Influence of different site symmetries of Eu centers on the luminescence properties of Anderson-based compounds

Two compounds, [Eu(H₂O)₇][Al(OH)₆Mo₆O₁₈] · 4H₂O (1) and {(C₂H₅NO₂)₂[Eu(H₂O)₅]}[Al(OH)₆Mo₆O₁₈] · 10H₂O (2), have been synthesized by conventional solution method and determined by single-crystal X-ray diffraction. Compound 1 shows a 1D chain structure built up of alternating Anderson-type polyanions [Al(OH)₆Mo₆O₁₈]³⁻ and hydrated rare-earth ions Eu³⁺. Compound 2 displays a 3D supramolecular network structure containing 1D sandglass-like channels along c axis, which were occupied by repetitive array of (H₂O)₈ clusters. Extensive hydrogen bonds play an important role in the formation of the 3D structures of 1 and 2. Luminescence measurements reveal that 1 and 2 exhibit intense red and orange fluorescent emission at room temperature, respectively. Origin of the distinct emission can be assigned to the different site symmetries of Eu³⁺ centers in the two compounds. These results are consistent with the crystal structures of the two compounds.     

The effect of N-terminal substitutions on the biological activity of MSH fragments.

In order to study the role of N-terminal substitutions of peptide sequences related to the active site of -melanotropin, [Glp⁵]-MSH(5–10), [Glp⁵, -Phe⁷]-MSH(5–10), [Sar⁵, -Phe⁷]-MSH(5–10), [Nle⁴, -Phe⁷]-MSH(4–10), [N-carbamoyl]-MSH(5–10), and formyl and acetyl derivatives of -MSH(5–10), [Gly⁵]-MSH(5–10) and [Gly⁵, -Phe⁷]-MSH(5–10), were synthesized in solution. The N-terminal acylations enhance by 2 to 10 times the melanin-dispersing activity of the unsubstituted sequences. Alkylation of the N-terminus does not change the biological activity of the parent peptide, suggesting the necessity of a carbonyl group for increasing the hormonal effect.     

Large and prolonged in vivo response of pancreatic secretion to phenylethylamide and phenylethylester derivatives of Boc-[Nle-Nle]CCK(26–33) in the rat

Supramaximal doses of cholecystokinin (CCK) induce in vitro submaximal biological responses (i.e., smaller by 50% than the response to a maximal dose of CCK), desensitization and residual stimulation, and in vivo secretory inhibition and edematous pancreatitis. It has been reported previously that supramaximal doses of Boc-[Nle²⁸-Nle³¹]CCK(27–32)/-phenylethylester (JMV180) do not produce these effects. The aim of this study was to analyze the in vivo response of pancreatic secretion of the rat to a wide dose range of Boc-[Nle²⁸-Nle³¹]CCK(26–33) (JMV118), an analog of CCK8 with the same activity spectrum as CCK8, to JMV180 and to Boc-[Nle²⁸-Nle³¹]CCK(27–32)-phenylethylamide (JMV170). The three peptides were administered as intravenous infusions and as bolus intravenous injections. In the case of infusions, the same maximal effect was observed with all three peptides. It was obtained with 22.5 pmol/kg · min of JMV118; JMV180 and JMV170 were about 700 times less potent. In the case of bolus injections, the maximal response to JMV118 was observed with 450 pmol/kg, and the response peaked 10–15 min after the injection. Higher doses of JMV118 induced a secretory peak that was smaller and delayed relative to the moment of injection. JMV180 and JMV170 were about 500 times less potent: the maximal response was observed with 218700 pmol/kg and peaked 10–15 min after the injection. Larger doses of JMV180 and JMV170 produced neither supramaximal inhibition nor a delayed peak response, but induced a sustained stimulation of pancreatic secretion that could last more than 3 h after the injection. These data indicate that single large doses of JMV180 and JMV170 can produce a large and long-lasting stimulation of pancreatic secretion in vivo, a goal that cannot be reached with JMV118 or CCK8.     

Properties of amino-terminal parathyroid hormone-related peptides modified at positions 11–13

Biological properties of amino-terminal PTHrP analogues modified in the region 11–13 were examined using ROS 17/2.8 cells. [Leu¹¹,D-Trp¹²,Arg¹³,Tyr³⁶]PTHrP(1–36)amide had a 17-fold lower binding affinity for the receptor (apparent K_d: 5 × 10⁻⁸ M) than [Tyr³⁶]PTHrP(1–36)amide or [Arg^11,13,Tyr³⁶]PTHrP(1–36)amide (apparent K_d for both: 2 × 10⁻⁹ M). Moreover, it is only a weak partial agonist despite completely inhibiting radioligand binding. [Leu¹¹,D-Trp¹²,Arg¹³,Tyr³⁶,Cys³⁸]PTHrP(7–38) and PTHrP(7–34)amide had similar receptor affinities (apparent K_ds: 5 × 10⁻⁸ M and 8 × 10⁻⁸ M), while that of [Nle^8,18,Tyr³⁴]bPTH(7–34)amide was more than 10-fold lower (apparent K_d: 2 × 10⁻⁶ M). These changes in biological properties suggest that high affinity receptor binding requires both amino- and carboxyl-terminal domains of the PTHrP(1–36) sequence and/or intramolecular interactions which are impaired by the D-Trp substitution for Gly¹².     

Degradation of cholecystokinin octapeptide by the neutral endopeptidase EC 3.4.24.11 and design of proteolysis-resistant analogues of the peptide

Inactivation of cholecystokinin octapeptide in vitro involves a metalloendopeptidase (EC 3.4.24.11) also called enkephalinase that inactivated the peptide both by a sequential pathway of hydrolysis (removal of Phe-NH₂ followed by cleavage of Trp-Met-Asp) and by an endopeptidase action (production of the tetrapeptides).

As enkephalinase cleaved CCK-8 at the Gly⁴-Trp⁵, Trp⁵-Met⁶ and Asp⁷-Phe⁸ bonds, we investigated the stability of analogues having: (1) substitutions of amino acids by a stereoisomer, (2) a substitution of Asp⁷ by a β Ala residue and (3) modifications of the Trp residue obtained by replacing the nitrogen atom in the indol ring by either an oxygen ([Bfa⁵]CCK-8) or a sulphur atom ([Bta⁵]CCK-8). Among these different CCK derivatives, [βAla⁷], [ Met⁶] and [ Trp⁵]CCK-8 were not hydrolyzed by enkephalinase: [ Ala^d]CCK-8 was rapidly cleaved by the enzyme. [Bta⁵] and [Bfa⁵]CCK-8 did not prove to be quite resistant; however the C-terminal tetrapeptides having the same modifications on the Trp residue were not cleaved although they interacted with the enzyme binding site. The stability and biological activity of the peptidase-resistant analogues of CCK-8 remain to be determined in vivo.     

Second sphere coordination behavior of aquo and amine ligands bound to a η-benzeneruthenium(II) cation

The bis(oxazoline) ligand, 2,2-bis[4(R)-phenyl-1,3-oxazolon-2-yl]propane (bpop), was introduced to the η⁶-benzenemthenium(II) moiety on treatment with [Ru(η⁶-C₆H₆)Cl₂]₂ to give [Ru(η⁶-C₆H₆)(bpop)Cl]⁺. Aquo and amine complexes [Ru(η⁶-C₆H₆)(bpop)(L)]²⁺ (L = H₂O (1), NH₂R; R = H (2) , Me (3) , and n-Bu (4) ) were prepared by treating the chloride complex with AgBF₄ in the presence of L. X-ray structure determinations of 1 and 3 were carried out. Both complexes possessed a three-leg piano stool structure with the N or O donors located at the three comers of a pseudo octahedron. The aquo complex 1 exhibited a dynamic NMR feature in which two magnetically nonequivalent oxazoline parts observed at lower temperatures were interchanged with each other at higher temperatures. This observation was ascribed to the formation of a C₂-symmetric 16-electron intermediate via Ru-OH₂ cleavage, which is slower in acetone than in dichloromethane owing to more effective solvation by acetone around hydrogens of the coordinated water molecule. The two diastereotopic N-hydrogens of 4 underwent deuterium exchange with CD₃OD with greatly different rates from each other owing to different energy of NHO (D) (CD₃) interaction. Carboxylate and sulfonate ions (A⁻) formed second sphere complexes with 4 by means of NHA⁻ hydrogen bonding, as evidenced by continuous shift of NH₂ resonances with increasing amounts of the anions added.     

CRF receptors in the rodent and human cardiovascular systems: species differences

CRF has powerful receptor-mediated cardiovascular actions. To evaluate the precise distribution of CRF receptors, in vitro CRF receptor autoradiography with ¹²⁵I-[Tyr⁰, Glu¹, Nle¹⁷]-sauvagine or [¹²⁵I]-antisauvagine-30 was performed in the rodent and human cardiovascular system. An extremely high density of CRF₂ receptors was detected with both tracers in vessels of rodent lung, intestine, pancreas, mesenterium, kidney, urinary bladder, testis, heart, brain, and in heart muscle. In humans, CRF₂ receptors were detected with ¹²⁵I- antisauvagine-30 at low levels in vessels of kidneys, intestine, urinary bladder, testis, heart and in heart muscle, while only heart vessels were detected with ¹²⁵I-[Tyr⁰, Glu¹, Nle¹⁷]-sauvagine. This is the first extensive morphological study reporting the extremely wide distribution of CRF₂ receptors in the rodent cardiovascular system and a more limited expression in man, suggesting a species-selective CRF receptor expression.     

Platinum(II) complexes of chelating and monodentate thiourea monoanions incorporating chiral, fluorescent or chromophoric groups

The reaction of cis-[PtCl₂(PPh₃)₂] with trisubstituted thioureas [R¹R²NC(=S)NHR³] in refluxing methanol with triethylamine base, followed by addition of NaBPh₄ gives the salts [Pt{SC(=NR¹R²)NR³}(PPh₃)₂]BPh₄ in high yield; a range of thiourea substituents, including chiral, fluorescent and chromophoric groups can be incorporated. The azo dye-derived complex [Pt{SC(=N(CH₂CH₂)₂O)NC₆H₄N=NC₆H₄NMe₂}(PPh₃)₂]BPh₄ has been characterised by a single-crystal X-ray diffraction study. The formation of a fluorescein-derivatised platinum–thiourea complex is also described. Reaction of cis-[PtCl₂(PPh₃)₂] with PhNHC(S)NHPh or EtNHC(S)NHEt, triethylamine and NaBPh₄ gives, respectively, [Pt{SC(=NHPh)NPh}(PPh₃)₂]⁺ and the known cation [Pt{SC(=NHEt)NEt}(PPh₃)₂]⁺, isolated as tetraphenylborate salts. Reaction of cis-[PtCl₂(PPh₃)₂] with an excess of Na[MeNHC(S)NCN] in methanol gives the bis(thiourea monoanion) complex trans-[Pt{SC(=N---CN)NHMe}₂(PPh₃)₂], characterised by NMR spectroscopy and an X-ray crystal structure determination. When cis-[PtCl₂(PPh₃)₂] is reacted with 1 equiv. of Na[MeNHC(S)N---CN] in methanol, with added NaBPh₄, a mixture of isomers of the [Pt{SC(=NHCN)NMe}(PPh₃)₂]⁺ cation is obtained.     

Characterization of growth hormone-releasing hormone (GHRH) binding to cloned porcine GHRH receptor

To study structure-activity relationships of growth hormone-releasing hormone (GHRH), a competitive binding assay was developed using cloned porcine adenopituitary GHRH receptors expressed in human kidney 293 cells. Specific binding of [His¹,¹²⁵I-Tyr¹⁰,Nle²⁷]hGHRH(1–32)-NH₂ increased linearly with protein concentration (10–45 μg protein/tube). Binding reached equilibrium after 90 min at 30°C and remained constant for at least 240 min. Binding was reversible to one class of high-affinity sites (K_d = 1.04 ± 0.19 nM, B_max = 3.9 ± 0.53 pmol/mg protein). Binding was selective with a rank order of affinity (IC₅₀) for porcine GHRH (2.8 ± 0.51 nM), rat GHRH (3.1 ± 0.69 nM), [N-Ac-Tyr¹, -Arg²]hGHRH(3–29)-NH₂ (3.9 ± 0.58 nM), and [ -Thr⁷]GHRH(1–29)-NH₂ (189.7 ± 14.3 nM), consistent with their binding to a GHRH receptor. Nonhydrolyzable guanine nucleotides inhibited binding. These data describe a selective and reliable method for a competitive GHRH binding assay that for the first time utilizes rapid filtration to terminate the binding assay.     

Characterization of Acetylcholine-induced Increases in Cytosolic Free Calcium Concentration in Individual Rat Pancreatic β-cells

The intracellular free Ca²⁺ ion concentration ([Ca²⁺]i) was measured using fura-2 microspec-trofluorimetry in individual rat pancreatic β-cells prepared by enzymatic digestion and fluorescence-activated cell sorting. The mean basal concentration of [Ca²⁺]i in β-cells in the presence of 4.4 mM glucose and 1.8 mM Ca²⁺ was 112±1.6 nM (n=207). The action of acetylcholine (ACh) was concentration-dependent, and raising the concentration resulted in [Ca²⁺]i spikes of increasing amplitude and duration in some, but not all of the β-cells. In addition, the β-cells demonstrated variable sensitivity to ACh. The increases in [Ca²⁺]i were rapid, transient and were blocked by atropine at 10^-6M. A brief exposure to 50 mM K⁺ resulted in a transient increase in [Ca²⁺]i similar to that induced by ACh, but resistant to atropine. A high concentration of ACh (100μL 10^-4M or 10^-3M) induced [Ca²⁺]i oscillations in 11 out of 57 β-cells in the presence of 4.4 mM glucose. Using calcium channel blockers and Ca²⁺ free medium, the source of the increase in [Ca²⁺]i was deduced to be from extracellular spaces. Changing the temperature from 22 to 37°C did not affect the action of ACh on [Ca²⁺]i. These data strongly suggest that ACh exerted a direct action on [Ca²⁺]i in normal rat pancreatic β-cells and support a role for Ca²⁺ as a second messenger in the action of ACh.     

Synthesis, structure, and heterogeneous catalytic activity of tungsten chalcogenide cubane cluster containing alkaline earth metal complex

A new compound containing a cubane tungsten chalcogenide cluster [W₄(μ₃-Te)₄(CN)₁₂]⁶⁻ and Ca²⁺ complex units has been prepared by the reaction of aqueous solution of K₆[W₄(μ₃-Te)₄(CN)₁₂] · 5H₂O with the solution of a Ca(NO₃)₂ and phen(1,10-phenanthroline) (1:2 molar ratio) in a solvent mixture of H₂O/EtOH. The structure of [{Ca(phen)₂(H₂O)}{Ca(phen)(H₂O)₄}{Ca(phen)₂(H₂O)₃}][W₄Te₄(CN)₁₂] · 5H₂O 1 has been determined by X-ray crystallography. Compound 1 contains [{Ca(phen)(H₂O)₄}{Ca(phen)₂(H₂O)₃}][W₄(μ₃- Te)₄(CN)₁₂] units bridged by {Ca(phen)₂(H₂O)}²⁺ units to form an one-dimensional zigzag chain structure. Interestingly, compound 1 showed a heterogeneous catalytic activity in the transesterification of a range of esters with methanol under the mild conditions. Moreover, it can be reused without any loss of activity through 10 runs with ester.     

Ligand induced P---H bond formation and a comparison of the reactivity of two isomers of the carbonyl hydride [Pt2(μ-PBu2)2(H)(CO)(PBu2H)]CF3SO3

The Pt₂ ^(II) isomeric terminal hydrides [(CO)(H)Pt(μ-PBu^t ₂)₂Pt(PBu^t ₂H)]CF₃SO₃ (1a), and [(CO)Pt(μ-PBu^t ₂)₂Pt(PBu^t ₂H)(H)]CF₃SO₃ (1b), react rapidly with 1 atm of carbon monoxide to give the same mixture of two isomers of the Pt₂ ^(I) dicarbonyl [Pt₂(μ-PBu^t ₂)(CO)₂(PBu^t ₂H)₂]CF₃SO₃ (3-Pt); the solid state structure of the isomer bearing the carbonyl ligands pseudo-trans to the bridging phosphide was solved by X-ray diffraction. A remarkable difference was instead found between the reactivity of 1a and 1b towards carbon disulfide or isoprene. In both cases 1b reacts slowly to afford [Pt₂(μ-PBu^t ₂)(μ,η²,η²-CS₂)(PBu^t ₂H)₂]CF₃SO₃ (4-Pt), and [Pt₂(μ-PBu^t ₂)(μ,η²,η²-isoprene) (PBu^t ₂H)₂]CF₃SO₃ (6-Pt), respectively. In the same experimental conditions, 1a is totally inert. A common mechanism, proceeding through the preassociation of the incoming ligand followed by the P---H bond formation between one of the bridging P atoms and the hydride ligand, has been suggested for these reactions.     

Nickel(II) and copper(II) complexes of mixed benzene-triazolehemiporphyrazines

The kinetics of substitution reactions of [η-CpFe(CO)₃]PF₆ with PPh₃ in the presence of R-PyOs have been studied. For all the R-PyOs (R = 4-OMe, 4-Me, 3,4-(CH)₄, 4-Ph, 3-Me, 2,3-(CH)₄, 2,6-Me₂, 2-Me), the reactions yeild the same product [η⁵-CpFe(CO)₂PPh₃]PF₆, according to a second-order rate law that is first order in concentrations of [η⁵-CpFe(CO)₃]PF₆ and of R-PyO but zero order in PPh₃ concentration. These results, along with the dependence of the reaction rate on the nature of R-PyO, are consistent with an associative mechanism. Activation parameters further support the bimmolecular nature of the reactions: ΔH^≠ = 13.4 ± 0.4 kcal mol⁻¹, ΔS^≠ = −19.1 ± 1.3 cal k⁻¹ mol⁻¹ for 4-PhPyO; ΔH^≠ = 12.3 ± 0.3 kcal mol⁻¹, ΔS^≠ = 24.7 ±1.0 cal K⁻¹ mol⁻¹ for 2-MePyO. For the various substituted pyridine N-oxides studied in this paper, the rates of reaction increase with the increasing electron-donating abilities of the substituents on the pyridine ring or N-oxide basicities, but decrease with increasing ¹⁷O chemical shifts of the N-oxides. Electronic and steric factors contributing to the reactivity of pyridine N-oxides have been quantitatively assessed.     

π-Arene complexes.: Part 12. Synthesis of chromiumtricarbonyl complexes of quinoline and N-methylindoles and selected metallation reactions

The lithiation of indole, using a slight excess of n-butyl lithium in THF, followed by methylation and reaction with [Cr(CO)₆] in refluxing dibutyl ether, resulted in the formation of [Cr(η⁶-N-methylindole)(CO)₃] (1a) and [Cr(η⁶-N-methyl-2-methylindole)(CO)₃] (1b). In contrast, lithiation of quinoline in THF, silylation and the subsequent reaction with [Cr(CO)₆] under similar reaction conditions, afforded [Cr(η⁶-N-trimethylsilyl-2-butyl-1,2-dihydroquinoline)(CO)₃] (2) and [Cr(η⁶-{2-butyl-1,2,3,4-tetrahydroquinoline})(CO)₃] (3). The formation of [Cr(η⁶-2,2′-bis{N-methylindolyl})(CO)₃] (4) implied lithiation at the 2-position of 1a. However, metallation at the 7-position was also indicated during the same reaction. In the presence of [Mn(CO)₅Br], product 4 and the transmetallation product [Cr(η⁶-{7-(N-methylindolyl)Mn(CO)₅})(CO)₃] (5) were isolated. Reaction with titanocene dichloride gave [Cr(η⁶-{2-(N-methylindolyl)TiCp₂Cl})(CO)₃] (6), which slowly converted into [TiCp₂{Cr(η⁶-2-(N-methylindolyl)(CO)₃}₂] (7).     

Synthesis, crystal structures and magnetic studies of dicyanamide bridged two new 1D copper(II) complexes

Two new dicyanamide bridged 1D polynuclear copper(II) complexes [Cu(L¹){μ_1,5-N(CN)₂}]_n (1) [L¹H = C₆H₅C(O)NHNC(CH₃)C₅H₄N] and [Cu(L²){μ_1,5-N(CN)₂}]_n (2) [L²H=C₆H₅C(O)CHC(CH₃)NCH₂CH₂N(CH₃)₂] have been synthesised and structures of both the complexes and their crystal packing arrangements have been established by X-ray crystallography. For complex 1, a tridentate hydrazone ligand (L¹H) obtained by the condensation of benzhydrazide and 2-acetylpyridine is used, whereas a tridentate Schiff base (L²H) derived from benzoylacetone and 2-dimethylaminoethylamine is employed for the preparation of complex 2. Variable temperature magnetic susceptibility measurement studies indicate there are weak antiferromagnetic interactions with J values −0.10 and −1.41 cm⁻¹ for 1 and 2, respectively.     

Crystal growth in aqueous hydrofluoric acid and (HF)x · pyridine solutions: syntheses and crystal structures of [Ni(H2O)6][MF6] (M = Ti, Zr, Hf) and Ni3(py)12F6 · 7H2O

The syntheses and structures of [Ni(H₂O)₆]²⁺[MF₆]²⁻ (M = Ti,Zr,Hf) and Ni₃(py)₁₂F₆·7H₂O are reported. The former three compounds are isostructural, crystallizing in the trigonal space group (No. 148) with Z = 3. The lattice parameters are a = 9.489(4), C = 9.764(7) Å, with V = 761(1) ų for Ti; a = 9.727(2), C = 10.051(3) Å, with V = 823.6(6) ų for Zr; and a = 9.724(3), C = 10.028(4)Å, with V = 821.2(8)ų for Hf. The structures consist of discrete [Ni(H₂O)₆]²⁺ and [MF₆]²⁻ octahedra joined by O---HF hydrogen bond Large single crystals were grown in an aqueous hydrofluoric acid solution. Ni₃(py)₁₂F₆·7H₂O crystallizes in the monoclinic space group I2/a (No. 15) with Z = 4. The lattice parameters are a = 16.117(4), B = 8.529(3), C = 46.220(7) Å, β = 92.46(2)°, and V = 6348(5) ų. The structure consists of discrete Ni(py)₄F₂ octahedra linked through H---O---HF and H---O---HO hydrogen bonding interactions. Single c were grown from a (HF)_x·pyridine/pyridine/water solution.     

Effect of clomiphene on Ca movement in human prostate cancer cells

The effect of clomiphene, an ovulation-inducing agent, on cytosolic free Ca²⁺ levels ([Ca²⁺]_i) in populations of PC3 human prostate cancer cells was explored by using fura-2 as a Ca²⁺ indicator. Clomiphene at concentrations between 10-50 μM increased [Ca²⁺]_i in a concentration-dependent manner. The [Ca²⁺]_i signal was biphasic with an initial rise and a slow decay. Ca²⁺ removal inhibited the Ca²⁺ signal by 41%. Adding 3 mM Ca²⁺ increased [Ca²⁺]_i in cells pretreated with clomiphene in Ca²⁺-free medium, confirming that clomiphene induced Ca²⁺ entry. In Ca²⁺-free medium, pretreatment with 50 μM brefeldin A (to permeabilize the Golgi complex), 1 μM thapsigargin (to inhibit the endoplasmic reticulum Ca²⁺ pump), and 2 μM carbonylcyanide m-chlorophenylhydrazone (to uncouple mitochondria) inhibited 25% of 50 μM clomiphene-induced store Ca²⁺ release. Conversely, pretreatment with 50 μM clomiphene in Ca²⁺-free medium abolished the [Ca²⁺]_i increase induced by brefeldin A, thapsigargin or carbonylcyanide m-chlorophenylhydrazone. The 50 μM clomiphene-induced Ca²⁺release was unaltered by inhibiting phospholipase C with 2 μM 1-(6-((17β-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122). Trypan blue exclusion assay suggested that incubation with clomiphene (50 μM) for 2-15 min induced time-dependent decrease in cell viability by 10-50%. Collectively, the results suggest that clomiphene induced [Ca²⁺]_i increases in PC3 cells by releasing store Ca²⁺ from multiple stores in an phospholipase C-independent manner, and by activating Ca²⁺ influx; and clomiphene was of mild cytotoxicity.     

4,5-Bis(diphenylthiophosphinoyl)-1,2,3-triazole, L: a new varidentate ligand containing diphenylthiophosphinoyl moieties

The novel ligand 4,5-bis(diphenylthiophosphinoyl)-1,2,3-triazole, L^T-S2H, has been synthesized, converted to the triethylamine salt, and to the palladium complexes Pd[L^T-S2]₂ and Pd[L^T-S2][η³-methallyl]. Structures of L^T-S2H, of its 2-acetyl derivative, of Pd[L^T-S2]₂ and Pd[L^T-S2][η³-methallyl] were determined by X-ray crystallography. In the last two complexes the L^T-S2 ligand was N,S-bonded.     

Structure and characterization of platinum(II) and platinum(IV) complexes with protonated nucleobase ligands

The reaction of H₂[PtCl₆] · 6H₂O and (H₃O)[PtCl₅(H₂O)] · 2(18C6) · 6H₂O (18C6 = 18-crown-6) with 9-methylguanine (MeGua) proceeded with the protonation of MeGua forming 9-methylguaninium hexachloroplatinate(IV) dihydrate (MeGuaH)₂[PtCl₆] · 2H₂O (1).The same compound was obtained from the reaction of Na₂[PtCl₆] with (MeGuaH)Cl.On the other hand, the reaction of guanosine (Guo) with (H₃O)[PtCl₅(H₂O)] · 2(18C6) · 6H₂O in methanol at 60 °C proceeded with the cleavage of the glycosidic linkage and with ligand substitution to give a guaninium complex of platinum(IV), [PtCl₅(GuaH)] · 1.5(18C6) · H₂O (2).Within several weeks in aqueous solution a slow reduction took place yielding the analogous guaninium platinum(II) complex, [PtCl₃(GuaH)] · (18C6) · 2Me₂CO (3).H₂[PtCl₆] · 6H₂O and guanosine was found to react in water, yielding (GuoH)₂[PtCl₆] (4) and in ethanol at 50 °C, yielding [PtCl₅(GuoH)] · 3H₂O (5).Dissolution of complexes 2 and 5 in DMSO resulted in the substitution of the guaninium and guanosinium ligands, respectively, by DMSO forming [PtCl₅(DMSO)]⁻.Reactions of 1-methylcytosine (MeCyt) and cytidine (Cyd) with H₂[PtCl₆] · 6H₂O and(H₃O)[PtCl₅(H₂O)] · 2(18C6) · 6H₂O resulted in the formation of hexachloroplatinates with N3 protonated pyrimidine bases as cation (MeCytH)₂[PtCl₆] · 2H₂O (6) and (CydH)₂[PtCl₆] (7), respectively. Identities of all complexes were confirmed by ¹H, ¹³C and ¹⁹⁵Pt NMR spectroscopic investigations, revealing coordination of GuoH⁺ in complex 5 through N7 whereas GuaH⁺ in complex 3 may be coordinated through N7 or through N9. Solid state structure of hexachloroplatinate 1 exhibited base pairing of the cations yielding (MeGuaH⁺)₂, whereas in complex 6 non-base-paired MeCytH⁺ cations were found. In both complexes, a network of hydrogen bonds including the water molecules was found. X-ray diffraction analysis of complex 3 exhibited a guaninium ligand that is coordinated through N9 to platinum and protonated at N1, N3 and N7. In the crystal, these NH groups form hydrogen bonds N–HO to oxygen atoms of crown ether molecules.     

The synthesis and structures of tantalum complexes that contain a triamido or a diamidoamine ligand

Addition of (Me₃SiNHCH₂CH₂)₂NH (H₃[N₃(TMS)]) or (Me₃SiNH-o-C₆H₄)₂NH (H₃[ArN₃(TMS)]) to a solution of TaMe₅ yields [N₃(TMS)]TaMe₂ or [ArN₃(TMS)]TaMe₂, respectively. An X-ray study of [ArN₃(TMS)]TaMe₂ showed it to have an approximate trigonal bipyramidal structure in which the two methyl groups are in equatorial positions and the triamido ligand is approximately planar. Addition of (C₆F₅NHCH₂CH₂)₂NH (H₃[N₃(C₆F₅)]) to TaMe₅ yields first [(C₆F₅NCH₂CH₂)₂NH]TaMe₃, which then decomposes to [(C₆F₅NCH₂CH₂)₂N]TaMe₂. An X-ray study of [(C₆F₅NCH₂CH₂)₂N]TaMe₂ shows it to be approximately a trigonal bipyramid, but the C₆F₅ rings are oriented so that they lie approximately in the TaN₃ plane and two ortho fluorines interact weakly with the metal. Trimethylaluminum attacks the central nitrogen atom in [N₃(TMS)]TaMe₂ to give [(Me₃SiNCH₂CH₂)₂NAlMe₃]TaMe₂, an X-ray study of which shows it to be a trigonal bipyramidal species similar to the first two structures, except that the C-Ta-C bond angle is approximately 30° smaller (106.6(12)°). Addition of B(C₆F₅)₃ to [(C₆F₅NCH₂CH₂)₂NH]TaMe₃ yields {[(C₆F₅NCH₂CH₂)₂NH]TaMe₂}⁺ {B(C₆F₅)₃Me}⁻, the structure of which most closely resembles that of [(Me₃SiNCH₂CH₂)₂NAlMe₃]TaMe₂ in that the C-Ta-C angle is 102.0(6)°. The C₆F₅ rings in {[(C₆F₅NCH₂CH₂)₂NH]TaMe₂}⁺ are turned roughly perpendicular to the TaN₃ plane, i.e. ortho fluorines do not interact with the metal in this molecule.