Pyridine Monocarboxylic Acids Research Articles

Volume Effects in Interactions between L-Histidine and Pyridine Monocarboxylic Acid Isomers in an Aqueous Buffer Solution

Volume Effects in Interactions between L-Histidine and Pyridine Monocarboxylic Acid Isomers in an Aqueous Buffer Solution

INTERACTION OF L-CARNOSINE WITH NICOTINIC AND ISONICOTINIC ACIDS IN AQUEOUS SOLUTIONS AT 298.15 K

Understanding the mechanism of interaction of drugs with proteins has drawn attention of numerous researchers. The thermodynamic investigations of liquid-phase systems containing peptide and drug make it possible to determine the nature and driving forces of the interaction between them. In this work, we present results of interaction study of peptide L-carnosine (Car), as model of polypeptide chains in protein, with isonicotinic and nicotinic acids, as the drug models, in aqueous solution using calorimetric method. Calorimetric measurements of the enthalpy of L-carnosine dissolution in water and aqueous solutions with two isomers of pyridine carboxylic acid additives were performed on an ampoule-type isoperibolic dissolution calorimeter at 298.15 K. The error of measuring single heat effects was below 0.2%. The relative combined uncertainty in the measurements of the enthalpies of dissolution was not more than 0.7%. Based on the obtained experimental data and the using the HEAT computer program, the thermodynamic parameters (lgKc, ΔcG, ΔcH, ΔcS) of the complex formation between the reagents were calculated. A comparison of the affinity of peptide to interaction with nicotinic acid and isonicotinic acid was carried out. It is shown that the interaction of L-carnosine with isonicotinic acid leads to the formation of a more stable complex than with nicotinic acid. This fact may be mainly explained by the changing of ionic state of the reagents in solution and the predominance of the zwitterionic forms of isonicotinic acid in compared with nicotinic acid. The data obtained reveal the presence of molecular complexes between Car and isomers of pyridine carboxylic acid with 1:2 stoichiometry in aqueous solutions. The complexes of Car with the isonicotinic acid are mainly enthalpically stabilized, while those of Car with nicotinic acid are stabilized by both enthalpic and entropic contributions to the free Gibbs energy. The main interactions in complexes stabilization are believed to be electrostatic forces and hydrogen bonds formation between peptide and pyridine monocarboxylic acids. For citation: Tyunina E.Yu., Mezhevoi I.N., Barannikov V.P. Interaction of L-carnosine with nicotinic and isonicotinic acids in aqueous solutions at 298.15 K. ChemChemTech [Izv. Vyssh. Uchebn. Zaved. Khim. Khim. Tekhnol.]. 2024. V. 67. N 7. P. 48-54. DOI: 10.6060/ivkkt.20246707.7010.

Effects of Structural Isomerism of Pyridine Monocarboxylic Acids on the Volume Properties of Their Buffer Solutions

Effects of Structural Isomerism of Pyridine Monocarboxylic Acids on the Volume Properties of Their Buffer Solutions

Effect of structure isomerism of pyridine monocarboxylic acids on thermodynamic properties of l-lysine complexation in aqueous buffer solution

The thermodynamic characteristics (lgKc, ΔcG, ΔcH, ΔcS) of complexation of l-lysine, a polar basic amino acid, with isomeric pyridine monocarboxylic acids (picolinic acid, nicotinic acid, isonicotinic acid) in buffer solution (pH 7.4) have been obtained at 298.15 K by calorimetry method. The results indicate the formation of molecular complexes between Lys and pyridine carboxylic acids (PyCOOH) with 1:1 stoichiometry in the buffer solution. The complexation of amino acid is influenced by position of –COOH group in the pyridine ring relative to the nitrogen atom. The binding affinity of Lys with PyCOOH isomers follows the order as PA < NA < INA. The measured density values were used to calculate the apparent molar and the partial molar volumes at infinite dilution for PyCOOH isomers in Lys buffer solutions. The results revealed formation of Lys complexes with above pyridine monocarboxylic acids. The positive transfer volumes for the PyCOOH isomers decrease in the series NA ≥ INA > PA. The effects of solute concentration and structure isomerism of PyCOOH on the volume properties were discussed in terms of predominant types of molecular interactions (hydrophilic, hydrophobic, ionic and zwitterionic) on the basis of co-spheres overlap model.

Voltammetric and spectroscopic analysis of interactions of pyridine mono-carboxylic acid isomers with cysteine at physiological pH

The interactions of pyridine mono-carboxylic acid isomers (PCAIs) (nicotinic acid (NA), isonicotinic acid (INA) and picolinic acid (PA)) with cysteine (RSH) at physiological pH (7.40) have been investigated by square-wave and cyclic voltammetry (SWV and CV), and UV-Vis and infrared spectroscopy. By the addition of isomeric pyridine mono-carboxylic acids, the reduction peak current of mercurous cysteine thiolate could be decreased and also its peak potential E p was shifted to more positive values. Also, the significant changes in formal potential E 0′, electron transfer coefficient α and electrode reaction standard rate constant k s of mercurous cysteine thiolate (Hg2(SR)2) in the presence and absence of PCAIs were observed. The results of voltammetric measurements indicated that binding reactions were occurred between PCAIs and RSH and new electroactive molecular complexes were formed, which resulted in the decrease of free cysteine concentration and the decrease of the reduction peak current of mercurous cysteine thiolate. The logarithmic values of binding constants of NA, INA and PA were calculated as 13.4, 17.7 and 18.9, respectively. The binding ratios for NA-RSH, INA-RSH and PA-RSH complexes were determined as 1: 3, 1: 4 and 1: 4, respectively. Both UV-Vis and FTIR studies also confirmed these interaction reactions.

Investigation of pyridine carboxylic acids in CM2 carbonaceous chondrites: Potential precursor molecules for ancient coenzymes

The distribution and abundances of pyridine carboxylic acids (including nicotinic acid) in eight CM2 carbonaceous chondrites (ALH 85013, DOM 03183, DOM 08003, EET 96016, LAP 02333, LAP 02336, LEW 85311, and WIS 91600) were investigated by liquid chromatography coupled to UV detection and high resolution Orbitrap mass spectrometry. We find that pyridine monocarboxylic acids are prevalent in CM2-type chondrites and their abundance negatively correlates with the degree of pre-terrestrial aqueous alteration that the meteorite parent body experienced. We also report the first detection of pyridine dicarboxylic acids in carbonaceous chondrites. Additionally, we carried out laboratory studies of proton-irradiated pyridine in carbon dioxide-rich ices (a 1:1 mixture) to serve as a model of the interstellar ice chemistry that may have led to the synthesis of pyridine carboxylic acids. Analysis of the irradiated ice residue shows that a comparable suite of pyridine mono- and dicarboxylic acids was produced, although aqueous alteration may still play a role in the synthesis (and ultimate yield) of these compounds in carbonaceous meteorites. Nicotinic acid is a precursor to nicotinamide adenine dinucleotide, a likely ancient molecule used in cellular metabolism in all of life, and its common occurrence in CM2 chondrites may indicate that meteorites may have been a source of molecules for the emergence of more complex coenzymes on the early Earth.

Nanostructured TiO2 modified with acetohydrazide zinc porphyrin well-arrays for supramolecular solar cells

In this work, employing the metal-mediated assembling strategy for organizing acetohydrazide zinc porphyrin (ZnP) and different organic acid (Ai) ligands on the nanostructured TiO2 electrode surfaces have been prepared, wherein the ZnP and Ai units are bound by a series of differently bivalent metal ions (M, M=Mn2+, Co2+, Ni2+, Cu2+, Zn2+, Cd2+ and Hg2+), resulting in a ZnP–M–Ai assembled approach. The photovoltaic performances of these assemblies-sensitized solar cells were performed under irradiance of 100mWcm−2 AM 1.5G sunlight. A significantly improved conversion efficiency of ZnP–Mn–A5 and ZnP–Cd–A5 devices occurs, indicating well-ordered arrangements of ZnP molecules on the TiO2 electrode surfaces for ZnP–Mn–A5 and ZnP–Cd–A5, where A5 is a pyridine–monocarboxylic acid ligand bearing longer arm. The results were also verified by the HOMO–LUMO gaps, UV–vis and fluorescence spectra.

Crystal structures of pyridinemonocarboxylic acid peroxosolvates

The crystal structures of new peroxosolvates of the following pyridinemonocarboxylic acids were studied: picolinic 2-C5H4NCOOH·H2O2 (1), nicotinic 3-C5H4NCOOH·H2O2 (2), and isonicotinic 4-C5H4NCOOH·2H2O2 (3). In these compounds, the acids exist exclusively as zwitterions, as opposed to non-solvated crystals. In compounds 1–3, the hydrogen peroxide molecules form two donor hydrogen bonds and, in some cases, one additional acceptor hydrogen bond. Peroxosolvate 2 can be considered as a novel drug formulation of vitamin B3.

Interaction of neptunium(V) with picolinic, nicotinic and isonicotinic acids

SummaryThe interaction of Np(V) with all isomers of pyridinemonocarboxylic acid has been investigated, stability constants have been calculated using NIR spectroscopy. Single crystals of [NpO2(Pic)(H2O)2] (1), Cs[NpO2(Pic)2(HPic)]·3H2O (2), [NpO2(Nic)(H2O)] (3), and [NpO2(iso-Nic)(H2O)] (4) have been synthesized. Compound1contains infinite chains; compound2consists of isolated Cs+, [NpO2(Pic)2(HPic)]-groups and water molecules. In both3and4neptunoyl-ion NpO2acts as monodentate ligand with one of the O atoms of NpO2group entering in coordination polyhedron of the adjacent Np atom. Compounds3and4have layered and three-dimensional topologies, respectively. Crystallographic data: [NpO2(Pic)(H2O)2], space groupP¯1, triclinic,a= 6.380(2),b= 7.733(2),c= 10.700(4) Å, α = 96.49(3), β = 106.78(3), γ = 103.83(3)°, andZ= 2 (1); Cs[NpO2(Pic)2(HPic)]·3H2O, space groupP¯1, triclinic,a= 8.707(2),b= 9.777(2),c= 14.640(3) Å, α = 76.633(15), β = 78.75(2), γ = 86.55(2)°, andZ= 2 (2); [NpO2(Nic)(H2O)], space groupP21/n, monoclinic,a= 11.901(4),b= 5.5628(15),c= 12.124(3) Å, β = 101.05(2)°, andZ= 4 (3); [NpO2(iso-Nic)(H2O)], space groupP212121, orthorhombic,a= 5.742(3),b= 8.550(5),c= 18.512(10) Å, andZ= 4 (4). Electron and IR spectra of solid compounds have been measured.

Investigations of the reactivity of pyridine carboxylic acids with diazodiphenylmethane in protic and aprotic solvents: Part II: Pyridine mono-carboxylic acid N-oxides

The rate constants for the reaction of three isomeric pyridine mono-carbocylic acid N-oxides with diazodiphenylmethane were determined at 30 ?C in thirty two protic and aprotic solvents by the well known UV spectrophotometric method. The rate constants are generally higher than for pyridine mono-carboxylic acids in a similar range of solvents, except for picolinic acid N-oxide, and also higher in protic than in aprotic solvents. The determined rate constants were correlated with solvent parameters using the Kamlet-Taft solvatochromic equation bymeans of multiple regression analysis. The sign of the equation coefficients were in agreement with the postulated reaction mechanism. The mode of the influences of the solvent is discussed on the basis of the correlation coefficients, taking into account the specific structures of the pyridine mono-carboxylic acid N-oxides.

Investigations of the reactivity of pyridine carboxylic acids with diazodiphenylmethane in protic and aprotic solvents. Part I. Pyridine mono-carboxylic acids

The rate constants for the reaction of three isomeric pyridine mono-carbo- cylic acid N-oxides with diazodiphenylmethane were determined at 30 oC in thirty two protic and aprotic solvents by the well known UV spectrophotometric method. The rate constants are generally higher than for pyridine mono-carboxylic acids in a similar range of solvents, except for picolinic acid N-oxide, and also higher in protic than in aprotic solvents. The determined rate constants were correlated with solvent parameters using the Kamlet-Taft solvatochromic equation by means of multiple re- gression analysis. The sign of the equation coefficients were in agreement with the postulated reaction mechanism. The mode of the influences of the solvent is discus- sed on the basis of the correlation coefficients, taking into account the specific struc- tures of the pyridine mono-carboxylic acid N-oxides.

Investigations of the reactivity of pyridine carboxylic acids with diazodiphenylmethane in protic and aprotic solvents, Part I: Pyridine mono-carboxylic acids

Rate constants for the reaction of diazodiphenylmethane with isomeric pyridine carboxylic acids were determined in chosen protic and aprotic solvents at 30 ?C, using the well known UV spectrophotometric method. The values of the rate constants of the investigated acids in protic solvents were higher than those in aprotic solvents. The second order rate constants were correlated with solvent parameters using the Kamlet-Taft solvatochromic equation in the form: logk = logk0 + s?*+ a? + b?. The correlation of the obtained kinetic data were performed by means of multiple linear regression analysis taking appropriate solvent parameters. The signs of the equation coefficients were in agreement with the postulated reaction mechanism. The mode of the influence of the solvent on the reaction rate in all the investigated acids are discussed on the basis of the correlation results.

On the electroreduction of the anions of pyridine monocarboxylic acid N-oxides on mercury electrodes in basic solutions

On the electroreduction of the anions of pyridine monocarboxylic acid N-oxides on mercury electrodes in basic solutions

The 1993 Upjohn Award Lecture. Quinolinic acid induced brain neurotransmitter deficits: modulation by endogenous excitotoxin antagonists

Excitotoxins constitute a group of agents that are capable of activating excitatory amino acid receptors and producing axonsparing neuronal lesions. Focal injections of the exogenous excitotoxins kainic acid and ibotenic acid result in depletion of neurotransmitter markers in neuronal cell bodies located in areas of injection or in terminal zones of their projections. The discovery of endogenous agents that behave as excitotoxins has generated interest in the idea that excitotoxicity may contribute to the neuronal degeneration associated with a number of neurological diseases (Alzheimer's disease, Huntington's disease, Parkinson's disease) which involve selective neurotransmitter deficits. Quinolinic acid (QUIN), a pyridine dicarboxylic acid and metabolite of tryptophan, which has been detected in the central nervous system (CNS), behaves as an excitotoxin. In the mammalian brain QUIN has been localized to glial and immune cells, and its content increases with age. The neuro-excitatory and neurotoxic actions of QUIN are mediated via the Mg(2+)-sensitive N-methyl-D-aspartate (NMDA) receptor. The toxicity of QUIN, like that of kainate, but not ibotenate, is dependent on the presence of an intact glutamate-aspartate afferent input to the target area. Focal injections of QUIN into the nucleus basalis magnocellularis (nbM), a major source of cholinergic innervation to diencephalic areas, produce sustained loss of cholinergic neuron markers in the neocortex and amygdala. The neurotoxic action of QUIN on nbM results in an impairment of performance on memory-related tasks. Cortical and amygdaloid projecting cholinergic neurons show differential sensitivity to QUIN and other excitotoxic agents. This factor may partly explain the reported discrepancy between mnemonic deficits and the loss of cholinergic markers in the cerebral cortex induced by intra-nbM injections of certain excitotoxins. Cortical muscarinic receptor function is not significantly influenced by QUIN injections into the nbM producing loss of cortical cholinergic neurons. In the striatum, focal QUIN injections have been found to largely replicate the neurotransmitter deficits prevailing in Huntington's disease, an inherited movement disorder. Intrastriatal QUIN produces a profound loss of the NADPH diaphorase staining neurons in the area of injection but relatively spares these in the adjacent transition zone. QUIN is also highly damaging to the striatopallidal enkephalinergic neurons. However, at doses that are neurotoxic to striatal neurons, QUIN and several other excitotoxins produce significant elevations in enkephalin levels both in the striatum and globus pallidus. This elevation reflects the presence of a plasticity in the striatal enkephalinergic neuron population. The metabolic pathway yielding QUIN produces a number of intermediates that act as excitotoxin antagonists.(ABSTRACT TRUNCATED AT 400 WORDS)

Comment on “Vibrational spectra of isomeric pyridinic carboxylic acids in solid state and in solution and their SERS studies in silver soil”

A recent claim that the solid pyridine(mono)carboxylic acids are composed of associated centrosymmetric (RCO2H)2 bimolecules is unfounded and incorrect. For solid picolinic acid (a hitherto not wholly solved problem), an ionic structure, NC5H4-2-CO−2.2′-HO2CC5H4N+H, is put forward here.

Study of the reduction mechanism of the N-oxides of pyridine monocarboxylic acids at mercury electrodes

The reduction mechanisms of the N-oxides of picolinic, nicotinic and isonicotinic acids were studied by dc and differential pulse polarography and voltammetry over a wide pH range. Tafel slopes and reaction orders were obtained at potentials corresponding to the foot of the waves. In addition, the UV absorption spectra of these N-oxides in strongly acidic solutions were recorded. From the variations of the absorbances with the pH, the acid dissociation constants of both the N-oxide and the carboxyl groups were obtained. The reduction products of the processes corresponding to the waves appearing at less negative potential were the corresponding carboxylic acids (picolinic, nicotinic and isonicotinic respectively). Polarographic and voltammetric results indicate that adsorption of the N-oxides occurs on the electrode. The results indicate that the protonated form of the N-oxide group is reduced in acidic media, whereas the unprotonated form is reduced at pH &>; 9. In both cases the reduction pathway is similar to that found for nicotinamide N-oxide.

Picolinic acid modulates kainic acid-evoked glutamate release from the striatum in vitro

Since picolinic acid, a tryptophan metabolite yielded by the kynurenine pathway, selectively attenuates quinolinic and kainic acid excitotoxicity that is dependent on the presence of a glutamatergic afferent input, it was hypothesized that this agent may inhibit the presynaptic release of glutamate. Using superfused rat striatal slices, this study examined the potential of picolinic acid, and related pyridine monocarboxylic acids, to modify kainic acid-induced glutamate release. Kainic acid (0.25, 0.5 and 1.0 mM) stimulated the release of glutamate, an effect which was calcium dependent and was attenuated in the presence of the kainate/AMPA receptor antagonist, 6,7-dinitroquinoxalene-2,3-dione (500 μM). Picolinic acid significantly decreased glutamic acid release evoked by exposure of striatal slices to 1 mM kainate in the presence of calcium. The inhibitory action of picolinic acid on kainate-induced release was also shared by nicotinic and isonicotinic acid. In the absence of external calcium, kainic acid-induced glutamate release was significantly reduced by approximately 65%. Under this condition, picolinic acid (100 μM) failed to influence kainic acid-induced release. Picolinic acid (100 μM) itself increased glutamate release by 35% over basal release. While the ability of picolinic acid to inhibit excitotoxin-induced release supports the notion that it may act presynaptically to modify excitotoxicity, lack of structural specificity in its action tends to cast doubt on this mechanism of action.

ChemInform Abstract: Self‐Association of Pyridine Monocarboxylic Acids and Their Esters in Aqueous Solution. A Study by Ultraviolet Spectroscopy.

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Action of picolinic acid and structurally related pyridine carboxylic acids on quinolinic acid-induced cortical cholinergic damage

Picolinic acid, a pyridine monocarboxylic acid derived from tryptophan metabolism by the kynurenine pathway, was shown to block cortical cholinergic neurotoxicity induced by quinolinic acid (QUIN), a pyridine dicarboxylic acid yielded by the same pathway. This study examined the specificity of the anti-toxic effect of picolinic acid by comparing its effect with several structurally related mono- and dicarboxylic acids, and by evaluating its potential to influence cholinergic neurotoxicity produced by kainic, ibotenic and quisqualic acid. Picolinic acid or related agents were injected alone or in combination with a fixed dose of QUIN into the right nucleus basalis magnocellularis (nbM) of rats anesthetized with halothane. Cholinergic neurotoxicity was assessed 7 days post injection by measuring choline acetyltransferase (ChAT) activity in the frontoparietal cortex on the injected and uninjected side. In picolinate experiments, the staining of nbM neurons by acetylcholinesterase (AChE) histochemistry was also examined. Focal injections of QUIN depleted cortical ChAT activity and staining of AChE in the nbM. Co-injection of picolinic acid with QUIN attenuated the decline in these two cholinergic neuron markers. Isonicotinate (4-pyridine monocarboxylate), but not nicotinate (3-pyridine monocarboxylate), significantly attenuated QUIN's effect on cortical ChAT activity. Among several dicarboxylic acids examined, only dipicolinate (2,6-pyridine dicarboxylate) showed activity. It produced a modest QUIN-like effect, but in co-injection experiments it attenuated the QUIN-induced decrease in cortical ChAT. When co-injected into the nbM with a neurotoxic dose of kainic, ibotenic or quisqualic acid which produced a neurotoxic response comparable to that of QUIN, picolinic acid attenuated kainic acid-induced neurotoxicity, but not ibotenate or quisqualate neurotoxicity. In contrast, kynurenic acid, which blocked QUIN's action, blocked the neurotoxicity of both kainate and ibotenate. The results suggest that actions of picolinic acid against QUIN show certain selectivity in regard to the chemical structure of picolinic acid. In addition, picolinic acid has selectivity against excitotoxins acting via different mechanisms. Its ability to influence only those excitotoxins which require an intact glutamatergic afferent input for their neurotoxic effect suggests that the protective effect of picolinic acid may involve an interaction with this input.

Self-association of pyridine monocarboxylic acids and their esters in aqueous solution. A study by ultraviolet spectroscopy

The ultraviolet spectra of pyridine monocarboxylic acids and their methyl or ethyl esters in aqueous solution, at different pH values, show an hypochromic effect over the range 10 −6–10 −1 M, which is interpreted in terms of dimerization and polymerization. In general, the values calculated for the association constants show that the studied interaction is a function of the nature and position of the substituent groups in the pyridine ring, and of the cationic, zwitterionic, anionic or neutral species which predominate at each of the selected pH values.