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PubMed1998

Interaction of Triphenyltin Hydride and Rhodium. Structure of [Rh(NCBPh(3))(H)(SnPh(3))(PPh(3))(2)] and NMR ((1)H, (15)N, (31)P, (103)Rh, (119)Sn) Study of Pyridine-Containing Derivatives.

The structure of [Rh(NCBPh(3))(H)(SnPh(3))(PPh(3))(2)] (1) (formed from [Rh(NCBPh(3))(PPh(3))(3)] and Ph(3)SnH) was determined by a single-crystal X-ray diffraction study which shows the geometry to be equally well described as a distorted tetragonal pyramid with tin at the apex or a distorted trigonal bipyramid with a hydrogen of one of the phosphine phenyl groups occupying the sixth coordination site. The tin-hydride distance of 2.31(5) Å is consistent with a weak interaction. Crystal data for 1: space group, P2(1)/c; a = 12.564(4), b = 26.942(4), c = 18.000(3) Å; beta = 92.93(2) degrees; V = 6085(2) Å(3); Z = 4; R = 0.050 for 5655 reflections with I >/= 2sigma(I). Complex 1 reacts with pyridine and substituted pyridines L (L = pyridine (py) (a), 4-(dimethylamino)pyridine (4-Me(2)Npy) (b), and 4-carbomethoxypyridine (4-MeO(2)Cpy) (c)) in dichloromethane at -25 degrees C to give trans-[Rh(NCBPh(3))(H)(SnPh(3))(PPh(3))(2)(L)] (2a-c). With L = 4-Me(2)Npy, the products cis-[Rh(NCBPh(3))(H)(SnPh(3))(PPh(3))(2)(4-Me(2)Npy)] (3) and cis- and trans-[Rh(NCBPh(3))(H)(SnPh(3))(PPh(3))(4-Me(2)Npy)(2)] (4 and 5, respectively) are also formed. At room temperature, [Rh(NCBPh(3))(H)(SnPh(3))(PPh(3))(L)] (6a-c) is the final product, decomposing over a period of hours. The pyridine-containing complexes were not isolated and were characterized by NMR spectroscopy, which showed the magnitude of the spin coupling constant J(Sn-H) to increase by factors of up to 5.5 compared with the value of 29 Hz observed for 1. At 50 degrees C, 6 (in the presence of L and PPh(3) originating from 1) undergoes reductive elimination of Ph(3)SnH to give cis-[Rh(NCBPh(3))(PPh(3))(2)(L)]; at this temperature 1 is stable, decomposing only at temperatures of 85 degrees C and above. A kinetic study of the dissociation of Ph(3)SnH from 6b (L = 4-Me(2)Npy) gave activation parameters DeltaH() = 97 +/- 6 kJ mol(-)(1) and DeltaS() = 1 +/- 20 J K(-)(1) mol(-)(1). The weakened interaction between Ph(3)SnH and rhodium is accounted for in terms of a three-center "agostic" bond.

Journal Article↗

PubMed2005

One-pot synthesis of metalated pyridines from two acetylenes, a nitrile, and a titanium(II) alkoxide.

Four-component coupling process involving two acetylenes, a nitrile, and a divalent titanium alkoxide reagent, Ti(O-i-Pr)(4)/2i-PrMgCl, directly yielded titanated pyridines in a highly selective manner. The reaction can be classified into four categories: (i) a combination of an internal acetylene, a terminal acetylene, sulfonylnitrile, and the titanium reagent to yield alpha-titanated pyridines, (ii) a combination of an internal acetylene, a (sulfonylamino)acetylene, a nitrile, and the titanium reagent to yield alternative alpha-titanated pyridines, (iii) a combination of an internal acetylene, a (sulfonylamino)acetylene, a nitrile, and the titanium reagent to yield titanated aminopyridines, and (iv) a combination of an acetylenic amide, a terminal acetylene, a nitrile, and the titanium reagent to yield pyridineamides with their side chain titanated. Some of these reactions enabled virtually completely regioselective coupling of two different, unsymmetrical acetylenes and a nitrile to form a single pyridine. Synthetic applications of these reactions have been illustrated in the preparation of optically active pyridines and medicinally useful compounds.

Journal Article↗

PubMed2005

Porphyrin-based organogels: control of the aggregation mode by a pyridine-carboxylic acid interaction.

To find a new strategy for designing porphyrin-based organogelators, hydrogen-bond-donating (carboxylic acid)/accepting (pyridine) substituents or electron-donating (dialkylamino)/withdrawing (pyridine) substituents were introduced into peripheral positions of a porphyrin (1cp or 1ep, respectively), and the gelation properties were compared with those of symmetrical reference compounds bearing two pyridyl substituents or two ester groups (1pp or 1ee, respectively). It was found that the symmetrical molecules show a solubility that is quite inferior to that of 1cp and 1ep having a dipole moment and precipitate from most organic solvents. 1cp, 1ep, and 1ee formed gels with cyclohexane, methylcyclohexane, and several alcoholic solvents, but scanning electron microscopy (SEM) and transmission electron microscopy (TEM) observations revealed that their superstructures constructed in the organogels are very different. In cyclohexane, 1cp resulted in a sheetlike structure, whereas 1ep and 1ee resulted in a fiberlike structure. The difference is attributed to the two-dimensional interactive forces in 1cp consisting of the porphyrin-porphyrin pi-pi stacking and the carboxylic acid-pyridine hydrogen bonding. In fact, when the hydrogen-bonding interaction was weakened by alcoholic solvents or by adding pyridine or N,N-(dimethylamino)pyridine, the sheetlike structure was transfigured to the fiberlike structure. Further detailed analyses of their aggregation modes were conducted by spectroscopic methods such as ultraviolet-visible (UV-vis) absorption, Fourier transform infrared (FT-IR), and X-ray diffraction (XRD). On the basis of these findings, the influence of these peripheral substituents on the gel formation and the aggregation mode was discussed.

Journal Article↗

PubMed2006

Excited state proton transfer (ESPT) from phenol to nitrogen and carbon in (2-hydroxyphenyl)pyridines.

ESIPT and ESPT are the only photochemical deactivation pathways of the singlet excited states of 2-, 3- and 4-(2'-hydroxyphenyl)pyridines. Due to the existence of an intramolecular hydrogen bond in 2-(2'-hydroxyphenyl)pyridine, ESIPT leads only to protonation of the pyridine nitrogen. On the other hand, the singlet excited states of 3- and 4-(2'-hydroxyphenyl)pyridine undergo protonation of both nitrogen and carbon atoms of the pyridine ring, via ESIPT or ESPT. The extent of ESIPT to carbon (as measured by extent of deuterium incorporation) can be controlled by the amount of water in the solvent system.

Journal Article↗

PubMed2006

Synthesis and application in asymmetric catalysis of camphor-based pyridine ligands.

This tutorial review deals with the synthesis and application in asymmetric catalysis of camphor-based pyridine ligands. These ligands can be roughly divided into two groups: those in which the camphor is annulated in the 2,3-positions to the beta-face of the pyridine ring and those in which the pyridine is contained as a pendant on the C2 or C3 of the camphor framework. Camphor-based pyridine ligands can also contain other donor centers located on the pyridine ring or camphor skeleton. Some of these ligands have provided interesting enantioselectivities in several asymmetric reactions, such as S(N)2' reactions, allylic oxidations, carbonyl additions with organozinc reagents and hydrogenations. This review contains a lot of chemistry on ligand synthesis and readers will find it of value and also perhaps an inspiration for the development of more active and improved versions.

Journal Article↗

PubMed2005

Photodissociation dynamics of pyridine.

Photodissociation of pyridine, 2,6-d2-pyridine, and d5-pyridine at 193 and 248 nm was investigated separately using multimass ion imaging techniques. Six dissociation channels were observed at 193 nm, including C5NH5 --> C5NH4 + H (10%) and five ring opening dissociation channels, C5NH5 --> C4H4 + HCN, C5NH5 --> C3H3 + C2NH2, C5NH5 --> C2H4 +C3NH, C5NH5 --> C4NH2 + CH3 (14%), and C5NH5 --> C2H2 + C3NH3. Extensive H and D atom exchanges of 2,6-d2-pyridine prior to dissociation were observed. Photofragment translational energy distributions and dissociation rates indicate that dissociation occurs in the ground electronic state after internal conversion. The dissociation rate of pyridine excited by 248-nm photons was too slow to be measured, and the upper limit of the dissociation rate was estimated to be 2x10(3) s(-1). Comparisons with potential energies obtained from ab initio calculations and dissociation rates obtained from the Rice-Ramsperger-Kassel-Marcus theory have been made.

Journal Article↗

PubMed2006

Structure and stability of Co(n)(pyridine)(m)- clusters: absence of metal inserted structures.

A synergistic approach combining the experimental photoelectron spectroscopy and theoretical electronic structure studies is used to probe the geometrical structure and the spin magnetic moment of Co(n)(pyridine)(m) (-) clusters. It is predicted that the ground state of Co(pyridine)(-) is a structure where the Co atom is inserted in a CH bond. However, the insertion is marked by a barrier of 0.33 eV that is not overcome under the existing experimental conditions resulting in the formation of a structure where Co occupies a site above the pyridine plane. For Co(2)(pyridine)(-), a ground-state structure is predicted in which the Co(2) diametric moiety is inserted in one of the CH bonds, but again because of a barrier, the structure which matches the photoelectron spectrum is a higher-energy isomer in which the Co(2) moiety is bonded directly to nitrogen on the pyridine ring. In all cases, the Co sites have finite magnetic moments suggesting that the complexes may provide ways of making cluster-based magnetic materials.

Journal Article↗

PubMed2003

The trans influence of the pyridine ligand on ruthenium(II)-porphyrin-carbene complexes.

In the two ruthenium(II)-porphyrin-carbene complexes (dibenzoylcarbenyl-kappaC)(pyridine-kappaN)(5,10,15,20-tetra-p-tolylporphyrinato-kappa(4)N)ruthenium(II), [Ru(C(15)H(10)O(2))(C(5)H(5)N)(C(48)H(36)N(4))], (I), and (pyridine-kappaN)(5,10,15,20-tetra-p-tolylporphyrinato-kappa(4)N)[bis(3-trifluoromethylphenyl)carbenyl-kappaC]ruthenium(II), [Ru(C(15)H(8)F(6))(C(5)H(5)N)(C(48)H(36)N(4))], (II), the pyridine ligand coordinates to the octahedral Ru atom trans with respect to the carbene ligand. The C(carbene)-Ru-N(pyridine) bonds in (I) coincide with a crystallographic twofold axis. The Ru-C bond lengths of 1.877 (8) and 1.868 (3) A in (I) and (II), respectively, are slightly longer than those of other ruthenium(II)-porphyrin-carbene complexes, owing to the trans influence of the pyridine ligands.

Journal Article↗

PubMed2000

Cofactor regeneration by a soluble pyridine nucleotide transhydrogenase for biological production of hydromorphone.

We have applied the soluble pyridine nucleotide transhydrogenase of Pseudomonas fluorescens to a cell-free system for the regeneration of the nicotinamide cofactors NAD and NADP in the biological production of the important semisynthetic opiate drug hydromorphone. The original recombinant whole-cell system suffered from cofactor depletion resulting from the action of an NADP(+)-dependent morphine dehydrogenase and an NADH-dependent morphinone reductase. By applying a soluble pyridine nucleotide transhydrogenase, which can transfer reducing equivalents between NAD and NADP, we demonstrate with a cell-free system that efficient cofactor cycling in the presence of catalytic amounts of cofactors occurs, resulting in high yields of hydromorphone. The ratio of morphine dehydrogenase, morphinone reductase, and soluble pyridine nucleotide transhydrogenase is critical for diminishing the production of the unwanted by-product dihydromorphine and for optimum hydromorphone yields. Application of the soluble pyridine nucleotide transhydrogenase to the whole-cell system resulted in an improved biocatalyst with an extended lifetime. These results demonstrate the usefulness of the soluble pyridine nucleotide transhydrogenase and its wider application as a tool in metabolic engineering and biocatalysis.

Alcohol Oxidoreductases↗

PubMed1966

Generation of reducing power in chemosynthesis. 3. Energy-linked reduction of pyridine nucleotides in Thiobacillus novellus.

Aleem, M. I. H. (Research Institute for Advanced Studies, Baltimore, Md.). Generation of reducing power in chemosynthesis. III. Energy-linked reduction of pyridine nucleotides in Thiobacillus novellus. J. Bacteriol. 91:729-736. 1966.-Cell-free extracts from Thiobacillus novellus. catalyzed an adenosine triphosphate (ATP)-dependent reduction of pyridine nucleotides anaerobically, or aerobically when the respiratory chain was inhibited by azide. The exogenous electron donor employed for the reduction of nicotinamide adenine dinucleotide or nicotinamide adenine dinucleotide phosphate (NADP) was thiosulfate, formate, or mammalian ferrocytochrome c. In the latter case, the oxidation of ferrocytochrome c was observed with the concomitant reduction of the pyridine nucleotide. Values calculated for the molar ratios of ATP utilized-NADP reduced and of cytochrome c oxidized-NADP reduced were 1:1 and 2:1, respectively. The energy-dependent reduction of the pyridine nucleotides was inhibited by Atabrine or amytal and by low concentrations of the uncouplers of oxidative phosphorylation such as 2,4-dinitrophenol and carbonyl cyanide m-chlorophenyl hydrazone. Evidence is presented showing that the reduced pyridine nucleotides are essential for providing the reducing power for the energy-dependent reduction of carbon dioxide in T. novellus.

Adenosine Triphosphate↗

PubMed1986

Pyridine nucleotide metabolism by extracts derived from Haemophilus parasuis and H. pleuropneumoniae.

A variety of biologically important pyridine nucleotides and precursors were examined for their capacities to serve as substrates for the synthesis of NAD by cell fractions derived from Haemophilus parasuis and H. pleuropneumoniae. Of the compounds tested, only NMN and nicotinamide riboside were converted to NAD. These reactions required ATP as co-substrate, and fractions from both organisms could also catalyze the ATP-dependent synthesis of NADP from NAD. In the absence of ATP, and depending on the pyridine compound under study, NAD, NMN, nicotinamide riboside, and also nicotinamide, were detected as products of catabolism. It is concluded that these haemophili possess either three-membered pyridine nucleotide cycles or two-membered cycles with synthetic branches originating with nicotinamide riboside. It is also possible that the pyridine nucleotide cycles of both organisms have nonrecycling branches resulting in the "waste" of usable pyridine compound in the form of nicotinamide.

Adenosine Triphosphate↗

PubMed1991

Inhibition of Ca2+ efflux by pyridine nucleotides.

The effects of pyridine nucleotides on the Mg-dependent ATP-stimulated Ca2+ pump and on the ATP-independent Na(+)-Ca2+ exchanger were investigated in rat brain synaptic plasma membranes. Both Ca2+ efflux mechanisms are inhibited by pyridine nucleotides, in the order NADPH greater than NADP greater than NADH greater than NAD with IC50 = ca. 3-4 mM for NADP or NADPH and ca. 5 mM for the other pyridine nucleotides in the case of the ATP-driven Ca(2+)-pump, and with IC50 = 8 to 10 mM for the Na(+)-Ca2+ exchanger. Oxidizing agents such as DCIP or FeCN also affect the Ca(2+)-efflux mechanisms. DCIP and FeCN inhibit the ATP-driven Ca2+ pump but not the Na(+)-Ca2+ exchanger. Inhibition of the ATP-dependent Ca2+ pump is optimal when both a reduced pyridine nucleotide and an oxidizing agent (e.g. DCIP or FeCN) were added together. Under similar experimental conditions the pyridine nucleotide-mediated inhibition of the Na(+)-Ca2+ exchanger is partially removed. Therefore Ca(2+)-efflux mechanisms appear to be controlled in part through the redox environment, probably by means of transplasma membrane dehydrogenases.

Animals↗

PubMed2002

Substrate specificity of mammalian pyridine nucleotide transglycosidases.

Spectrophotometrical analysis of pyridine nucleotide transglycosidase in mammalian tissues indicated that the enzyme activity was observed to be distributed ubiquitously among the mammalian tissues analyzed, although the velocity ratio of transglycosidation/hydrolysis (vT/vH) and the partitioning of nicotinic acid against water differed with the pyridine nucleotide substrate and the mammalian species, and also with the organ from which the enzyme was extracted. A clarification of their enzymatic properties reveals that pyridine nucleotide transglycosidases were purified from rabbit spleen and guinea pig spleen, after which a kinetic analysis of the transglycosidases was performed. The resulting values, including Km, maximal transglycosidation velocity, and vT/vH, indicated that the enzymes differ in their substrate specificities toward pyridine nucleotide and pyridine base structures.

Animals↗

PubMed1992

N-acetyl-p-benzoquinone imine induces Ca2+ release from mitochondria by stimulating pyridine nucleotide hydrolysis.

The mechanism of N-acetyl-p-benzoquinone imine (NAPQI)-induced release of Ca2+ from rat liver mitochondria was investigated. The addition of NAPQI or 3,5-Me2-NAPQI (a dimethylated analogue of NAPQI with only oxidizing properties) to mitochondria resulted in the rapid and extensive oxidation of NADH and NADPH. High-performance liquid chromatographic analysis of mitochondrial pyridine nucleotides revealed that the formation of NAD+ and NADP+ was followed by a time-dependent net loss of total pyridine nucleotides as a result of their hydrolysis, with the formation of nicotinamide. Preincubation of the mitochondria with cyclosporin A completely prevented the quinone imine-stimulated release of sequestered Ca2+ from mitochondria. Cyclosporin A did not affect the ability of NAPQI or 3,5-Me2-NAPQI to oxidize NAD(P)H but prevented the quinone imine-induced hydrolysis of the pyridine nucleotides. Although there was no detectable change in total protein-bound ADP-ribose content during quinone imine-induced Ca2+ release from mitochondria, meta-iodobenzylguanidine, a competitive inhibitor of protein mono(ADP-ribosylation), prevented Ca2+ release by NAPQI and 3,5-Me2-NAPQI; meta-iodobenzylguanidine did not inhibit the quinone imine-induced NAD(P)H oxidation and only partially blocked hydrolysis of the oxidized pyridine nucleotides. It is concluded that NAPQI causes the oxidation of mitochondrial NADH and NADPH, and stimulates Ca2+ release as a result of the further hydrolysis of the oxidized pyridine nucleotides and protein mono(ADP-ribosylation).

3-Iodobenzylguanidine↗

PubMed1989

Imidazopyridines: roles of pyridine nitrogen position and methylsulfinyl oxygen for in vitro positive inotropic mechanism and chronotropic activity.

The role of structural features of sulmazole, an imidazo(4,5-b)pyridine, in its inotropic action was examined by comparison with its reduced (4-methylthiophenyl) analog EMD 46512 and the corresponding imidazo(4,5-c)pyridine isomers isomazole and EMD 41000 on isolated guinea-pig papillary muscles and right atria and on Na,K-ATPase and phosphodiesterase III isolated from guinea-pig hearts. The pyridine nitrogen position in sulmazole was crucial for affinity to Na,K-ATPase (IC50 = 350 microM) because the imidazo(4,5-c)pyridines had little effect. Participation of Na,K-ATPase inhibition in sulmazole's inotropic effect (EC50 = 180 microM) was suggested by synergism with the Na channel activator germitrine. The methylsulfinyl oxygen at the phenyl ring decreased the affinity to Na,K-ATPase of sulmazole 40-fold: The reduced analog EMD 46512 was a potent inhibitor of Na,K-ATPase (IC50 = 8.5 microM) and a more potent inotropic agent (EC50 = 8.2 microM) that appeared to act predominantly through Na,K-ATPase inhibition. Micromolar through Na,K-ATPase inhibition. Micromolar IC50s for inhibition of phosphodiesterase III were 49 (sulmazole), 34 (EMD 46512), 18 (isomazole), and 13 (EMD 41000). Participation of this mechanism in the inotropic effect of sulmazole, isomazole, and EMD 41000, but not EMD 46512, was indicated by augmentation of slow action potentials, synergism with histamine, inhibition by carbachol, and (with the exception of EMD 41000) a positive chronotropic effect on the right atrium. Sulmazole appeared to combine the actions of its 4-methylthiophenyl analog EMD 46512 (an inhibitor of Na,K-ATPase) and of its imidazo(4,5-c)pyridine isomer isomazole (an inhibitor of phosphodiesterase III).

Action Potentials↗

PubMed1993

Detrimental effects of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, a mutagenic agent, on mitochondrial respiration among various rat tissues.

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine is a potent mutagenic agent produced during thermal processing of meats. Since 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine has a similar structure to tetrahydroisoquinoline, a mitochondria toxic compound, we determined whether or not this compound shows detrimental effects on mitochondrial electron transport activities in various rat tissues. Administration of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, 100 mg/kg twice a week for 4 weeks, decreased significantly the activity of complex I in mitochondrial electron transport chain of heart, diaphragm, and psoas major, while it did not affect the activities of complex I in the liver mitochondria. Concerning the activities of complexes II, III, and IV, no significant effects were observed irrespective of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine administration. Age-related deterioration of mitochondrial function seems to be a major contributor to age-related decline in cellular function. From our results, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine might act as an accelerator of age-related decline in mitochondrial function.

Aging↗

PubMed1997

Olfactory dysfunction for pyridine and dementia progression in Alzheimer disease.

OBJECTIVE: To investigate whether odor detection sensitivity for pyridine, suggested by previous research not to be affected, is impaired in Alzheimer disease (AD) and whether an association exists between odor threshold and both degree of dementia and rate of dementia progression in AD. METHOD: The method of constant stimuli was used to determine odor thresholds for pyridine in 18 patients with AD (Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised and National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders Association criteria) and 16 healthy elderly control subjects. All participants were carefully examined with medical and neuropsychological tests. RESULTS: Six patients with AD but none of the controls were anosmic (total olfactory loss) to pyridine, and the 12 nonanosmic patients had significantly higher detection thresholds (50% probability for detection, 323 parts per billion [ppb]) than did the controls (50% probability for detection, 105 ppb). In addition, an association was found between odor threshold and both degree of dementia and rate of dementia progression in AD. CONCLUSIONS: In contrast to previous findings, our results provide evidence that odor sensitivity in AD is impaired for pyridine. Odor sensitivity, in addition to other suggested predictors of progression rate, may be of interest for defining subgroups of AD or for clinical prognostic judgments of single patients.

Aged↗

PubMed1994

Effect of pyridine and its methylated derivatives on storage by rat pineal nerves of monoaminergic neurotransmitter.

In previous work of our laboratory, it was demonstrated that collidine (2-4-6-trimethylpyridine) applied briefly to fresh tissues extracted noradrenaline or closely related compound/s of neuronal origin. This effect gave rise to the abolition of osmiophilia and chromaffin reaction of electron-dense cores of monoaminergic synaptic vesicles and to the extraction of radioactive compounds in tissues that had previously taken up tritiated noradrenaline. In this work, the role of the pyridine ring and its progressive methylation on the monoamine releasing effect was investigated. For this purpose, the effect of pyridine, two picolines (2 and 4 monomethylpyridines) and a lutidine (2-6-dimethylpyridine) was compared to the effect of collidine. It was found that pyridine has a much smaller effect than collidine on the histochemical reactivity of monoaminergic synaptic vesicles and on the extraction of tritiated compounds and that its extent was dependent upon the number of methyl groups incorporated in the pyridine ring.

Animals↗