Photoluminescence of Cu(I)(PPh3)2(8-quinolinolate)

The complex Cu(I)(PPh₃)₂(oxinate) with oxine = 8-quinolinole is luminescent under ambient conditions. In the solid state it shows an emission which originates from the lowest-energy oxinate ILCT state. It consists of a fluorescence and a phosphorescence. In solution saturated with argon, a single broad emission band appears which seems to be composed of a more intense fluorescence and a much weaker phosphorescence at longer wavelength. If this solution is saturated with air, the complete emission band becomes less intense. This is quite surprising, since the oxinate ILCT fluorescence of other oxinate complexes is not quenched by oxygen. It is conceivable that the fluorescence largely consists of a delayed fluorescence. When the emitting triplet is depopulated by a thermally activated transition to the fluorescent singlet, both emissions, the delayed fluorescence and the phosphorescence, may undergo a luminescence quenching. For a simple comparison, the photoluminescence of Ag(PPh₃)₂(oxinate) was also briefly examined. The absorption and emission spectra of this silver complex in solution at r.t. resemble those of the copper complex.     

Photoluminescence and electron-beam excitation induced cathodoluminescence properties of novel green-emitting Ba4La6O(SiO4)6:Tb3+phosphors

Tb³⁺ions activated Ba₄La₆O(SiO₄)₆ (BLSO:Tb³⁺) phosphors were synthesized by a citrate sol-gel method. The X-ray diffraction pattern confirmed their oxyapatite structure. The field-emission scanning electron microscope image established that the BLSO:Tb³⁺phosphor particles were closely-packed and acquired irregular shapes. The photoluminescence (PL) excitation spectra of BLSO:Tb³⁺phosphors showed intense f–d transitions along with low intense peaks corresponding to the f–f transitions of Tb³⁺ions in the lower energy region. The PL emission spectra displayed the characteristic emission bands of Tb³⁺ions, and the optimized concentrations were found to be at 1 and 6 mol% for blue and green emission peaks, respectively. The cathodoluminescece (CL) spectra exhibited a similar behavior that was observed in the PL spectra except the intensity variations in the blue and green regions. The CL spectra of the BLSO:6 mol% Tb³⁺phosphor unveiled accelerating voltage induced luminescent properties.     

Calcium(II)(3) (3,5-Diisopropylsalicylate)(6)(H(2)O)(6) Activates Nitric Oxide Synthase: An Accounting for its Action in Decreasing Platelet Aggregation

Purposes of these studies were first; to determine whether or not Calcium(II)(3) (3,5- diisopropylsalicylate)(6)(H(2)O)(6) [Ca(II)(3)(3,5-DIPS)(6)], a lipophilic calcium complex, could decrease activated-platelet aggregation, and second; to determine whether or not it is plausible that Ca(II)(3)(3,5-DIPS)(6) decreases activated-platelet aggregation by facilitating the synthesis of Nitric Oxide (NO) by Nitric Oxide Synthase (NOS). The influence of Ca(II)(3)(3,5-DIPS)(6) on the initial rate of activated-platelet aggregation was determined by measuring the decrease in rate of increase in transmission at 550 nm for a suspension of Thrombin-CaCl(2) activated platelets following the addition of 0, 50, 100, 250, or 500 muM Ca(II)(3)(3,5-DIPS)(6). To establish that the Ca(lI)(3)(3,5- DIPS)(6)-mediated decrease in aggregation was due to activation of NOS, the effect of L-NMMA, an inhibitor of NOS, on the inhibition of platelet aggregation by Ca(II)(3)(3,5-DIPS)(6) was determined using a suspension of activated platelets contaimng 0 or 250 muM Ca(II)(3)(3,5-DIPS)(6) without or with 1 mM L-NMMA. An in vitro Bovine Brain NOS reaction mixture, containing CaCl(2) for the activation of Phosphodiesterase-3' ,5'-Cyclic Nucleotide Activator required for the activation of NOS, was used to determine whether or not Ca(II)(3)(3,5-DIPS)(6) could be used as a substitute for the addition of Ca. The decrease in absorbance at 340 nm, lambda maximum for NADPH, was measured to determine NOS activity following the addition of NOS to the complete reaction mixture containing either CaCl(2), Ca(II)(3)(3,5-DIPS)(6), or neither Ca compound. Increasing the concentration of Ca(II)(3)(3,5-DIPS)(6) caused a concentration related decrease in activated platelet aggregation. The addition of L-NMMA to activated platelets, in the absence of Ca(II)(3)(3,5-DIPS)(6), caused a 129% increase in initial rate of platelet aggregation. The initial rate of platelet aggregation decreased 74% with the addition of 250 muM Ca(II)(3)(3,5-DIPS)(6) and the addition of L-NMMA plus 250 muM Ca(II)(3)(3,5-DIPS)(6) caused a 197% decrease in initial rate of aggregation compared to the initial rate observed width the presence of 1 mM L-NMMA alone. There was only a small, 27%, increase in initial rate of 0.4 mM NADPH oxidation when 0.9 mM CaCl(2) was added to the NOS reaction mixture in comparison to the initial rate of NADPH oxidation with no addition of CaCI(2). Addition of an equivalent amount of Ca in the form of Ca(II)(3)(3,5-DIPS)(6), 333 muM, caused a 37% increase in initial rate of NADPH oxidation compared to the addition of 0.9 mM CaCl(2). Addition of increasing concentrations of L-NMMA plus 0.9 mM CaCl(2) or 333 muM Ca(II)(3)(3,5-DIPS)(6) to the NOS reaction mixture caused a concentration related increase in initial rate of NADPH oxidation. Addition of L-NMMA while expected to decrease NADPH oxidation actually increased the rate of NADPH oxidation. Additions of 133 muM or 267 muM Ca(II)(3)(3,5- DIPS)(6) also caused concentration related increases in initial rate of NADPH oxidation in the presence of 113 muM L-NMMA. However, the addition of 533 muM Ca(II)(3)(3,5-DIPS)(6) caused a dramatic decrease in initial rate of NADPH oxidation by NOS. It is concluded that: 1) Ca(II)(3)(3,5- DIPS)(6) activates platelet NOS in preventing platelet aggregation, 2) in vitro NOS activity can be observed spectrophotometrically by following the consumption of NADPH as a decrease in absorbance at 340 nm, 3) Ca(II)(3)(3,5-DIPS)(6) plays a role in enhancing Bovine Brain NOS activity resulting in an increased rate of NADPH oxidation by NOS, 4) Ca(II)(3)(3,5-DIPS)(6) is a useful form of Ca in activating NOS and superior to CaCl(2) with regard to the facilitation of a NADPH oxidation, and 5) L-NMMA stimulates Bovine Brain NOS activity rather than causing an inhibition of this enzyme and must serve as a reducible substrate for Bovine Brain NOS.     

Interaction of [Rh(2)(O(2)CCH(3))(4)(H(2)O)(2)] and [Rh(2)(O(2)CCH(OH)Ph)(2)(phen)(2)(H(2)O)(2)](O(2)C-CH(OH)Ph)(2) With Sulfhydryl Compounds and Ceruloplasmin

The interaction of binuclear rhodium(II) complexes [Rh(2)(OOCCH(3))(4)(H(2)O)(2)], [Rh(2){OOCCH(OH)Ph}(2)(phen)(2)(H(2)O)(2)] {OOCCH(OH)Ph}(2), [Rh(2)(OOCCH(3))(2)(bpy)(2)(H(2)O)(2)](OOCCH(3))(2) and [Rh(2)Cl(2)(OOCMe)(2)(bpy)(2)](3H(2)O) with ceruloplasmin, cysteine, glutathione and coenzyme A have been investigated using. UV-Vis and CD spectroscopies. The complexes containing phen or bpy at pH = 7.4 and 4.0 are readily reduced with sulfhydryl compounds, while rhodium(II) acetate is relatively stable in these conditions. Complex [Rh(2){OOCCH(OH)Ph}(2)(phen)(2)(H(2)O)(2)] strongly changes structure of ceruloplasmin leading to the decrease of of alpha-helix content and loss of oxidase activity.     

Second-sphere Coordination of [Pt(bipy)(NH3)2]2+ by Dibenzo-crown Ethers. Solution Spectroscopic Studies and the Crystal and Molecular Structures of [Pt(bipy)(NH3)2.dibenzo-30-crown-10] [PF6]2.0.6 H2O and [Pt(bipy)(NH3)2.dibenzo-24-crown-8] [PF6]2

In addition to hydrogen bonding and Coulombic forces, charge transfer interactions stabilise the 1:1 adducts formed between [Pt(bipy)(NH₃)₂] ²⁺ and a series of dibenzo-3n-crown-n (n = 6–12) ethers as evidenced by ¹H NMR and UV-visible spectra in solution and by X-ray crystal structures (for n = 8 and 10) in the solid state. Mutual diamagnetic (ring current) shielding by the aromatic systems of host and guest results in dramatic upfield shifts of certain aromatic proton resonances on adduct formation, especially when n = 10 or 11. A broad charge-transfer absorption band at 350 nm attains its maximum intensity at n = 11 though stability constant measurements indicate optimum binding when n = 10. X-ray diffraction studies reveal that, when n = 8, only one of the crown ether benzo-rings interacts with the bipyridyl ligand in a charge-transfer sense. However, when n = 10, the macrocycle is sufficiently large and flexible to allow both benzo-rings to enter into stabilising interactions with the bipyridyl ligand such that the platinum complex is encapsulated by the host in a U-shaped cavity.     

Immobilization of Ru(II)(salen)(PPh3)2 on Mesoporous MCM-41/SBA-15: Characterization and Catalytic Applications

Ru(II)(salen)(PPh₃)₂ immobilized on MCM-41 and SBA-15 modified with aminopropyl groups as linkers has been synthesized and characterized by elemental analysis, TEM, FTIR, BET, and TGA. Elemental analysis shows that the grafted samples contain 0.7–0.8 wt.% Ru. The retaining of long range ordering of the mesoporous MCM-41 and SBA-15 supporting materials after grafting is evident from TEM and N₂ adsorption/desorption measurements. FTIR and TGA spectra show the formation of metal salen complexes with the amino groups acting as connectors to the SiO₂ surface. Both grafted materials were successfully applied as catalysts for the olefination of various aldehydes with very good yields and high E-selectivity. The catalyst materials are recyclable for several catalytic runs.     

Down-Regulation of Porcine Heart Diaphorase Reactivity by Trimanganese Hexakis(3,5-Diisopropylsalicylate), Mn(3)(3,5-DIPS)6, and Down-Regulation of Nitric Oxide Synthase Reactivity by Mn(3)(3,5-DIPS)(6) and Cu(II)(2)(3,5-DIPS)(4)

Purposes of this work were to examine the plausible down-regulation of porcine heart diaphorase (PHD) enzyme reactivity and nitric oxide synthase (NOS) enzyme reactivity by trimanganese hexakis(3,5-diisopropylsalicylate), [Mn(3)(3,5-DIPS)(6)] as well as dicopper tetrakis(3,5- diisopropylsalicylate, [Cu(II)(2)(3,5-DIPS)(4)] as a mechanistic accounting for their pharmacological activities.Porcine heart disease was found to oxidize 114 muM reduced nicotinamide-adenine- dinucleotide-'(3)-phosphate (NADPH) with a corresponding reduction of an equivalent concentration of 2,6-dichlorophenolindophenol (DCPIP). As reported for Cu(II)(2) (3,5-DIPS)(4), addition of Mn(3)(3,5-DIPS)(6) to this reaction mixture decreased the reduction of DCPIP without significantly affecting the oxidation of NADPH. The concentration of Mn(3)(3,5-DIPS)(6) that produced a 50% decrease in DCPIP reduction (IC(50)) was found to be 5muM. Mechanistically, this inhibition of DCPIP reduction with ongoing NADPH oxidation by PHD was found to be due to the ability of Mn(3)(3,5-DIPS)(6) to serve as a catalytic electron acceptor for reduced PHD as had been reported for Cu(II)(2)(3,5-DIPS)(4). This catalytic decrease in reduction of DCPIP by Mn(3)(3,5-DIPS)(6) was enhanced by the presence of a large concentration of DCPIP and decreased by the presence of a large concentration of NADPH, consistent with what had been observed for the activity of Cu(II)(2)(3,5-DIPS)(4)Oxidation of NADPH by PHD in the presence of Mn(3)(3,5-DIPS)(6) and the absence of DCPIP was linearly related to the concentration of added Mn(3)(3,5-DIPS)(6) through the concentration range of 2.4 muM to 38muM with a 50% recovery of NADPH oxidation by PHD at a concentration of 6 muM Mn(3)(3,5-DIPS)(6)Conversion of [(3)H] L-Arginine to [(3)H] L-Citrulline by purified rat brain nitric oxide synthase (NOS) was decreased in a concentrated related fashion with the addition of Mn(3)(3,5-DIPS)(6) as well as Cu(II)(2)(3,5-DIPS)(4) which is an extention of results reported earlier for Cu(II)(2)(3,5-DIPS)(4). The concentration of these two compounds required to produce a 50% decrease in L-Citrulline synthesis by NOS, which may be due to down-regulation of NOS, were 0.1 mM and 8muM respectively, consistent with the relative potencies of these two complexes in preventing the reduction of Cytochrome c by NOS.It is concluded that Mn(3)(3,5-DIPS)(6), as has been reported for Cu(II)(2) (3,5-DIPS)(4) , serves as an electron acceptor in down-regulating PHD and both of these complexes down-regulate rat brain NOS reactivity. A decrease in NO synthesis in animal models of seizure and radiation injury may account for the anticonvulsant, radioprotectant, and radiorecovery activities of Mn(3)(3,5-DIPS)(6) and Cu(II)(2)(3,5-DIPS)(4).     

Synthesis and crystal structure of mer-nitroaquatriamminenitrosylruthenium(II) nitrate [RuNO(NH3)3(NO2)(H2O)](NO3)2

The reaction between mer-[RuNO(NH₃)₃(NO₂)(OH)]Cl·0.5H₂O and an excess of 16 M HNO₃ leads to the protonation of the starting complex and crystallization of the complex with a coordinated water molecule and nitrite anion. The crystal structure of the product has been determined. The coordinated water molecule tends to be a weak acid with a measured pK_a of 2.4.     

Hydrothermal synthesis and crystal structure of a new copper(II) molybdenum(VI) arsenate(III), (C5H5NH)2(H3O)2[(CuO6)Mo6O18(As3O3)2]

A new copper(II) molybdenum(VI) arsenate(III), (C₅H₅NH)₂(H₃O)₂[(CuO₆)Mo₆O₁₈(As₃O₃)₂], has been hydrothermally synthesized and characterized by single crystal X-ray diffraction and TG analysis. The compound crystallizes in the monoclinic space group P2₁/n with a=9.303(2), b=20.731(4), c=12.617(3) Å, β=104.17(3)°, V=2359.3(8) ų, Z=2 and R1(wR2)=0.0296(0.0683). The structure is composed of pyridinium cations, proton hydrates and [(CuO₆)Mo₆O₁₈(As₃O₃)₂]⁴⁻ polyanions. The polyanion framework derives from the Anderson type; the central octahedron is filled up by copper(II) and is capped on both sides by a cyclic As₃O₆ group.     

Photoluminescence of [Pt(C3Ph3)Ln]PF6 with L = phenylphosphine ligands. Emission from a (Pt0 to C3Ph3+) MLCT triplet

The complex cations [Pt⁰(C₃Ph₃)(PPh₃)₂]⁺ and [Pt⁰(C₃Ph₃)(tripod)]⁺ with tripod = CH₃C(CH₂PPh₂)₃ contain the smallest Hückel aromat C₃R₃⁺ (with n = 0) as ligand. Since this cation is a CT acceptor, the complexes are characterized by low-energy (Pt⁰ to C₃Ph₃⁺) MLCT states. The complexes show a photoluminescence which originates from the lowest MLCT triplet.     

C5/C6烷烃异构化Pt/Al2O3-Cl催化剂的性能

采用浸渍法制备了Pt/Al₂O₃,在300℃、CCl₄氯化1h,制备出Pt/Al₂O₃-Cl催化剂。采用FT-IR、XRD、TEM、CO-IR、Py-IR和TPD等方法表征了催化剂,并与中温型RISO催化剂的催化性能进行比较。结果表明,在氯化处理过程中氯取代了氧化铝的表面羟基,导致3000～3800cm^-1红外吸收峰强度大幅度减小,但催化剂的晶相不发生改变;氯化使Pt粒子的平均粒径增大,粒径分布变宽,金属分散度降低;氯化后金属Pt主要以+2价的PtCl₂的形式出现,其中一部分生成了易升华的PtCl₂·2AlCl₃,从而导致Pt含量降低;氯化后的催化剂上只有L酸,评价后既有L酸,又有B酸;氯化后的催化剂热稳定不高,随着温度升高,3种类型的氯化物相继脱出;Pt/Al₂O₃-Cl相对于中温型RISO催化剂表现出较好的异构化性能,正己烷转化率达88.17%,2,2-二甲基丁烷选择性达29.68%,裂化和氢解几乎没有发生。     

Synthesis and Anti-Candida Activity of Cobalt(II) Complexes of Benzene-1,2-Dioxyacetic Acid (bdoaH(2)). X-Ray Crystal Structures of [Co(bdoa)(H(2)O)(3)] 3.5H(2)O and {[CO(phen)(3)](bdoa)}(2)24H(2)O (phen = 1,10-Phenanthroline)

Co(CH(3)CO(2))(2)4H(2)O reacts with benzene-1,2-dioxyacetic acid (bdoaH(2)) to give the Co(2+) complexes [Co(bdoa)(H(2)O)(3)]H(2)O (1a) and [Co(bdoa)(H(2)O)(3)] 3.5H(2)O (1b). Subsequent reaction of 1a with 1,10- phenanthroline produces [CO(phen)(3)] bdoa10H(2)O (2a) and {[CO(phen)(3)](bdoa)}(2)24H(2)O (2b). Molecular structures of 1b and 2b were determined crystallographically. In 1b the bdoa(2-)- ligates the metal by two carboxylate oxygens and two ethereal oxygens, whereas in 2b the bdoa(2-) is uncoordinated. The Mn(2+) and Cu(2+) complexes [Mn(bdoa)(phen)(2)]H(2)O (3) and [Cu(pdoa)(imid)(2)] (4) were also synthesised, 1a-4 and other metal complexes of bdoa H(2) (metal = Mn(2+), Co(2+) ,Cu(2+), Cu(+) ) were screened for their ability to inhibit the growth ofhe yeast Candida albicans. Complexes incorporating the 1,10-phenanthroline ligand were the most active.     

Isomerism in bis(phenylselenolato)bis(triphenylphosphine)platinum(II): the crystal and molecular structures of cis- and trans-[Pt(SePh)2(PPh3)2]

The reaction of cis-[PtCl₂(PPh₃)₂] and NaSePh in benzene produces a mixture of cis- and trans-isomers of the monomeric platinum complex [Pt(SePh)₂(PPh₃)₂]. The low-temperature X-ray structures of both isomers are reported. The structure of cis-[Pt(SePh)₂(PPh₃)₂] is the first crystallographic characterized cis-isomer of mononuclear platinum(II) complex containing only non-chelating organoselenolato and phosphine ligands.     

MgO-supported cluster catalysts with Pt–Ru interactions prepared from Pt3Ru6(CO)21(μ3-H)(μ-H)3

Bimetallic MgO-supported catalysts were prepared by adsorption of Pt₃Ru₆(CO)₂₁(μ₃-H)(μ-H)₃ on porous MgO. Characterization of the supported clusters by infrared (IR) spectroscopy showed that the adsorbed species were still in the form of metal carbonyls. The supported clusters were decarbonylated by treatment in flowing helium at 300 °C, as shown by IR and extended X-ray absorption fine structure (EXAFS) data, and the resulting supported PtRu clusters were shown by EXAFS spectroscopy to have metal frames that retained Pt–Ru bonds but were slightly restructured relative to those of the precursor; the average cluster size was almost unchanged as a result of the decarbonylation. These are among the smallest reported bimetallic clusters of group-8 metals. The decarbonylated sample catalyzed ethylene hydrogenation with an activity similar to that reported previously for γ-Al₂O₃-supported clusters prepared in nearly the same way and having nearly the same structure. Both samples were also active for n-butane hydrogenolysis, with the MgO-supported catalyst being more active than the γ-Al₂O₃-supported catalyst.     

Hydrothermal synthesis,crystal structure and photoluminescent property of a novel 3-D [La2(C2O4)2(NO3)(OH)(H2O)] · 3H2O

A novel 3D [La₂(C₂O₄)₂(NO₃) (OH)(H₂O)] · 3H₂O 1 has been synthesized under hydrothermal conditions and characterized by elemental analyses, IR, TGA, X-ray powder diffraction, X-ray single crystal diffraction and photoluminescence. The bridging modes of both nitrates and oxalates in compound 1 are uncommon. We have unexpectedly generated an unusual compound by using the simplest ligands, oxalates and nitrates in the presence of nicotinate (HIN).     

[Fe(C7H5O3)(C9H6NO)2]三元配合物的合成及抑菌性能

本文以水杨酸、8-羟基喹啉为配体与铁(Ⅲ)合成了三元配合物,用元素分析、红外光谱、紫外可见光谱、荧光光谱等手段对其进行表征,确定其化学组成为[Fe(C7H5O3)(C9H6NO)2]。其中水杨酸脱质子以羧酸根与Fe3+成键,酚羟基不参与配位,而8-羟基喹啉脱质子以酚羟基氧和杂环上的氮原子双齿配位,形成五元螯环。配合物在整个可见光区都有较强吸收,粉末及其浓溶液均呈黑色,稀溶液显紫色。以300 nm为激发波长时,三元配合物在409 nm处有较强的发射荧光。采用分光光度法研究其对大肠杆菌生长的作用,配合物摩尔浓度低于2 mmol/L时,促进大肠杆菌的生长,高于2 mmol/L时抑制其生长,浓度越大抑制作用越强,即配合物对大肠杆菌的生长具有双向生物效应。     

[Fe(C7H5O3)(C9H6NO)2]三元配合物的合成及抑菌性能

以水杨酸、8-羟基喹啉为配体与铁(Ⅲ)合成了三元配合物,用元素分析、红外光谱、紫外可见光谱、荧光光谱对其进行表征,确定其化学组成为[Fe(C7H5O3)(C9H6NO)2]。其中,水杨酸脱质子以羧酸根与Fe3+成键,酚羟基不参与配位,而8-羟基喹啉脱质子以酚羟基氧和杂环上的氮原子双齿配位,形成五元螯环。配合物在整个可见光区都有较强吸收,粉末及其浓溶液均呈黑色,稀溶液呈紫色。以300 nm为激发波长时,三元配合物在409 nm处有较强的发射荧光。采用分光光度法研究其对大肠杆菌生长的作用,配合物浓度低于2 mmol/L时,促进大肠杆菌的生长,高于2 mmol/L时抑制其生长,浓度越大抑制作用越强,即配合物对大肠杆菌的生长具有双向生物效应。     

Intramolecular hydrogen bond controlled coordination of N-thiophosphorylated thiourea 2,6-Me2C6H3NHC(S)NHP(S)(OiPr)2 with Ni(II)

Reaction of O,O′-diisopropylthiophosphoric acid isothiocyanate (iPrO)₂P(S)NCS with 2,6-dimethylaniline 2,6-Me₂C₆H₃NH₂ leads to the new N-thiophosphorylated thiourea 2,6-Me₂C₆H₃NHC(S)NHP(S)(OiPr)₂ (HL). Reaction of the potassium salt of HL with Ni(II) in aqueous EtOH leads to the complex of formula [Ni(L-N,S)₂]. The molecular structures of the thiourea HL and the complex [Ni(L-N,S)₂] were elucidated by single crystal X-ray diffraction analysis, ¹H and ³¹P NMR spectroscopy and microanalysis. In the complex [Ni(L-N,S)₂], the metal center is found to be in a square-planar N₂S₂ environment formed by the CS sulfur atoms and the P–N nitrogen atoms of two deprotonated L ligands. The ligands are in a trans-configuration.     

Synthesis and Biological Activity of Manganese (II) Complexes of Phthalic and Isophthalic Acid: X-Ray Crystal Structures of [Mn(ph)(Phen)(2)(H(2)O)]. 4H(2)O, [Mn(Phen)(2)(H(2)O)(2)](2)(Isoph)(2)(Phen). 12H(2)O and {[Mn(Isoph)(bipy)](4). 2.75biby}(n)(phH(2) = Phthalic Acid; isoph = Isophthalic Acid; phen = 1,10-Phenanthroline; bipy = 2,2-Bipyridine)

Manganese(II) acetate reacts with phthalic acid (phH(2)) to give [Mn(ph)].0.5H(2)O (1). Reaction of 1 with 1,10-phenanthroline produces [Mn(ph)(phen)].2H(2)O (2) and [Mn(ph)(phen)(2)(H(2)O)].4H(2)O (3). Reaction of isophthalic acid (isophH(2)) with manganese(II) acetate results in the formation of [Mn(isoph)].2H(2)O (4). The addition of the N,N-donor ligands 1,10-phenanthroline or 2,2'-bipyridine to 4 leads to the formation of [Mn(2) (isoph)(2)(phen)(3))].4H(2)O (5), [(Mn(phen)(2)(H(2)O)(2)](2)(isoph)(2)(phen).12H(2)O (6) and {[Mn(isoph)(bipy)](4).2.75 biby}(n) (7), respectively. Molecular structures of 3, 6 and 7 were determined crystallographically. In 3 the phthalate ligand is bound to the manganese via just one of its carboxylate groups in a monodentate mode with the remaining coordination sites filled by four phenanthroline nitrogen and one water oxygen atoms. In 6 the isophthalates are uncoordinated with the octahedral manganese center ligated by two phenanthrolines and two waters. In 7 the Isophthalate ligands act as bridges resulting in a polymeric structure. One of the carboxylate groups is chelating a single manganese with the other binding two metal centres in a bridging bidentate mode. The phthalate and isophthalate complexes, the metal free ligands and a number of simple manganes salts were each tested for their ability, to inhibit the growth of Candida albicans. Only the "metal free" 1,10-phenanthroline and its manganese complexes were found to be active.     

Ag(I)(Et(2)PCH(2)CH(2)PPh(2))(2)]NO(3): An Antimitochondrial Silver Complex

The silver(I) complex [Ag(eppe)(2)]NO(3) (eppe = Et(2)PCH(2)CH(2)PPh(2)) is shown by X-ray crystallography to be tetrahedral with Ag - PEt(2) and Ag - P Ph(2) bond lengths of 2.482 and 2.518 A, respectively. The complex is selectively antimitochondrial and inhibits the growth of a number of yeast strains in non-fermentable media at concentrations as low as 2.5 muMu and induces the mitochondrial mutation petite The effect is largely reversed by the presence of aspirin. The complex is shown to be stable in the cell culture media and in the presence of glutathione, but readily reacts with disulfides of oxidized glutathione and serum albumin. Surprisingly, neither [Au(eppe)(2)]Cl nor [Au(eppe)(2)]Cl (dppe = Ph(2)PCH(2)CH(2)PPh(2)) showed any mitochondrial selectivity in the same screening protocol.