Picolinic acid hydroxylase of Arthrobacter picolinophilus.
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Arthrobacter↗
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The effects of some alpha picolinic acid derivatives on growth and sporulation of bacilli.
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Amides↗
In vivo activation of macrophages but not natural killer cells by picolinic acid (PLA).
Intraperitoneal injection of PLA into C57BL/6 mice induced high levels of macrophage-mediated cytostatic activity. Maximal cytostatic activity was found 3 days after injection of 100 mg/kg of PLA. In contrast, natural killer cell activity was not affected by PLA. Thus, PLA selectively modulates macrophage activity without influencing NK activity.
Animals↗
The reaction of [Fe(pic)3] with hydrogen peroxide: a UV-visible and EPR spectroscopic study (Hpic = picolinic acid).
The Gif family of catalysts, based on an iron salt and O2 or H2O2 in pyridine, allows the oxygenation of cyclic saturated hydrocarbons to ketones and alcohols under mild conditions. The reaction between [Fe(pic)3] and hydrogen peroxide in pyridine under GoAgg(III)(Fe(III)/Hpic catalyst) conditions was investigated by UV-visible spectrophotometry. Reactions were monitored at 430 and 520 nm over periods ranging from a few minutes to several hours at 20 degrees C. A number of kinetically stable intermediates were detected, and their relevance to the processes involved in the assembly of the active GoAgg(III) catalyst was determined by measuring the kinetics in the presence and absence of cyclohexane. EPR measurements at 110 K using hydrogen peroxide and t-BuOOH as oxidants were used to further probe these intermediates. Our results indicate that in wet pyridine [Fe(pic)3] undergoes reversible dissociation of one picolinate ligand, establishing an equilibrium with [Fe(pic)2(py)(OH)]. Addition of aqueous hydrogen peroxide rapidly generates the high-spin complex [Fe(pic)2(py)(eta1-OOH)] from the labilised hydroxy species. Subsequently the hydroperoxy species undergoes homolysis of the Fe-O bond, generating HOO. and [Fe(pic)2(py)2], the active oxygenation catalyst.
Electron Spin Resonance Spectroscopy↗
Flavopiridol inhibits vascular endothelial growth factor production induced by hypoxia or picolinic acid in human neuroblastoma.
Human neuroblastoma (NB) tumors elaborate angiogenic peptides, and enhanced angiogenesis correlates with their aggressive behavior, metastatic spread and poor clinical outcome. Hence, inhibition of angiogenic factor production may represent a potential therapeutic target for NB treatment. There is currently little information regarding the stimuli that control NB production of angiogenic mediators. In this study, we analyzed the effects of hypoxia, a common feature of solid tumors and a major drive to tumor angiogenesis, and of PA, a tryptophan catabolite produced under inflammatory conditions and endowed with several biologic properties, on the production of the angiogenic activator VEGF by advanced-stage human NB cell lines. We demonstrate that both stimuli are potent inducers of VEGF expression and secretion. VEGF upregulation by PA involved iron chelation because iron sulfate prevented this effect whereas the iron-chelating agent DFX induced VEGF production. Conversely, the CDK inhibitor Flp completely blocked VEGF induction by hypoxia. This effect occurred as early as 3 hr after stimulation and did not require de novo protein synthesis. Moreover, Flp exerted similar inhibitory activity on VEGF induction by PA or DFX, suggesting that this compound targets an essential step in the signaling pathway that leads to VEGF expression. Our findings demonstrate that PA can modulate angiogenic factor production by tumor cells and establish the importance of Flp as an inhibitor of VEGF production by human NB.
Antineoplastic Agents↗
Inhibition of glucose-6-phosphate phosphohydrolase by 3-mercaptopicolinate and two analogs is metabolically directive.
3-Mercaptopicolinae (3-MP) blocks gluconeogenesis from lactate, pyruvate, alanine, and other substrates through its inhibition of phosphoenolpyruvate carboxykinase. Nevertheless, we observed increased glycogenesis, net glucose uptake, and glucose-6-P levels in livers perfused with glucose in the presence of 3-MP. In perfusions with 20 mM dihydroxyacetone, increased glycogenesis and decreased glucose production were observed with 3-MP. These metabolic effects suggested additional site(s) of action of 3-MP. Further studies showed that 3-MP inhibits glucose-6-P phosphohydrolase activity of intact liver microsomes. Several compounds with structural similarities to 3-MP (2-mercaptonicotinic acid, picolinic acid, cysteine, reduced glutathione, nicotinic acid, quinolinic acid, tryptophan, and pyridine) were tested for their effect on glucose-6-P phosphohydrolase activity. Two of these compounds, 2-mercaptonicotinic acid and picolinic acid, were found to inhibit. In perfusions including 7.5 mM fructose, the addition of 3-MP, 2-mercaptonicotinic acid, or picolinic acid increased glycogenesis, decreased glucose production, and increased hepatic glucose-6-P concentrations. These observations indicate that the inhibition of glucose-6-P phosphohydrolase may play a role in enhanced glycogenesis from glucose, dihydroxyacetone, and fructose in isolated livers from 48-h fasted rats perfused with 3-MP or certain sulfhydryl-containing and sulfhydryl-devoid analogs.
Animals↗
Experimental matrix isolation study and quantum-mechanics-based normal-coordinate analysis of the anharmonic infrared spectrum of picolinic acid N-oxide.
This work is, according to our knowledge, the first experimental matrix isolation study of a molecular system with a very short and strong intramolecular OH...O hydrogen bond. It also includes a satisfying interpretation of its entire infrared spectrum. The interpretation relies on the calculation at the DFT/B3LYP/6-31G(d,p) level of the harmonic spectrum and of the anharmonic relaxed potential energy for the stretching motion of the hydrogen-bonded proton, used with our recently modified quantum-mechanics-based normal-coordinate analysis. An important observation about the anharmonic spectrum obtained from this procedure is that the OH stretch coordinate contributes to several normal modes, mixing extensively with other in-plane internal coordinates, in particular OH-bending and C=O-stretching. The two intense normal modes with the largest contributions from the OH-stretching coordinate to the potential energy distribution and to the intensity are located near 1700 and 1500 cm(-1). A calculated anharmonic spectrum obtained from this procedure agrees with the experimental spectrum (frequencies and intensity distribution), within the limits of the estimated uncertainties for the calculation and experiment, allowing the interpretation of the latter. The agreement for the frequencies is about 1-3%. The anharmonic spectrum calculated using the anharmonic keyword in Gaussian 03w is not in satisfactory agreement with experiment insofar as the OH-stretching mode is concerned.
Journal Article↗
Separation and direct UV detection of lanthanides complexed with pyridine-2-carboxylic acid by capillary electrophoresis.
Separation and detection of lanthanides by capillary zone electrophoresis in the presence of pyridine-2-carboxylic acid (picolinic acid) as UV-absorbing complexing agent were investigated. The resolution of partially complexed positively charged complexes is improved by using two buffer ligands competing with picolinic acid for metal ions. When hydroxyisobutyric acid (HIBA) and formic acid are used together as competing ligands, this provides complete separation of all 14 lanthanides with good peak shapes. An on-column separation of 14 lanthanides was achieved in only 9 min using 0.8 mmol/l picolinic acid, 10 mmol/l HIBA and 25 mmol/l formic acid at pH 4.7. Determination of lanthanide complexes was performed by direct detection at 210 nm. Detection limits (signal-to-noise ratio=3) are ca. 0.53-0.96 microg/ml.
Electrophoresis, Capillary↗
Antagonism of kynurenine-induced seizures by picolinic, kynurenic and xanthurenic acids.
Picolinic, kynurenic, xanthurenic and anthranilic acids are metabolites of L-kynurenine which, when administered intraperitoneally (i.p.) antagonized (in descending order of potency) the seizures induced by intracerebroventricular (i.c.v.) injections of l-kynurenine sulfate in SHR and C57BL/6 mice. Picolinic and anthranilic acids were also effective after oral administration. Picolinic acid completely prevented seizures. Kynurenic acid, when injected i.c.v. prior to l-kynurenine sulfate, appeared to be more effective than after i.p. administration while picolinic and anthranilic acids were less effective. This suggest that the antikynurenine effect of metabolites of kynurenine (kynurenines) is related to different brain structures, i.e. kynurenic acid predominantly affects structures adjacent to ventricles (e.g. hippocampus, caudate nucleus) while picolinic and anthranilic acids act on other brain structures or the periphery. Xanthurenic, kynurenic and picolinic acids merely prolonged the latency of seizures induced by i.c.v. quinolinic acid (another metabolite of kynurenine) or by subcutaneous strychnine sulfate and i.p. pentylenetetrazole, and did not modify seizures induced by i.p. caffeine and thiosemicarbazide. This selective antagonism of the tested kynurenines against kynurenine might be an important anticonvulsant factor in kynurenine-dependent seizures. It is suggested that increased excretion of xanthurenic, kynurenic and picolinic acids in patients with convulsive states may be manifestations of compensatory processes.
Animals↗
In vitro competition between calcium phytate and the soluble fraction of rat small intestine contents for cadmium, copper and zinc.
Calcium phytate precipitates were mixed with cadmium (Cd), copper (Cu), or zinc (Zn); in each case most of the trace metal was found to bind to the precipitate. In the presence of some amino acids, picolinic acid or soluble contents of rat intestine, binding was reduced. The solubility effects were low for Cd and Zn, but much higher for Cu. The extent to which Cd was solubilized by intestinal extract was correlated with calcium concentration, but for Cu and Zn it appeared that the concentration of amino groups was the most important factor.
Amino Acids↗
Pentafluorobenzylation method for quantification of acidic tryptophan metabolites using electron capture negative ion mass spectrometry.
An improved pentafluorobenzylation method was developed for derivatization of L-tryptophan and its acidic metabolites (L-kynurenine, kynurenic acid, anthranilic acid, xanthurenic acid, 3-hydroxyanthranilic acid, picolinic acid, quinolinic acid) present at trace levels in aqueous samples. This method employs lyophilization of aqueous samples in the presence of excess tetrabutylammonium hydrogen sulfate, followed by base-catalyzed anhydrous pentafluorobenzylation. A comparison with other published methods shows the advantage of this modification for the derivatization of kynurenine metabolites. The derivatives were analyzed by gas chromatography/electron capture negative ion mass spectrometry (GC/ECNI-MS) or liquid chromatography/particle beam/ECNI-MS (LC/ECNI-MS). The detection limits for injected standards are in the femtogram range by GC/ECNI-MS and in the low picogram range by LC/ECNI-MS. GC/ECNIMS is 3.6 (xanthurenic acid) to 66 (quinolinic acid) times more sensitive than LC/ECNI-MS. The simultaneous determination of two neuroactive metabolites, quinolinic and kynurenic acids, in culture medium is presented. The minimum measurable concentrations of these metabolites in 100 microL of culture medium are 0.11 nM for quinolinic acid and 0.21 nM for kynurenic acid.
Fluorobenzenes↗
Peptide nucleic acid characterization by MALDI-TOF mass spectrometry.
Peptide nucleic acids (PNAs) are a new class of DNA mimics in which the regular nucleobases of adenine, thymine, cytosine, and guanine are connected via a peptide-like backbone. PNA molecules retain the same Watson-Crick base pairing as regular oligonucleotides, with the added benefits of greater specificity and resistance to enzymatic digestion. While the use of PNAs has grown rapidly because of their potential applications in biotechnology, little work has been done on developing analytical procedures for characterizing them. We have found matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry to be an effective tool for PNA analysis. PNA molecules survive the MALDI process intact and are easily ionized with almost no multiply-charged species. These features allow mixtures to be easily characterized. Traditional protein matrices (e.g., sinapinic acid,2,5-dihydroxybenzoic acid, alpha-cyano-4-hydroxycinnamic acid) were found to be superior to DNA matrices (e.g., trihydroxy-acetophenone, 3-hydroxypicolinic acid, picolinic acid). In addition, the new DNA matrix 6-aza-2-thiothymine worked well. The ability of MALDI-TOF-MS to ascertain PNA purity and sequence information at low picomole levels will be important as greater quality control of PNA synthesis is needed (e.g., when PNAs are used as antisense or antigene drugs).
Base Sequence↗
Copper bioavailability and requirements.
Knowledge of factors affecting the bioavailability of dietary copper is limited. Intestinal absorption of copper appears to be facilitated by L-amino acids. Picolinic acid has a favorable binding affinity for copper and may facilitate its absorption. Measurements of the dietary requirements for copper in adult men have shown the requirement to range from about 1.5 to 2.0 mg daily, levels similar to the 2.0 mg estimate suggested in the past. Comparison of the copper requirements with the levels of copper present in some contemporary diets suggests that marginal copper nutriture may not be rare. Persons who consume diets high in zinc and low in protein are at risk of copper deficiency. High intakes of sources of dietary fiber apparently increase the dietary requirement for copper. Studies in one man have shown that signs of mild copper deficiency can be produced experimentally when a conventional diet containing about 0.8 mg of copper is fed. At this time, the 2 to 3 mg daily intake of dietary copper suggested by the National Research Council (63) seems appropriate.
Adult↗
Aquabromo(6-carboxypyridine-2-carboxylato-O,N,O')mercury(II).
The title compound, [HgBr(C7H4NO4)(H2O)], was obtained by the reaction of an aqueous solution of mercury(II) bromide and pyridine-2,6-dicarboxylic acid (picolinic acid, dipicH(2)). The shortest bond distances to Hg are Hg-Br 2.412 (1) A and Hg-N 2.208 (5) A; the corresponding N-Hg-Br angle of 169.6 (1) degrees corresponds to a slightly distorted linear coordination. There are also four longer Hg-O interactions, three from dipicH(-) [2.425 (4) and 2.599 (4) A within the asymmetric unit, and 2.837 (4) A from a symmetry-related molecule] and one from the bonded water molecule [2.634 (4) A]. The effective coordination of Hg can thus be described as 2+4. The molecules are connected to form double-layer chains parallel to the y axis by strong O-H.O hydrogen bonds between carboxylic acid groups of neighbouring molecules, and by weaker hydrogen bonds involving both H atoms of the water molecule and the O atoms of the carboxylic acid groups.
Crystallography, X-Ray↗
EFFECTS OF ANTI-RHEUMATIC COMPOUNDS AND PYRIDINE DERIVATIVES ON THE CUTANEOUS RESPONSE TO THURFYL NICOTINATE IN THE GUINEA-PIG.
The effects of certain anti-rheumatic drugs and compounds related to nicotinic acid on the cutaneous response to locally applied thurfyl nicotinate in guinea-pigs were investigated. Sodium salicylate, aspirin or phenylbutazone administered orally each reduced the response to thurfyl nicotinate at about half the dose needed for equivalent protection against the cutaneous effects of exposure to ultra-violet light. Nicotinic acid or thurfyl nicotinate given orally flushed the skin and reduced the intensity of the local reaction to thurfyl nicotinate without affecting the response to ultra-violet light. Nicotinamide, isonicotinic acid, picolinic acid and quinolinic acid were less effective in producing flushes and in reducing the effect of locally applied thurfyl nicotinate. The flush induced in guinea-pigs by oral nicotinic acid was reduced by the previous administration of phenylbutazone. Possible mechanisms for these effects are discussed.
Animals↗
Aluminium distribution and excretion: a comparative study of a number of chelating agents in rats.
The present study was conducted to assess in rats the comparative effects of a number of chelating agents on the urinary excretion and tissue distribution of A1. Adult male Sprague-Dawley rats received a single intraperitoneal dose of aluminium (A1) nitrate nonahydrate (0.24 mmol/kg). Ten min. after A1 injection 1,2-dimethyl-3-hydroxypyrid-4-one, 2,3-dihydroxybenzoic acid, picolinic acid, methylmalonic acid, ethylenediamine-di(o-hydroxyphenylacetic) acid, 1-benzyl-2-methyl-3-hydroxypyrid-4-one, 1-(p-methylbenzyl)-2-methyl-3-hydroxypyrid-4-one, 1-(p-methoxy-benzyl)-2-methyl-3-hydroxypyrid-4-one, 1-(p-chlorobenzyl)-2-methyl-3-hydroxypyrid-4-one, 1-benzyl-2-ethyl-3-hydroxypyrid-4-one, 1-(p-methyl-benzyl)-2-ethyl-3-hydroxypyrid-4-one, 1-[3-hydroxy-2-methyl-4-oxopyridyl]-2-ethanesulfonic acid and 1-benzyl-(4-carboxylic acid)-3-hydroxy-2-methyl-4-oxopyridine were given by gavage at 1.79 mmol/kg. A control group received similar volumes of distilled water. An additional group of rats received a subcutaneous injection of desferrioxamine at 1.79 mmol/ kg. Urine samples were collected daily for three consecutive days and the animals were killed after this period. Samples of brain, bone, liver, kidney and spleen were collected. Although desferrioxamine, 1,2-dimethyl-3-hydroxypirid-4-one, 1-(p-methylbenzyl)-2-methyl-3-hydroxypyrid-4-one, 1-(p-methoxybenzyl)-2-methyl-3- hydroxypyrid-4-one, 1-(p-methylbenzyl)-2-ethyl-3-hydroxypyrid-4-one, 1-[3-hydroxy-2-methyl-4-oxopyridyl]-2-ethanesulfonic acid and 1-benzyl-(4-carboxylic acid)-3-hydroxy-2-methyl-4-osopyridine significantly enhanced the total excretion of A1 into urine, only treatment with 1-(p-chlorobenzyl)-2-methyl-3-hydroxypyrid-4-one and 1-benzyl-2-ethyl-3-hydroxypyrid-4-one significantly reduced A1 concentrations in all analyzed tissues. No beneficial effects of the remaining chelators on Al mobilization were observed. Further studies on the effects of some 3-hydoxrypyrid-4-ones on A1 removal can be of interest for the treatment of A1 accumulation and toxicity.
Aluminum↗
Metabolic pathways linked to sarcopenia in the Bushehr Elderly Health Program: kynurenine, nicotinamide, B-vitamins, and sulfur amino acids.
BACKGROUND: Sarcopenia, characterized by the loss of muscle mass and function, is a common condition in the elderly, associated with increased morbidity and mortality. Metabolic pathways, including the kynurenine, nicotinamide, B-vitamins, and sulfur amino acid pathways, may play a significant role in the development and progression of sarcopenia. This study investigates the relationship between metabolic pathways and sarcopenia, aiming to identify potential therapeutic targets. METHOD: Four hundred participants over 60 years were randomly selected from the second stage of the Bushehr Elderly Health Program (BEH). Frozen plasma samples were used to measure metabolomics. We used factor analysis and logistic regression analysis to determine the kynurenine-tryptophan metabolites associated with sarcopenia and its components. RESULT: Study participants included 89 sarcopenic subjects aged 72.92 ± 7.32 years and 307 non-sarcopenic subjects aged 68.12 ± 5.56 years. In full model adjustment, factor 3, which included methionine, tryptophan, 3-hydroxyanthranilic acid, picolinic acid, and xanthurenic acid, was associated with 38.3% lower risk of sarcopenia (OR = 0.617 [95%CI = 0.436–0.875]); Factor 6, which included methylmalonic acid and total homocysteine, was associated with a 33.7% increased risk of sarcopenia (OR = 1.337 [95%CI = 1.031–1.735]); and factor 7, consisting of nicotinamide, were related to a 25.2% lower risk of developing sarcopenia (OR = 0.748 [95%CI = 0.571–0.979]). Additionally, factor 1, which included quinolinic acid, kynurenine, 3-hydroxykynurenine, neopterin, kynurenic acid, anthranilic acid, cystathionine, and total cysteine, was linked to a 49.2% higher risk of low muscle strength, while factors 3 and 7 were associated with approximately a 24% decrease in risk of low muscle strength. Factors 5, consisting of serine and glycine, and factor 7 were related to 43% and 27.7% lower risk of low skeletal muscle index, respectively. While factor 6 was related to a 32.8% higher risk of low skeletal muscle index. Factor 1 was also related to a 32.9% higher risk of low walking speed, while factor 3 was related to a 28.5% lower risk of low walking speed. CONCLUSION: Specific metabolites from the kynurenine, nicotinamide, B-vitamin, and sulfur amino acid pathways are significantly associated with sarcopenia and its key parameters, such as muscle strength, skeletal muscle index, and walking speed. These findings suggest that metabolic profiling could offer valuable insights for early detection and targeted interventions for sarcopenia in elderly populations.
Humans↗
Effects of kynurenine metabolites on the electrocorticographic activity in the rat.
We examined the effects of kynurenine metabolites administered into the right cerebroventricle (1 micromol) on the electrocorticogram (ECoG) of rats to establish the role of kynurenines on brain function. Kynurenine, anthranilic acid, quinaldic acid, xanthurenic acid or 8-hydroxyquinaldic acid showed no effect on ECoG throughout the recording period of 4 hours. 3-Hydroxykynurenine had a transient suppressive effect on the ECoG, while kynurenic acid caused a slight suppression of ECoG activity. 3-Hydroxyanthranilic acid (3-OH-An), a metabolite of 3-hydroxykynurenine, induced spike discharges with a long latency (60-230 min). 3-OH-An is thought to be metabolized to o-aminophenol, 3-methoxyanthranilic acid, quinolinic acid, 2-ketoadipic acid and picolinic acid. Among 3-OH-An metabolites, only o-aminophenol induced spike discharges several minutes after administration, lasting for 60 min. On the other hand, quinolinic acid suppressed ECoG, though 3-methoxyanthranilic acid, 2-ketoadipic acid and picolinic acid had no effects on ECoG. These electrocorticographic findings suggest that 3-OH-An may induce spike discharges after it is metabolized in the brain to o-aminophenol.
3-Hydroxyanthranilic Acid↗