, we showed simvastatin exerts an antidepressant effect and inhibits neuroinflammation. Given the role of synaptic impairment in depression development, we investigate the effect of simvastatin on synaptic plasticity in depression and the related mechanisms. METHODS: Electrophysiological analysis, Golgi staining, and transmission electron microscope were performed to analyze the effect of simvastatin on synaptic impairment in depression. In addition, the localization and reactivity of N-methyl-D-aspartate receptor (NMDAR) subunits and the downstream signaling were investigated to explore the mechanism of simvastatin's effect on synaptic plasticity. RESULTS: Simvastatin ameliorated the reduction of the magnitude of long-term potentiation (LTP) in Schaffer collateral-CA1, restored hippocampal dendritic spine density loss, improved the number of spine synapses, reversed the reduction in BrdU-positive cells in chronic mild stress (CMS)-induced depressed mice, and ameliorated NMDA-induced neurotoxicity in hippocampal neurons. Dysfunction of NMDAR activity in the hippocampus is associated with depression. Simvastatin treatment reversed the surface expression and phosphorylation changes of NMDAR subunits in NMDA-treated hippocampal neurons and depressed mice. In addition, simvastatin further increased the levels of mature BDNF, activating TrkB-Akt-mTOR signaling, which is critical for synaptic plasticity. CONCLUSIONS: These findings suggest that simvastatin can improve the dysfunction of NMDAR and ameliorate hippocampal synaptic plasticity impairment in depressed mice.

Two new cadmium(II) coordination polymers based on imidazole-containing ligands: synthesis, structural characterization and fluorescence properties.

The judicious selection of suitable ligands is vitally important in the construction of novel metal-organic frameworks (MOFs) with fascinating structures and interesting properties. Recently, imidazole-containing multidentate ligands have received much attention. Two new CdII coordination frameworks, namely, poly[tris{µ-1,4-bis[(1H-imidazol-1-yl)methyl]benzene-κ2N3:N3'}tetrakis(nitrato-κ2O,O')dicadmium], [Cd2(NO3)4(C14H14N4)3]n, (I), and poly[[bis{µ3-1,3,5-tris[(1H-imidazol-1-yl)methyl]benzene-κ3N3:N3':N3''}cadmium] hexafluorosilicate], {[Cd(C18H18N6)2](SiF6)}n, (II), have been synthesized and characterized by elemental analysis, IR spectroscopy and single-crystal X-ray diffraction. In polymer (I), the 1,4-bis[(1H-imidazol-1-yl)methyl]benzene ligand bridges Cd2+ ions with a distorted seven-coordinated pentagonal bipyramidal geometry, forming a one-dimensional ladder chain, and the nitrate anions coordinate to the Cd2+ ions in a terminal bidentate fashion. In the crystal, adjacent chains are further connected by C-H...O hydrogen bonds to generate a two-dimensional (2D) supramolecular structure. Polymer (II) exhibits a 2D layered structure in which 1,3,5-tris[(1H-imidazol-1-yl)methyl] benzene ligands join Cd2+ centres having a six-coordinated octahedral structure. The layers are connected by hexafluorosilicate anions via C-H...F hydrogen-bond interactions, giving rise to a three-dimensional supramolecular network structure in the solid state. In addition, powder X-ray diffraction (PXRD) patterns were recorded, thermogravimetric analyses (TGA) carried out and fluorescence properties investigated.

New views and possibilities of antidiabetic drugs in treating and/or preventing mild cognitive impairment and Alzheimer's Disease.

Mounting evidence suggests that diabetes mellitus (DM) is associated with mild cognitive impairment (MCI), vascular dementia and Alzheimer's disease (AD). Biological, clinical and epidemiological data support a close link between DM and AD. Increasingly, studies have found that several antidiabetic agents can promote neurogenesis, and clinically ameliorate cognitive and memory impairments in different clinical settings. Data has shown that these antidiabetic drugs positively affect mitochondrial and synaptic function, neuroinflammation, and brain metabolism. Evidence to date strongly suggests that these antidiabetic drugs could be developed as disease-modifying therapies for MCI and AD in patients with and without diabetes.

A new one-dimensional NiII coordination polymer with a two-dimensional supra-molecular architecture.

A new one-dimensional NiII coordination polymer of 1,3,5-tris-(imidazol-1-ylmeth-yl)benzene, namely catena-poly[[aqua-(sulfato-κO)hemi(µ-ethane-1,2-diol-κ2O:O')[µ3-1,3,5-tris-(1H-imidazol-1-ylmeth-yl)benzene-κ3N3,N3',N3'']nickel(II)] ethane-1,2-diol monosolvate monohydrate], {[Ni(SO4)(C18H18N6)(C2H6O2)0.5(H2O)]·C2H6O2·H2O} n , was synthesized and characterized by elemental analysis, IR spectroscopy and single-crystal X-ray diffraction. The NiII cation is coordinated by three N atoms of three different 1,3,5-tris-(imidazol-1-ylmeth-yl)benzene ligands, one O atom of an ethane-1,2-diol mol-ecule, by a sulfate anion and a water mol-ecule, forming a distorted octa-hedral NiN3O3 coordination geometry. The tripodal 1,3,5-tris-(imidazol-1-ylmeth-yl)benzene ligands link the NiII cations, generating metal-organic chains running along the [100] direction. Adjacent chains are further connected by O-H⋯O hydrogen bonds, resulting in a two-dimensional supermolecular architecture running parallel to the (001) plane. Another water mol-ecule and a second ethane-1,2-diol mol-ecule are non-coordinating and are linked to the coordinating sulfate ions via O-H⋯O hydrogen bonds.

A new three-dimensional manganese(II) coordination polymer based on the 1,3,5-tris[(1H-imidazol-1-yl)methyl]benzene ligand.

The self-assembly of coordination polymers and the crystal engineering of metal-organic coordination frameworks have attracted great interest, but it is still a challenge to predict and control the compositions and structures of the complexes. Employing multidentate organic ligands and suitable metal ions to construct inorganic-organic hybrid materials through metal-ligand coordination and hydrogen-bonding interactions has become a major strategy. Recently, imidazole-containing multidentate ligands that contain an aromatic core have received much attention. A new three-dimensional MnII coordination polymer based on 1,3,5-tris[(1H-imidazol-1-yl)methyl]benzene, namely poly[(ethane-1,2-diol-κO)(µ-sulfato-κ2O:O'){µ3-1,3,5-tris[(1H-imidazol-1-yl)methyl]benzene-κ3N:N':N''}manganese(II)], [Mn(SO4)(C18H18N6)(C2H6O2)]n, was synthesized and characterized by elemental analysis, IR spectroscopy and single-crystal X-ray diffraction. Crystal structural analysis shows that there are two kinds of crystallographically independent MnII centres, each lying on a centrosymmetric position and having a similar six-coordinated octahedral structure. One is coordinated by four N atoms from four 1,3,5-tris[(1H-imidazol-1-yl)methyl]benzene (timb) ligands and two O atoms from two different bridging sulfate anions. The second is surrounded by two timb N atoms and four O atoms, two from sulfate anions and two from two ethane-1,2-diol ligands. The tripodal timb ligand bridges neighbouring MnII centres to generate a two-dimensional layered structure running parallel to the ab plane. Adjacent layers are further bridged by sulfate anions, resulting in a three-dimensional structure with 3,4,6-c topology. Thermogravimetric analysis of the title polymer shows that it is stable up to 533 K. The first weight loss between 533 and 573 K corresponds to the release of coordinated ethane-1,2-diol molecules, and further decomposition occurred at 648 K.

Antidiabetic drugs restore abnormal transport of amyloid-ß across the blood-brain barrier and memory impairment in db/db mice.

Previous studies have shown significant changes in amyloid-ß (Aß) transport across the blood-brain barrier (BBB) under diabetic conditions with hypoinsulinemia, which is involved in diabetes-associated cognitive impairment. Present study employed db/db mice with hyperinsulinemia to investigate changes in Aß transport across the BBB, hippocampal synaptic plasticity, and restorative effects of antidiabetic drugs. Our results showed that db/db mice exhibited similar changes in Aß transport across the BBB to that of insulin-deficient mice. Chronic treatment of db/db mice with antidiabetic drugs such as metformin, glibenclamide and insulin glargine significantly decreased Aß influx across the BBB determined by intra-arterial infusion of (125)I-Aß(1-40), and expression of the receptor for advanced glycation end products (RAGE) participating in Aß influx. Insulin glargine, but not, metformin or glibenclamide increased Aß efflux across the BBB determined by stereotaxic intra-cerebral infusion of (125)I-Aß(1-40), and expression of the low-density lipoprotein receptor related protein 1 (LRP1) participating in Aß efflux. Moreover, treatment with these drugs significantly decreased hippocampal Aß(1-40) or Aß(1-42) and inhibited neuronal apoptosis. The drugs also ameliorated memory impairment confirmed by improved performance on behavioral tasks. However, insulin glargine or glibenclamide, but not metformin, restored hippocampal synaptic plasticity characterized by enhancing in vivo long-term potentiation (LTP). Further study found that these three drugs significantly restrained NF-κB, but only insulin glargine enhanced peroxisome proliferator-activated receptor γ (PPARγ) activity at the BBB in db/db mice. Our data indicate that the antidiabetic drugs can partially restore abnormal Aß transport across the BBB and memory impairment under diabetic context.

PPARγ agonists regulate bidirectional transport of amyloid-ß across the blood-brain barrier and hippocampus plasticity in db/db mice.

BACKGROUND AND PURPOSE: There is emerging evidence suggesting that abnormal transport of amyloid-ß (Aß) across the blood-brain barrier (BBB) is involved in diabetes-associated cognitive decline. We investigated whether PPARγ agonists restore Aß transport across the BBB and hippocampal plasticity in db/db mice. EXPERIMENTAL APPROACH: Efflux and influx of Aß across the BBB were determined by stereotaxic intra-cerebral or i.a. infusion of [(125) I]-Aß1-40 respectively. Receptor for advanced glycation end products (RAGE) and low-density lipoprotein receptor-related protein 1 (LRP1), which are involved in Aß influx and efflux, PPARγ and NF-κB p65 at the BBB, as well as hippocampal Aß, caspase-3, Bax and Bcl-2 were assayed by Western blot, immunohistochemistry and RT-PCR. In vivo, hippocampal LTP was recorded, and Morris water maze and Y-maze tasks were performed. KEY RESULTS: Treatment with PPARγ agonists, rosiglitazone (0.8 mg·kg(-1) ) and pioglitazone (9.0 mg·kg(-1) ), for 6 weeks significantly increased Aß efflux and decreased Aß influx across the BBB in db/db mice. Concomitantly, they decreased hippocampal Aß1-40 and Aß1-42 , suppressed neuronal apoptosis, as indicated by decreased caspase-3 activity and increased ratio of Bcl-2/Bax, and increased hippocampal plasticity, characterized by an enhanced in vivo LTP and better performance in behavioural tests. Furthermore, the PPARγ agonists induced the expression of LRP1 gene by activation of PPARγ and suppressed RAGE gene expression by inactivation of NF-κB signalling at the BBB of db/db mice. CONCLUSIONS AND IMPLICATIONS: PPARγ agonists modify abnormal Aß transport across the BBB and this is accompanied by amelioration of ß-amyloidosis and an improvement in hippocampal plasticity in diabetic mice.

Pretreatment with antiasthmatic drug ibudilast ameliorates Aß 1-42-induced memory impairment and neurotoxicity in mice.

Amyloid-ß peptide (Aß) is thought to be associated with the progressive neuronal death observed in Alzheimer's disease (AD). However, effective neuroprotective approaches against Aß neurotoxicity are unavailable. Here, we investigated possible preventive effects of ibudilast, as a pharmacologic phosphodiesterase inhibitor, currently used for treatment of inflammatory diseases such as asthma, on Aß 1-42-induced neuroinflammatory, apoptotic responses and memory impairment. We found that pretreatment with ibudilast (4 or 12 mg/kg, i.p.) significantly ameliorated impaired spatial learning and memory in intracerebroventricularly (ICV) Aß 1-42-injected mice, as evidenced by decrease in escape latency during acquisition trials and increase in exploratory activities in the probe trial in Morris water maze (MWM) task, and by increase in the number of correct choices and decrease in latency to enter the shock-free compartment in Y-maze test. Further study showed that ibudilast prevented generation of pro-inflammatory cytokines such as NF-κB p65 and TNF-α as well as pro-apoptotic molecule caspase-3 activation and anti-apoptotic protein Bcl-2 downregulation in both hippocampus and cortex of ICV Aß 1-42-injected mice. Taken together, our findings suggest that ibudilast has preventive effects on Aß-induced cognitive impairment via inhibiting neuroinflammatory and apoptotic responses.

Bis(6-nitro-1,10-phenanthrolin-1-ium) 2,5-di-carb-oxy-terephthalate.

In the structure of the title 2:1 proton-transfer compound, 2C12H8N3O2 (+)·C10H4O8 (2-), the 6-nitro-1,10-phenanthroline mol-ecules act as proton sponges, accepting protons from pyromellitic acid. The -NO2 group of one of the 6-nitro-1,10-phenanthrolin-1-ium cations is disordered and was refined with a site-occupancy ratio of 0.624 (15):0.376 (15). Two -COOH(-COO(-)) groups of the 2,5-di-carb-oxy-terephthalate dianion are disordered and were refined with site-occupancy ratios of 0.769 (4):0.231 (4) and 0.766 (5):0.234 (5). The -NO2 group of the second cation is also disordered about a pseudo-twofold rotation axis and was refined with a site-occupancy ratio of 0.903 (3):0.097 (3). There is an intra-molecular O-H⋯O hydrogen bond in the anion. The phenanthroline rings of the two cations are inclined to one another by 31.3 (1)°. In the anions, considering the major components only, the carb-oxy-lic acid groups (-COOH) are inclined to the benzene ring by 17.3 (2) and 22.3 (3)°. The carboxyl-ate groups (-COO(-)) are twisted by 9.3 (2) and 13.6 (6)° with respect to the benzene ring. In the crystal, adjacent 2,5-di-carb-oxy-terephthalate anions are linked via O-H⋯O hydrogen bonds, forming chains propagating along [010]. The cations are attached to the chain of anions by N-H⋯O hydrogen bonds.

A novel three-dimensional Zn(II) coordination polymer with 1,3,5-tris(imidazol-1-ylmethyl)benzene and cyclohexane-1,3,5-tricarboxylate ligands.

In the Zn(II) compound poly[[bis(µ3-cyclohexane-1,3,5-tricarboxylato)bis[µ3-1,3,5-tris(imidazol-1-ylmethyl)benzene]trizinc(II)] hexahydrate], {[Zn3(C18H18N6)2(C9H9O6)2]·6H2O}n, based on mixed 1,3,5-tris(imidazol-1-ylmethyl)benzene and cyclohexane-1,3,5-tricarboxylate ligands, there are two types of crystallographically independent Zn(II) centres, one in a general position and one on a crystallographic twofold axis. They have similar fourfold distorted tetrahedral coordination geometries, ligated by two monodentate carboxylate groups from two cyclohexane-1,3,5-tricarboxylate ligands and by two N atoms from two 1,3,5-tris(imidazol-1-ylmethyl)benzene ligands. The cyclohexane-1,3,5-tricarboxylate anions link the Zn(II) cations to generate a two-dimensional layered metal-organic structure running parallel to the (201) plane. Adjacent layers are further connected by tripodal 1,3,5-tris(imidazol-1-ylmethyl)benzene ligands, resulting in a three-dimensional network. The solvent water molecules are linked to the cyclohexane-1,3,5-tricarboxylate ligands via water-carboxylate O-H···O hydrogen bonds.

Two-dimensional hydrogen-bonded supramolecular networks in the compounds of benzene-1,2,4,5-tetracarboxylic acid (pyromellitic acid) with 2,2'-biimidazole and 4,4'-dimethyl-2,2'-bipyridine.

Two products from the proton-transfer reactions of benzene-1,2,4,5-tetracarboxylic acid (pyromellitic acid, PMA) with 2,2'-biimidazole and 4,4'-dimethyl-2,2'-bipyridine, namely 2,2'-biimidazole-3,3'-diium 2,5-dicarboxybenzene-1,4-dicarboxylate, C6H8N4(2+),C10H4O8(2-), (I), and 4-methyl-2-(4-methylpyridin-2-yl)pyridinium 2,4,5-tricarboxybenzoate monohydrate, C12H13N2(+)·C10H5O8(-)·H2O, (II), have been prepared and their structures determined. Both compounds crystallize in the space group P1. The asymmetric unit of (I) is composed of two independent ion pairs. Both the 2,2'-biimidazole-3,3'-diium dication and the PMA(2-) anion are located on special positions (inversion centres). The protonated 2,2'-biimidazole-3,3'-diium ring H atoms are involved in hydrogen bonding with carboxylate O atoms to form one-dimensional hydrogen-bonded chain structures. Adjacent chains are further linked via carboxyl-carboxyl O-H···O hydrogen bonding, resulting in a two-dimensional supramolecular sheet with the R6(5)(34) motif extending in the (1-21) plane. In (II), classical O-H···O hydrogen-bond-linked anion-anion units are extended into a one-dimensional chain running parallel to the [100] direction, giving an R2(2)(8)R4(4)(30) motif. The chains are connected by water-carboxyl O-H···O hydrogen bonds to form a two-dimensional network parallel to the (011) plane. The 4-methyl-2-(4-methylpyridin-2-yl)pyridinium cations lie between the two-dimensional supramolecular layers linked via N-H···O hydrogen-bonding interactions.

Bis(1,10-phenanthroline-κ(2) N,N')(sulfato-κO)zinc(II) propane-1,2-diol monosolvate.

In the title compound, [Zn(SO4)(C12H8N2)2]·C3H8O2, the Zn(II) ion is in a distorted square-pyramidal coordination environment composed of four N atoms from two chelating 1,10-phenanthroline ligands and one O atom from a monodentate sulfate ligand. The Zn(II) ion lies on a twofold rotation axis. The sulfate ligand and propane-1,2-diol mol-ecules are disordered across the twofold rotation axis. The dihedral angle between the two chelating N2C2 groups is 83.26 (13)°. In the crystal, the complex mol-ecule and the propane-1,2-diol mol-ecule are connected through a pair of O-H⋯O hydrogen bonds.

Poly[diaqua-bis-(µ-4,4'-bipyridine-κ(2) N:N')bis-(ethane-1,2-diol-κO)bis(µ-sulfato-κ(2) O:O')dicobalt(II)].

In the title compound, [Co2(SO4)2(C10H8N2)2(C2H6O2)2(H2O)2] n , there are two crystallographically independent Co(II) ions, each of which lies on a twofold rotation axis and has a slightly distorted octa-hedral environment. One Co(II) ion is coordinated by two N atoms from two bridging 4,4'-bipyridine (4,4'-bipy) ligands, two O atoms from two sulfate ions and two O atoms from aqua ligands. The second Co(II) ion is similar but with ethane-1,2-diol ligands in place of water mol-ecules. The sulfate anions act as bridging ligands to link two adjacent Co(II) ions together, leading to the formation of linear ⋯Co1Co2Co1Co2⋯chains along the a axis. Adjacent chains are further bridged by 4,4'-bipy ligands, which are also located on the twofold rotation axis, resulting in a two-dimensional layered polymer extending parallel to (001). In the crystal, the layers are linked by extensive O-H⋯O hydrogen-bonding inter-actions involving the O atoms of the water mol-ecules and ethane-1,2-diol mol-ecules, resulting in a three-dimensional supra-molecular network.

Bis(1,10-phenanthroline-κ(2) N,N')(sulfato-κ(2) O,O')cobalt(II) propane-1,2-diol monosolvate.

In the title compound, [Co(SO4)(C12H8N2)2]·C3H8O2, the Co(II) atom (site symmetry 2) has a distorted octa-hedral coordination composed of four N atoms from two chelating 1,10-phenanthroline ligands and two O atoms from an O,O'-bidentate sulfate ligand, in which the S atom has site symmetry 2. The dihedral angle between the two chelating N2C2 groups is 84.46 (15)°. The complex and solvent mol-ecules are connected through O-H⋯O hydrogen bonds. The solvent mol-ecule is equally disordered over two positions and is also located on a twofold axis.

Bis(1,10-phenanthroline-κ(2) N,N')(sulfato-O)copper(II) butane-2,3-diol monosolvate.

The title compound, [Cu(SO4)(C12H8N2)2]·C4H10O2, is comprised of neutral monomeric complex and butane-2,3-diol solvent mol-ecules. In the complex, the Cu(II) ion is in a distorted square-pyramidal coordination environment defined by four N atoms from two chelating 1,10-phenanthroline ligands and one O atom from a monodentate sulfate anion; the O atom is at the apex. The two chelating N2C2 groups subtend a dihedral angle of 85.8 (4)°. In the crystal, the neutral monomeric complex and butane-2,3-diol solvent mol-ecules are held together by O-H⋯O hydrogen bonding, which leads to additional stabilization of the structure. The presence of pseudosymmetry in the structure suggests the higher symmetry space group C2/c, but attempts to refine the structure in this space group resulted in an unsatisfactory model and high R and wR values. The sulfate anion is disordered over two sets of sites with occupancies of 0.55 (1) and 0.45 (1).

Poly[aqua-(µ2-4,4'-bipyridine-κ(2) N:N')(ethane-1,2-diol-κO)(µ2-sulfato-κ(2) O:O')nickel(II)].

The title compound, [Ni(SO4)(C10H8N2)(C2H6O2)(H2O)] n , contains two crystallographically unique Ni(II) atoms, each lying on a twofold rotation axis and having a slightly distorted octa-hedral environment. It is isotypic with the previously reported Cu(II) analog [Zhong et al. (2011 ▶). Acta Cryst. C67, m62-m64]. One Ni(II) atom is coordinated by two N atoms from two bridging 4,4'-bipyridine (4,4'-bipy) ligands, two O atoms from two sulfate ions and two aqua O atoms. The second Ni(II) atom is surrounded by two N atoms from 4,4'-bipy ligands and four O atoms, two from bridging sulfate ions and from two ethane-1,2-diol ligands. The sulfate anion acts as a bridging ligand, linking adjacent Ni(II) atoms, leading to the formation of linear ⋯Ni1-Ni2-Ni1-Ni2⋯ chains along the a-axis direction. Adjacent chains are further bridged by 4,4'-bipy ligands, resulting in a two-dimensional layered polymer parallel to (001). In the crystal, the polymeric layers are linked by extensive O-H⋯O hydrogen-bonding inter-actions involving the O atoms of the water mol-ecules and the ethane-1,2-diol mol-ecules, resulting in a three-dimensional supra-molecular network.

Bis(1,10-phenanthroline-κ(2) N,N')(sulfato-κ(2) O,O')nickel(II) propane-1,2-diol monosolvate.

In the title compound, [Ni(SO4)(C12H8N2)2]·C3H8O2, the Ni(II) atom exhibits a distorted octa-hedral coordination by four N atoms from two chelating 1,10-phenanthroline ligands and two O atoms from an O,O'-bidentate sulfate group. A twofold rotation axis passes through the Ni and S atoms and the mid-point of the hydroxyl C-C bond of the propane-1,2-diol solvent mol-ecule. The dihedral angle between the two chelating N2C2 groups is 85.61 (8)°. The [NiSO4(C10H8N2)2] and propane-1,2-diol units are held together by a pair of symmetry-related inter-molecular O-H⋯O hydrogen bonds involving the uncoordinating O atoms of the sulfate ion. Due to symmetry, the solvent mol-ecule is equally disordered over two positions.

2,9-Dimethyl-1,10-phenanthrolin-1-ium 2,4,5-tri-carb-oxy-benzoate monohydrate.

In the preparation of the title hydrated salt, C14H13N2 (+)·C10H5O8 (-)·H2O, a proton has been transfered to the 2,9-dimethyl-1,10-phenanthrolinium cation, forming a 2,4,5-tri-carb-oxy-benzoate anion. In the anion, the mean planes of the protonated carboxyl-ate groups form dihedral angles of 11.0 (5), 4.4 (5) and 80.3 (4)° with the benzene ring to which they are attached. The mean plane of the deprotonated carboxyl-ate group forms a dihedral angle of 10.6 (5)° with the benzene ring. In the crystal, the anions are involved in carb-oxy-lic acid O-H⋯Ocarbox-yl hydrogen bonds, generating a two-dimensional network parallel to (001) containing R 4 (4)(28) and R 4 (4)(32) motifs. The 2,9-dimethyl-1,10-phenanthrolinium cations and water mol-ecules reside between the anion layers and are connected to the anions via N-H⋯Owater and Owater-H⋯Ocarbox-yl hydrogen bonds. An intra-molecular O-H⋯O hydrogen bond is also observed in the anion.

Tris(1,10-phenanthroline-κ2N,N')iron(II) bis(2,4,5-tricarboxybenzoate) monohydrate and tris(2,2'-bipyridine-κ2N,N')iron(II) 2,5-dicarboxybenzene-1,4-dicarboxylate-benzene-1,2,4,5-tetracarboxylic acid-water (1/1/2).

The title compounds, tris(1,10-phenanthroline-κ(2)N,N')iron(II) bis(2,4,5-tricarboxybenzoate) monohydrate, [Fe(C(12)H(8)N(2))(3)](C(10)H(5)O(8))(2)·H(2)O, (I), and tris(2,2'-bipyridine-κ(2)N,N')iron(II) 2,5-dicarboxybenzene-1,4-dicarboxylate-benzene-1,2,4,5-tetracarboxylic acid-water (1/1/2), [Fe(C(10)H(8)N(2))(3)](C(10)H(4)O(8))·C(10)H(6)O(8)·2H(2)O, (II), were obtained during an attempt to synthesize a mixed-ligand complex of Fe(II) with an N-containing ligand and benzene-1,2,4,5-tetracarboxylic acid via a solvothermal reaction. In both mononuclear complexes, each Fe(II) metal ion is six-coordinated in a distorted octahedral manner by six N atoms from three chelating 1,10-phenanthroline or 2,2'-bipyridine ligands. In compound (I), the Fe(II) atom lies on a twofold axis in the space group C2/c, whereas (II) crystallizes in the space group P2(1)/n. In both compounds, the uncoordinated carboxylate anions and water molecules are linked by typical O-H···O hydrogen bonds, generating extensive three-dimensional hydrogen-bond networks which surround the cations.

A novel one-dimensional Co(II) coordination polymer: catena-poly[[hexaaquacobalt(II)] [[diaquabis(sulfato-κO)cobalt(II)]-µ-4,4'-bipyridine-κ2N:N'] [[triaqua(sulfato-κO)cobalt(II)]-µ-4,4'-bipyridine-κ2N:N']].

The title compound, {[Co(H(2)O)(6)][Co(SO(4))(C(10)H(8)N(2))(H(2)O)(3)][Co(SO(4))(2)(C(10)H(8)N(2))(H(2)O)(2)]}(n), contains three crystallographically unique Co(II) centres, all of which are in six-coordinated environments. One Co(II) centre is coordinated by two bridging 4,4'-bipyridine (4,4'-bipy) ligands, one sulfate ion and three aqua ligands. The second Co(II) centre is surrounded by two N atoms of two 4,4'-bipy ligands and four O atoms, i.e. two O atoms from two monodentate sulfate ions and two from water molecules. The third Co(II) centre forms part of a hexaaquacobalt(II) ion. In the crystal structure, there are two different one-dimensional chains, one being anionic and the other neutral, and adjacent chains are arranged in a cross-like fashion around the mid-point of the 4,4'-bipy ligands. The structure features O-H···O hydrogen-bonding interactions between sulfate anions and water molecules, resulting in a three-dimensional supramolecular network.