Discriminative affinity labelling of opioid receptors by enkephalin and morphiceptin analogues containing 3-nitro-2-pyridinesulphenyl-activated thiol residues.

The thiol groups of leucinthiol, cysteamine and cysteine incorporated into opioid peptides enkephalin and morphiceptin were activated by the 3-nitro-2-pyridinesulphenyl (Npys) group to form mixed disulphides highly reactive to a free thiol. Enkephalin analogues containing Npys-leucinthiol or -cysteine at positions 4, 5 and 6 exhibited high affinities for both mu and delta receptors, while morphiceptin analogues containing Npys-cysteine at positions 4 and 5 showed relatively weak affinity only for mu receptors. When these S-activated opioid peptides were incubated with rat brain membrane preparations, it was found, by binding assay using radiolabelled and non-labelled [D-Ala2,MePhe4,Gly-ol5]enkephalin, that they label mu opioid receptors in a dose-dependent manner. The concentrations required to label half of the receptors were 0.2-2 microM for enkephalins and 10-30 microM for morphiceptins. These results suggested that the thiol group labelled by S-activated enkephalins and morphiceptins is present in the ligand binding site of receptor protein, but not in GTPase-binding protein.     

In vivo imaging of brain dopaminergic neurotransmission system in small animals with high-resolution single photon emission computed tomography.

High-resolution single photon emission computed tomography (SPECT) provides a unique capability to image the biodistribution of radiolabeled molecules in small laboratory animals. Thus, we applied the high-resolution SPECT to in vivo imaging of the brain dopaminergic neurotransmission system in common marmosets using two radiolabeled ligands, [123I]2beta-carbomethoxy-3beta-(4-iodophenyl)tropane (beta-CIT) as a dopamine transporter (DAT) ligand and [123I]iodobenzamide (IBZM) as a dopamine D2 receptor (D2R) ligand. Specific images of the striatum, a region with a high density of dopaminergic synapses, were obtained at 240 min and 60 min after injection of [123I]beta-CIT and [123I]IBZM, respectively. Furthermore, a significantly low accumulation of [123I]beta-CIT in the striatum was observed in MPTP-treated animals compared with results for a control group, and a similar accumulation in the control group was observed with the pretreatment of deprenyl in the MPTP-treated animals. However, the striatal accumulation of [123I]IBZM showed no changes among the control, MPTP-treated, and deprenyl-MPTP-treated groups. These SPECT imaging results agreed well with those of DA concentration and motor behavior. Since MPTP destroys nigrostriatal dopamine nerves and produces irreversible neurodegeneration associated with Parkinsonian syndrome, SPECT imaging data in this study demonstrated that deprenyl shows its neuroprotective effect on Parkinsonism by protecting against the destruction of presynaptic dopamine neurons.     

Biological properties of opioid peptides replacing Tyr at position 1 by 2,6-dimethyl-Tyr.

To understand the effect of the replacement of Tyr residue at position 1 in opioid peptides by 2,6-dimethyl-Tyr (Dmt) on the biological property, chiral (D or L) Dmt1 analogs of Leu-enkephalin (Enk) and Tyr-D-Arg-Phe-beta Ala-NH2 (YRFB) were synthesized and their enzymatic stabilities, in vitro bioactivities and receptor binding affinities compared with those of parent peptides. [L-Dmt1]Enk (1) exhibited 4-fold higher stability against aminopeptidase-M and possessed dramatically increased activities in guinea pig ilium (GPI) (187-fold) and mouse vas deferens (MVD) (131-fold) assays, and in rat brain receptor binding assays (356-fold at mu receptor and 46-fold at delta receptor) as compared to Enk. [L-Dmt1]YRFB (3) also exhibited increased activities in GPI (46-fold) and MVD (177-fold) assays, and in the binding assays (69-fold at mu receptro and 341-fold at delta receptor) as compared to the parent peptide. [D-Dmt1]Enk (2) and [D-Dmt1]YRFB (4) exhibited activities with diminished or lesser potency than the parent peptide in all assays. These results indicate that there is a tendency for mu affinity to be enhanced more than delta affinity with introduction of L-Dmt into delta ligand peptide (Enk), and for delta affinity to be enhanced more than mu affinity in case of mu ligand peptide (YRFB), resulting in reduced receptor selectivities at the receptors.     

Simple, rapid and reliable preparation of [¹¹C]-(+)-α-DTBZ of high quality for routine applications

[11C]-(+)-α-DTBZ has been used as a marker of dopaminergic terminal densities in human striatum and expressed in islet beta cells in the pancreas. We aimed to establish a fully automated and simple procedure for the synthesis of [11C]-(+)-α-DTBZ for routine applications. [11C]-(+)-α-DTBZ was synthesized from a 9-hydroxy precursor in acetone and potassium hydroxide with [11C]-methyl triflate and was purified by solid phase extraction using a Vac tC-18 cartridge. Radiochemical yields based on [11C]-methyl triflate (corrected for decay) were 82.3% ± 3.6%, with a specific radioactivity of 60 GBq/μmol. Time elapsed was less than 20 min from end of bombardment to release of the product for quality control.     

Determination of O and OH adsorption sites and coverage in situ on Pt electrodes from Pt L(2,3) X-ray absorption spectroscopy

The adsorption of atomic oxygen and hydroxide on a platinum electrode in 0.1 M HClO4 or H2SO4 electrolytes was studied in situ with Pt L(2,3) X-ray absorption spectroscopy (EXAFS and XANES). The Pt L3 edge absorption data, mu, were collected at room temperature in transmission mode on beamline X-11A at the National Synchrotron Light Source using a custom built cell. The Pt electrode was formed of highly dispersed 1.5-3 nm particles supported on carbon. A novel difference procedure (delta mu = mu(O[H]/Pt) - mu(Pt)) utilizing the L3 XANES spectra at different applied voltages was used to isolate the effects of O[H] (O or OH) adsorption in the XANES spectra. The Deltamu results are compared with results obtained from real-space full-multiple scattering calculations utilizing the FEFF8 code on model clusters. The experimental results, when compared with theoretical calculations, allow the adsorption site to be identified. At low coverages OH adsorbs primarily in 1-fold coordinated atop sites. As the coverage increases, O binds in the bridge/fcc sites, and at still higher coverages above 1.05 V RHE, O adsorbs into a higher coordinated n-fold or subsurface site, which is thought to be the result of Pt-O site exchange and oxide formation. These results are similar to those found in the gas phase. Direct specific adsorption of bisulfate anions in H2SO4 is spectroscopically seen in both the EXAFS and XANES data and is seen to impede oxygen adsorption consistent with previous reports.     

Endogenous synthesis of N-methylsalsolinol, an analogue of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, in rat brain during in vivo microdialysis with salsolinol, as demonstrated by gas chromatography-mass spectrometry.

N-Methylsalsolinol, an analogue of 1,2,3,6-tetrahydropyridine, is present in the brains of patients with Parkinson's disease. To determine the metabolic pathway for the synthesis of N-Methylsalsolinol in the brain, salsolinol was perfused through the striatum or the substantia nigra of the rat brain by in vivo microdialysis. N-Methylsalsolinol was detected in the brain dialysate samples during microdialysis with salsolinol using gas chromatography-mass spectrometry with selected-ion monitoring. These results demonstrate that endogenous N-methylation of salsolinol into N-methylsalsolinol occurs in the brain in vivo.     

Specific binding of beta-endorphin to the isolated renal basolateral membranes in vitro

Binding of human beta-endorphin (beta-EP) to rat renal basolateral membranes was characterized using [125I]Tyr27-beta-EP ([125I]beta-EP) as a primary ligand. Ten millimolar of ethylenediaminetetra acetic acid (EDTA) completely inhibited the degradation of [125I]beta-EP in the incubation mixture at 4 degrees C, thus making it possible to quantitatively examine the [125I]beta-EP binding. The specific binding of [125I]beta-EP to the basolateral membranes was reversible and saturable, and a nonlinear least-squares regression analysis of a saturation isotherm revealed two different classes of specific binding sites. One class had an apparent dissociation constant (Kd) of 0.68 nM and a lower number of binding sites (33 fmol/mg protein), whereas the other class had a lower affinity (apparent Kd of 210 nM) and a higher number of binding sites (7.3 pmol/mg protein). Inhibition of the [125I]beta-EP binding by naloxone (10 microM) was approximately only 20%, and that by D-Ala2-D-Leu5-enkephalin (10 microM) was null, suggesting the major role of a non-opioid binding component in specific [125I]beta-EP binding to basolateral membranes. Moreover, a 50% inhibition by 10 microM of dynorphin(1-13) suggests that a certain region of the primary structure of beta-EP, excluding at least the NH2-terminal enkephalin sequence, is of particular importance for the [125I]beta-EP binding. These lines of evidence suggest the existence of two different classes of specific binding sites for beta-EP on the renal basolateral membranes, and the high-and low-affinity bindings may be attributed to opioid and non-opioid receptors, respectively, as judged by known characteristics of opioid and non-opioid receptors in other peripheral tissues.     

Immunological and binding studies on chloroform--methanol extracts from electroplax of Torpedo marmorata and from rat brain cortex. Comparison of the material solubilized by organic solvents with the receptor proteins solubilized by detergents

We have investigated a chloroform--methanol extracted material from electric organ of Torpedo marmorata with respect to binding of [3H]-acetyl-alpha-neurotoxin and [3H]-acetylcholine. No binding was observed which is in contrast to observations with detergent extracted receptor. Further, no crossreactivity could be demonstrated between the chloroform--methanol extracted proteolipid and antibodies against the detergent extracted receptor. Labelling in the membrane with [3H]-acetyl-alpha-neurotoxin before extraction with chloroform--methanol gave a very low yield of extracted labelled compound. The protein yield is about 0.3% of the total in the homogenate and only 0.04% of the specifically bound neurotoxin. Using the alkylating affinity label [3H]-N-propylbenzilylcholine mustard (1) and also [3H]-atropine, which both bind, at low concentrations, specifically to the muscarinic acetylcholine receptor, binding was studied to the chloroform--methanol extracted proteolipid from rat brain cortex. No specific binding could, however, be demonstrated. Prelabelling in the membrane with 1 and subsequent extraction with chloroform--methanol gave a protein yield of about 1% and an extraction of 26% of the specifically bound label.     

Studies on analgesic oligopeptides. VI. Further studies of synthesis and biological properties of tripeptide alkylamides, Tyr-D-Arg-Phe-X

Nine analogs based on a structure of Tyr-D-Arg-Phe-X (X = alkylamides or alkylhydrazide containing electron-withdrawing atoms or groups) were newly synthesized and their biological properties were examined by the opioid receptor binding properties of mu-, delta- and kappa-receptors, guinea-pig ileum (GPI) assay and analgesic activity in the tail pinch test after subcutaneous administration in mice. Analogs with X = NHCF2CF3, Sar-ol, or NH(CH2)2CN showed potent activities in the GPI and analgesic assays and high affinity for mu-receptor. An analog with X = taurinamide was found to possess 4-fold higher mu-receptor selectivity than that of [D-Ala2, MePhe4, Gly-ol5]enkephalin (DAGO). The receptor binding properties of previously reported analogs [Chem. Pharm. Bull., 33, 1528 (1985); ibid., 33, 4865 (1985); ibid., 36, 4834 (1988)] were also examined for overall discussion of the structure-activity relationships of this series of tripeptide amides.     

Systemic LPS administration induces brain inflammation but not dopaminergic neuronal death in the substantia nigra

It has been suggested that brain inflammation is important in aggravation of brain damage and/or that inflammation causes neurodegenerative diseases including Parkinson's disease (PD). Recently, systemic inflammation has also emerged as a risk factor for PD. In the present study, we evaluated how systemic inflammation induced by intravenous (iv) lipopolysaccharides (LPS) injection affected brain inflammation and neuronal damage in the rat. Interestingly, almost all brain inflammatory responses, including morphological activation of microglia, neutrophil infiltration, and mRNA/protein expression of inflammatory mediators, appeared within 4-8 h, and subsided within 1-3 days, in the substantia nigra (SN), where dopaminergic neurons are located. More importantly, however, dopaminergic neuronal loss was not detectable for up to 8 d after iv LPS injection. Together, these results indicate that acute induction of systemic inflammation causes brain inflammation, but this is not sufficiently toxic to induce neuronal injury.     

Noscapine Prevents Rotenone-Induced Neurotoxicity: Involvement of Oxidative Stress,Neuroinflammation and Autophagy Pathways

Parkinson’s disease is characterized by the loss of dopaminergic neurons in substantia nigra pars compacta (SNpc) and the resultant loss of dopamine in the striatum. Various studies have shown that oxidative stress and neuroinflammation plays a major role in PD progression. In addition, the autophagy lysosome pathway (ALP) plays an important role in the degradation of aggregated proteins, abnormal cytoplasmic organelles and proteins for intracellular homeostasis. Dysfunction of ALP results in the accumulation of α-synuclein and the loss of dopaminergic neurons in PD. Thus, modulating ALP is becoming an appealing therapeutic intervention. In our current study, we wanted to evaluate the neuroprotective potency of noscapine in a rotenone-induced PD rat model. Rats were administered rotenone injections (2.5 mg/kg, i.p.,) daily followed by noscapine (10 mg/kg, i.p.,) for four weeks. Noscapine, an iso-qinulinin alkaloid found naturally in the Papaveraceae family, has traditionally been used in the treatment of cancer, stroke and fibrosis. However, the neuroprotective potency of noscapine has not been analyzed. Our study showed that administration of noscapine decreased the upregulation of pro-inflammatory factors, oxidative stress, and α-synuclein expression with a significant increase in antioxidant enzymes. In addition, noscapine prevented rotenone-induced activation of microglia and astrocytes. These neuroprotective mechanisms resulted in a decrease in dopaminergic neuron loss in SNpc and neuronal fibers in the striatum. Further, noscapine administration enhanced the mTOR-mediated p70S6K pathway as well as inhibited apoptosis. In addition to these mechanisms, noscapine prevented a rotenone-mediated increase in lysosomal degradation, resulting in a decrease in α-synuclein aggregation. However, further studies are needed to further develop noscapine as a potential therapeutic candidate for PD treatment.     

Automated method to estimate catecholamine and indoleamine content and turnover rates

A double-label isotopic method for estimation of the rate of formation of serotonin (5-HT) and dopamine (DA) in mouse striatum, hippocampus and cortex was standardized. Mice received an intravenous pulse injection of [3H]tryptophan (TRP) and [3H]tyrosine (TYR) at 2.5, 5, 10 or 20 min before sacrifice by microwave irradiation. Compounds of interest were separated by automated high-performance liquid chromatography and their contents were determined by electrochemical detection. Programmed collection of the TYR, DA, 5-HT and TRP peaks allowed determination of their radioactivity by liquid scintillation. Conversion of [3H]TYR to [3H]DA was nearly ten times greater in striatum than cortex, whereas the formation of [3H]5-HT from [3H]TRP was similar in striatum, cortex and hippocampus.     

Positron-emitting N-[18F]fluoroalkyl and [18F]fluoropyrrolidinyl analogues of eticlopride as potential in vivo radioligands for dopamine D2 receptors.

N-Fluoroalkyl and 4-fluoropyrrolidinyl eticlopride analogues with high affinity toward central nervous system dopamine D2 receptors in vitro were labelled with positron emitting fluorine-18 (t1/2 = 110 min), and their in vivo biodistribution was investigated in rats. N-[18F]Fluoro-ethyl and -propyl eticlopride derivatives showed poor in vivo selectivity in the rat brain. On the other hand, 4-[18F]fluoropyrrolidinyl eticlopride exhibited almost constant and relatively high striatal concentration. The striatal/cerebellar radioactivity ratio, which corresponds to the ratio of a brain D2 receptor-rich to poor region, gradually increased to 5.2-6.4, 90 min after the injection. The striatal accumulation was selectively inhibited by pre-injection of haloperidol, a dopamine D2 antagonist, without affecting accumulation in other tissues. Thus, the selective striatal accumulation of 4-[18F]fluoropyrrolidinyl eticlopride in striatal tissue appears to be due to the specific binding to dopamine D2 receptors.     

Reactivity of alkynes containing alpha-hydrogen atoms with a triruthenium hydrido carbonyl cluster: alkenyl versus allyl cluster derivatives

The reactions of the hydrido-triruthenium cluster complex [Ru3(mu-H)(mu3-kappa(2)-HNNMe2)(CO)9] (1; H2NNMe2 = 1,1-dimethylhydrazine) with alkynes that have alpha-hydrogen atoms give trinuclear derivatives containing edge-bridging allyl or face-capping alkenyl ligands. Under mild conditions (THF, 70 degrees C) the isolated products are as follows: [Ru3(mu3-kappa(2)-HNNMe2)(mu-kappa(3)-1-syn-Me-3-anti-EtC3H3)(mu-CO)2(CO)6] (2) and [Ru3(mu3-kappa(2)-HNNMe2)(mu-kappa(3)-1-syn-Me-3-syn-EtC3H3)(mu-CO)2(CO)6] (3) from 3-hexyne; [Ru3(mu3-kappa(2)-HNNMe2)(mu-kappa(3)-3-anti-PhC3H4)(mu-CO)2(CO)6] (4), [Ru3(mu3-kappa(2)-HNNMe2)(mu-kappa(2)-MeCCHPh)(mu-CO)2(CO)6] (5) and [Ru3(mu3-kappa(2)-HNNMe2)(mu3-kappa(2)-PhCCHMe)(mu-CO)2(CO)6] (6) from 1-phenyl-1-propyne; [Ru3(mu3-kappa(2)-HNNMe2)(mu-kappa(2)-3-anti-PrC3H4)(mu-CO)2(CO)6] (7), [Ru3(mu3-kappa(2)-HNNMe2)(mu3-kappa(2)-BuCCH2)(mu-CO)2(CO)6] (8), and [Ru3(mu3-kappa(2)-HNNMe2)(mu3-kappa(2)-HCCHBu)(mu-CO)2(CO)6] (9) from 1-hexyne; [Ru3(mu3-kappa(2)-HNNMe2)(mu3-kappa(2)-HOH2CCCH2)(mu-CO)2(CO)6] (10) from propargyl alcohol; and [Ru3(mu3-kappa(2)-HNNMe2)(mu3-kappa(2)-MeOCH2CCH2)(mu-CO)2(CO)6] (11) from 3-methoxy-1-propyne. The regioselectivity of these reactions depends upon the nature of the alkyne reagent, which affects considerably the kinetic barriers of important reaction steps and the stability of the final products. It has been established that the face-capped alkenyl derivatives are not precursors to the allyl products, which are formed via edge-bridged alkenyl intermediates. At higher temperature (toluene, 110 degrees C), the complexes that have allyl ligands with an anti substituent are isomerized into allyl derivatives with that substituent in the syn position, for example, 4 into [Ru3(mu3-kappa(2)-HNNMe2)(mu-kappa(3)-3-syn-PhC3H4)(mu-CO)2(CO)6] (14). The diene complex [Ru3(mu-H)(mu3-kappa(2)-HNNMe2)(mu-kappa(4)-trans-EtC4H5)(CO)7] (13) has been obtained from the thermolysis of compounds 2 and 7 at 110 degrees C (3 and [Ru3(mu3-kappa(2)-HNNMe2)(mu-kappa(2)-3-syn-PrC3H4)(mu-CO)2(CO)6] (12) are also formed in these reactions). A DFT theoretical study has allowed a comparison of the thermodynamic stabilities of isomeric compounds and has helped rationalize the experimental results. Mechanistic proposals for the synthesis of the allyl complexes and their isomerization processes are also provided.     

2 + 2] cross coupling of benzene and tropylium ligands in reductively activated piano stool complexes of Mn,Cr, and W

We have established cation/anion coupling reactions between the tropylium ligand in [M(eta7-C7H7)(CO)3]+ (M = Cr, W) and the reductively activated eta4-benzene ligand in [Mn(eta4-C6H6)(CO)3]- (3-) to form [M(CO)3(mu2-eta6:eta5-C7H7-C6H6)Mn(CO)3]; [Cr(CO)3(mu2-eta6:eta5-C7H7-C6H6)Mn(CO)3] can be further reduced to [Cr(CO)3(mu2-eta5:eta4-C7H7-C6H6)Mn(CO)3]2-, in which the tropylium and benzene ligands have undergone a [2 + 2] cross coupling reaction.     

Rhodium/iridium-titanium azaheterometallocubanes

Treatment of [[Ti(eta5-C5Me5)(mu-NH)]3(mu3-N)] (1) with the diolefin complexes [[MCl(cod)]2] (M = Rh, Ir; cod = 1,5-cyclooctadiene) in toluene afforded the ionic complexes [M-(cod)(mu3-NH)3Ti3(eta5-C5Me5)3(mu3-N)]Cl [M = Rh (2), Ir (3)]. Reaction of complexes 2 and 3 with [Ag(BPh4)] in dichloromethane leads to anion metathesis and formation of the analogous ionic derivatives [M(cod)(mu3-NH)3Ti3-(eta5-C5Me5)3(mu3-N)][BPh4] [M = Rh (4), Ir (5)]. An X-ray crystal structure determination for 5 reveals a cube-type core [IrTi3N4] for the cationic fragment, in which 1 coordinates in a tripodal fashion to the iridium atom. Reaction of the diolefin complexes [[MCl(cod))2] (M = Rh, Ir) and [[RhCl(C2H4)2]2] with the lithium derivative [[Li(mu3-NH)2(mu3-N)-Ti3(eta5-C5Me5)3(mu3-N)]2] x C7H8 (6 C7H8) in toluene gave the neutral cube-type complexes [M(cod)(mu-NH)2(mu3-N)Ti3-(eta5-C5Me5)3(mu3-N)] [M = Rh (7), Ir (8)] and [Rh(C2H4)2(mu3-NH)2(mu3-N)Ti3(eta5-C5Me5)3(mu3-N)] (9), respectively. Density functional theory calculations have been carried out on the ionic and neutral azaheterometallocubane complexes to understand their electronic structures.     

Glucose binding isotope effects in the ternary complex of brain hexokinase demonstrate partial relief of ground-state destabilization

Isotope effects can yield detailed information about contacts made between a bound compound and its host receptor or enzyme. In this study, we have measured isotope effects upon the equilibrium constant for the association of glucose and human brain hexokinase [E.C.2.7.1.1] in the presence of beta,gamma-CH(2)-ATP and compared these with data for the same equilibrium in the absence of ATP-analogue. We have found isotope effects of 1.012, 0.929, 1.031, 1.052, 0.998, and 1.032 for the competitive binding of [1-(3)H]-, [2-(3)H]-, [3-(3)H]-, [4-(3)H]-, [5-(3)H]-, or [6,6-(3)H(2)]- and either [2-(14)C]- or [6-(14)C]glucose to brain hexokinase. We observed changes only at H1, H5, and H6, and we attribute these to a slight change in the position of Asn683 and Glu742 due to nucleotide binding and to partial satisfaction of activated OH6 by the terminal nucleotide phosphorus.     

A simple and sensitive high‐performance liquid chromatography–electrochemical detection assay for the quantitative determination of monoamines and respective metabolites in six discrete brain regions of mice

A rapid, sensitive, and reproducible assay is described for the quantitative determination of the monoamine neurotransmitters dopamine, norepinephrine and serotonin, their metabolites, and the internal standard 3,4‐dihydroxybenzlyamine hydro‐bromide in mouse brain homogenate using high‐performance liquid chromatography with electrochemical detection. The method was validated in the following brain areas: frontal cortex, striatum, nucleus accumbens, hippocampus, substantia nigra pars compacta and ventral tegmental area. Biogenic amines and relevant metabolites were extracted from discrete brain regions using a simple protein precipitation procedure, and the chromatography was achieved using a C₁₈ column. The method was accurate over the linear range of 0.300–30 ng/mL (r = 0.999) for dopamine and 0.300–15 ng/mL (r = 0.999) for norepinephrine, 3,4‐dihydroxybenzlyamine hydro‐bromide, homovanillic acid and 5‐hydroxyindolacetic acid, with detection limits of ~0.125 ng/mL (5 pg on column) for each of these analytes. Accuracy and linearity for serotonin were observed throughout the concentration range of 0.625–30 ng/mL (r = 0.998) with an analytical detection limit of ~0.300 ng/mL (12 pg on column). Relative recoveries for all analytes were approximately ≥90% and the analytical run time was <10 min. The described method utilized minimal sample preparation procedures and was optimized to provide the sensitivity limits required for simultaneous monoamine and metabolite analysis in small, discrete brain tissue samples.     

Unsupported gold(I)-copper(I) interactions through eta1 Au-[Au(C6F5)2]- coordination to Cu+ Lewis acid sites

The reaction of the complex [Au2Ag2(C6F5)4)N[triple bond]CCH3)2]n (1) with 1 equiv of CuCl in the presence of 1 equiv of pyrimidine ligand leads to the formation of the heteronuclear Au(I)-Cu(I) organometallic polymer [Cu{Au(C6F5)2}(N[triple bond]CCH3)(mu2-C4H4N2)]n (2) through a transmetalation reaction. Complex 2 displays unprecedented unsupported Au(I)...Cu(I) interactions of [Au(C6F5)2]- units with the acid Cu(I) sites in a [Cu(N[triple bond]CCH3)(mu2-pyrimidine)]n+(n) polymeric chain. Complex 2 has a rich photophysics in solution and in the solid state.     

Oxygen capture by lithiated organozinc reagents containing aromatic 2-pyridylamide ligands

The sequential reaction of ZnMe2 with a 2-pyridylamine (HN(2-C5H4N)R, R = Ph: 1; 3,5-Xy (=3,5-xylyl): 2; 2,6-Xy: 3; Bz (=benzyl): 4; Me: 5), tBuLi and thereafter with oxygen affords various lithium zincate species, the solid-state structures of which reveal a diversity of oxo-capture modes. Amine 1 reacts to give both dimeric THF [Li(Me)OZn[N(2-C5H4N)Ph]2] (6), wherein oxygen has inserted into the Zn-C bond of a [MeZn[N(2-C5H4N)-Ph]2] ion, and the trigonal Li2Zn complex, bis(OtBu)-capped (THF x Li)2-[[(mu3-O)tBu]2Zn[N(2-C5H4N)Ph]2] (7). The structural analogue of 6 (8) results from the employment of 2, while the use of more sterically congested 3 yields a pseudo-cubane dimer [(THF x [Li(tBu)OZn(OtBu)Me]]2] (9) notable for the retention of labile Zn-C(Me). Amines 4 and 5 afford the oxo-encapsulation products [mu4-O)Zn4[(2-C5H4N)-NBz]6] (10b), and [tBu(mu3-O)-Li3(mu6-O)Zn3[(2-C5H4N)NMe]6] (11), respectively, with concomitant oxo-insertion into a Li-C interaction resulting in capping of the fac-isomeric (mu6-O)M3M'3 distorted octahedral core of the latter complex by a tert-butoxide group.