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PubMed2006

Synthetic and structural comparisons of bismuth(III) carboxylates synthesised under solvent-free and reflux conditions.

Two synthetic approaches to the formation of bismuth(III) carboxylates have been explored and compared. Ph(3)Bi was reacted with a series of carboxylic acids (RCO(2)H) of varying pK(a) and functionality (R = PhCH[double bond, length as m-dash]CH, o-MeOC(6)H(4), m-MeOC(6)H(4), o-H(2)NC(6)H, o-O(2)NC(6)H(4), p-O(2)NC(6)H(4), 2-(C(5)H(4)N)) under reflux conditions in toluene and solvent-free. The thermochemical profiles of the solvent-free reactions were also studied by DSC-TGA. All reactions produced the tri-substituted bismuth carboxylates in comparable yields and purity with the exceptions of picolinic acid and p-nitrobenzoic acid. 2-Picolinic acid exclusively formed the di-substituted complex, [PhBi(2-(C(5)H(4)N)CO(2))(2)](4), by both methods, while p-nitrobenzoic acid gave the tri-substituted complex through reflux and the di-substituted complex under solvent-free conditions. Two of the complexes were structurally authenticated by single crystal X-ray diffraction: [PhBi(2-(C(5)H(4)N)CO(2))(2)](4) is tetrameric formed through five membered chelate rings involving the pyridyl N and O(-C) rather than the less stable carboxylate (-CO(2)) chelates, while [Bi(o-MeOC(6)H(4)CO(2))(3)](infinity), is a polymer in which dimeric units, constructed around two chelating and one unsymmetrical bridging carboxylate on each Bi centre, are then joined together through longer intermolecular Bi-O bridging bonds.

Journal Article↗
PubMed2003

Synthesis of alpha-amino acids via asymmetric phase transfer-catalyzed alkylation of achiral nickel(II) complexes of glycine-derived Schiff bases.

Achiral, diamagnetic Ni(II) complexes 1 and 3 have been synthesized from Ni(II) salts and the Schiff bases, generated from glycine and PBP (7) and PBA (11), respectively, in MeONa/MeOH solutions. The requisite carbonyl-derivatizing agents pyridine-2-carboxylic acid(2-benzoyl-phenyl)-amide 7 (PBP) and pyridine-2-carboxylic acid(2-formyl-phenyl)-amide 11 (PBA) were readily prepared from picolinic acid and o-aminobenzophenone or picolinic acid and methyl o-anthranilate, respectively. The structure of 1 was established by X-ray crystallography. Complexes 1 and 3 were found to undergo C-alkylation with alkyl halides under PTC conditions in the presence of beta-naphthol or benzyltriethylammonium bromide as catalysts to give mono- and bis-alkylated products, respectively. Decomposition of the complexes with aqueous HCl under mild conditions gave the required amino acids, and PBP and PBA were recovered. Alkylation of 1 with highly reactive alkyl halides, carried out under the PTC conditions in the presence of 10% mol of (S)- or (R)-2-hydroxy-2'-amino-1,1'-binaphthyl 31a (NOBIN) and/or its N-acyl derivatives and by (S)- or (R)-2-hydroxy-8'-amino-1,1'-binaphthyl 32a (iso-NOBIN) and its N-acyl derivatives, respectively, gave rise to alpha-amino acids with high enantioselectivities (90-98.5% ee) in good-to-excellent chemical yields at room temperature within several minutes. An unusually large positive nonlinear effect was observed in these reactions. The Michael addition of acrylic derivatives 37 to 1 was conducted under similar conditions with up to 96% ee. The (1)H NMR and IR spectra of a mixture of the sodium salt of NOBIN and 1 indicated formation of a complex between the two components. Implications of the association and self-association of NOBIN for the observed sense of asymmetric induction and nonlinear effects are discussed.

Alkylation↗
PubMed1982

Effect of pyridines on phenotypic properties of Bordetella pertussis.

Several conditions of growth of Bordetella pertussis cause a reversible phenotypic alteration in properties termed modulation. Growth in medium containing nicotinic acid induces normal (X-mode) cells to change to modulated (C-mode) cells. We examined several pyridines and compounds resembling pyridines for their ability to affect modulation, using envelope protein patterns and serological reactivity as indicators of modulation. We found that 6-chloronicotinic acid and quinaldic acid were more effective modulating stimuli than was nicotinic acid on a molar basis. Both 2-chloronicotinamide and isoniazid interfered with nicotinic acid-induced modulation, and can be called antimodulators. Picolinic acid inhibited growth.

Agglutination Tests↗
PubMed1977

The anticonvulsant action of methazolamide in mice: antagonism by various inhibitors of dopamine beta-hydroxylase.

The dopamine beta-hydroxylase inhibitors, FLA-63 and picolinic acid, antagonized the anticonvulsant action of methazolamine in mice; disulfiram and pyrimidinethiol were inactive. FLA-63 and picolinic acid, but not disulfiram or pyrimidinethiol prevented pheniprazine restoration of the anticonvulsant action of methazolamide in reserpinized mice. The present findings clearly demonstrate that differences exist among inhibitors of dopamine beta-hydroxylase regarding their ability to antagonize the anticonvulsant action of methazolamide under various test conditions.

Animals↗
PubMed1984

[Antilipolytic activity in vitro of various analogs of nicotinic acid. Structure-activity relationship].

The antilipolytic activity of a series of N aryl-nicotinamides and of alpha picolinic acid, has been tested in vitro. Lipolysis was stimulated by epinephrine (20 micrograms/ml of incubation medium) using rat's epididymal adipose tissue slices. Only N(2-carboxy methyl phenyl) nicotinamide showed antilipolytic effect comparable to that of nicotinic acid at similar concentrations (2 X 10(-5) M). Picolinic acid (10(-4) M) showed no antilipolytic effect. These results, together with those of the literature, are discussed in regard to the relations between structure and antilipolytic activity.

Adipose Tissue↗
PubMed2002

Cytotoxicity and oxidative mechanisms of different forms of chromium.

Chromium exists mostly in two valence states in nature: hexavalent chromium [chromium(VI)] and trivalent chromium [chromium(III)]. Chromium(VI) is commonly used in industrial chrome plating, welding, painting, metal finishes, steel manufacturing, alloy, cast iron and wood treatment, and is a proven toxin, mutagen and carcinogen. The mechanistic cytotoxicity of chromium(VI) is not completely understood, however, a large number of studies demonstrated that chromium(VI) induces oxidative stress, DNA damage, apoptotic cell death and altered gene expression. Conversely, chromium(III) is essential for proper insulin function and is required for normal protein, fat and carbohydrate metabolism, and is acknowledged as a dietary supplement. In this paper, comparative concentration- and time-dependent effects of chromium(VI) and chromium(III) were demonstrated on increased production of reactive oxygen species (ROS) and lipid peroxidation, enhanced excretion of urinary lipid metabolites, DNA fragmentation and apoptotic cell death in both in vitro and in vivo models. Chromium(VI) demonstrated significantly higher toxicity as compared with chromium(III). To evaluate the role of p53 gene, the dose-dependent effects of chromium(VI) were assessed in female C57BL/6Ntac and p53-deficient C57BL/6TSG p53 mice on enhanced production of ROS, lipid peroxidation and DNA fragmentation in hepatic and brain tissues. Chromium(VI) induced more pronounced oxidative damage in multiple target organs in p53 deficient mice. Comparative studies of chromium(III) picolinate and niacin-bound chromium(III), two popular dietary supplements, reveal that chromium(III) picolinate produces significantly more oxidative stress and DNA damage. Studies have implicated the toxicity of chromium picolinate in renal impairment, skin blisters and pustules, anemia, hemolysis, tissue edema, liver dysfunction; neuronal cell injury, impaired cognitive, perceptual and motor activity; enhanced production of hydroxyl radicals, chromosomal aberration, depletion of antioxidant enzymes, and DNA damage. Recently, chromium picolinate has been shown to be mutagenic and picolinic acid moiety appears to be responsible as studies show that picolinic acid alone is clastogenic. Niacin-bound chromium(III) has been demonstrated to be more bioavailable and efficacious and no toxicity has been reported. In summary, these studies demonstrate that a cascade of cellular events including oxidative stress, genomic DNA damage and modulation of apoptotic regulatory gene p53 are involved in chromium(VI)-induced toxicity and carcinogenesis. The safety of chromium(III) is largely dependent on the ligand, and adequate clinical studies are warranted to demonstrate the safety and efficacy of chromium(III) for human consumption.

Animals↗
PubMed1983

Synthesis and antihypertensive activity of 5-O-substituted derivatives of 5-hydroxypicolinic acid.

5-O-Substituted derivatives of 5-hydroxypicolinic acids were synthesized from nojirimycin and studied for their antihypertensive activity in unanesthetized spontaneously hypertensive rats (SHRs) restrained in wire mesh cage and acute toxicity in mice. 5-n-Butoxy-picolinic acid (ND-186) was found to have antihypertensive activity comparable to fusaric acid and lesser acute toxicity. Introduction of halogeno group, in particular trifluoromethyl group to the omega-position of 5-n-butoxy group resulted in the enhancement of antihypertensive activity. The acute toxicity was also lowered 3-5 times compared to that of fusaric acid. Replacement of alkyl group with phenyl group resulted in a slight increment of activity. Some of ester derivatives of ND-186 potentiated the antihypertensive activity and reduced the acute toxicity. There was good correlation between partition coefficient (log P) of ester groups and their antihypertensive activities; compound with higher lipophilicity showed higher antihypertensive activity under the condition of oral administration. However, esterification of other compounds such as 5-halogenoalkoxy- and 5-(substituted) phenoxypicolinic acid was not accompanied with activity increment. Considering from the balance of the antihypertensive activity in SHRs and the acute toxicity in mice, 5-(5',5',5'-trifluoropentoxy)-picolinic acid was selected as a candidate for further evaluation.

Animals↗
PubMed1993

Ligands influence Zn transport into cultured endothelial cells.

Experimental results were obtained that demonstrate the importance of the relative concentrations of Zn ligands and their affinities for Zn to the rate of Zn transport across a biological membrane. The transport rate into cultured endothelial cells became saturated near a Zn concentration of 30 microM in the presence or absence of 14% serum. However, the maximum transport rate identified by the saturation plateau was nearly twice as fast from serum-free medium. The addition of histidine or picolinic acid to the medium with serum resulted in the coincidental shift of Zn from high molecular weight ligands to low molecular weight ligands and increased the overall transport rate. In serum-free medium, adding histidine or picolinic acid slowed the transport rate. This indicates that the rate of Zn transport is influenced by the ligand to which it is associated and that altering the relative proportions of specific ligands influences the Zn transport rate. The rate of Zn transport decreased in a stepwise fashion as the albumin to Zn ratio increased from 0 to 4:1, with further increases having little effect. This suggests that albumin has a special role as modulator of Zn transport into endothelial cells. These studies underscore the importance of controlling the relative concentrations of Zn and its ligands in Zn transport kinetic research and suggest that varying their concentrations in a physiological range may be a method of regulating the distribution of Zn into specific cells and tissues.

Analysis of Variance↗
PubMed2003

Dipicolinic acid prevents the copper-dependent oxidation of low density lipoprotein.

Effect of dipicolinic acid (pyridine 2,6-dicarboxylic acid) and pyridine compounds on the copper-dependent oxidation of human low density lipoprotein was analyzed in relation to the inhibition of copper reduction. Dipicolinic acid inhibited copper-dependent LDL oxidation completely, but the LDL oxidation was slightly inhibited by pyridine compounds with one carboxyl group at 2 or 6-position. Reduction of copper by LDL itself and ascorbate was inhibited completely by dipicolinic acid, but only partially by picolinic acid, quinolinic acid and isocinchomeronic acid with 2- or 6-carboxylic group. Pyridine compounds without 2- or 6-carboxyl group did not show any inhibitory effect on the LDL oxidation and the copper reduction. Protective effect of dipicolinic acid on the LDL oxidation was closely correlated with the copper-reducing activity. Dipicolinic acid shows an antioxidant action by the formation of a chelation complex with copper. This may have implications in understanding mechanisms of preventing LDL oxidation during the early phase of atherosclerosis.

Antioxidants↗
PubMed1982

Zinc dependency as a cause of chronic diarrhea in variant acrodermatitis enteropathica.

Two siblings with chronic diarrhea, growth failure, mood changes, and occasional cheilosis responded repeatedly to treatment with either pharmacologic doses of zinc or pancreatin (Viokase), and their symptoms were exacerbated after withdrawal of therapy. Pancreatic exocrine deficiency was ruled out in both cases. Proteolytic activity was 20% of normal in one infant tested. Plasma zinc concentration was normal. Plasma picolinic acid concentration was low in these two patients and in one previously reported patient (mean 3.6, normal 12.4 +/- 3.3 mumoles/liter). This is a characteristic shared with acrodermatitis enteropathica. The response to Viokase may be due to its content of picolinic acid and/or zinc or the correction of a deficiency of carboxypeptidase, a zinc-requiring enzyme.

Child, Preschool↗
PubMed2000

Apoptosis induced by nicotinamide-related compounds and quinolinic acid in HL-60 cells.

In our previous paper, we have reported that niacin-related compounds, particularly picolinic acid, dipicolinic acid, and isonicotinamide, induced apoptosis in HL-60 cells but that niacin did not. Moreover, picolinamide, N1-methylnicotinamide, 6-aminonicotinamide, quinolinic acid, and cinchomeronic acid also had the function of DNA fragmentation in HL-60 cells analyzed by flow cytometry, the ratio of DNA fragmentation finally being about 40% after treatment with these compounds at 10 mM for 24 h. In this study, we found that these compounds also induced apoptosis in HL-60 cells. The wide-spectrum caspase inhibitors prevented DNA fragmentation induced by these compounds. Interestingly, 6-aminonicotinamide induced apoptosis at a comparatively low concentration, while picolinic acid, dipicolinic acid, and isonicotinamide did not at 1 mM. Our results suggest that both NAD metabolism and NAD biosynthesis may be related to the process of apoptosis induced by niacin-related compounds.

Apoptosis↗
PubMed1986

Zinc-amino acid complexes for swine.

Two experiments were conducted to determine the effect of sources of dietary zinc on gain, feed conversion and blood and bone traits of swine. In the first experiment 96 pigs were used in a 28-d study. The pigs were fed diets with no supplemental Zn or with either 9 or 12 ppm supplemental Zn from zinc sulfate (ZnSO4), zinc methionine (ZnMet) or zinc methionine with picolinic acid (ZnMet w/PA), each with or without 5% added corn oil. There were differences (P less than .05) in average daily gain (ADG) and average daily feed intake (ADFI) between the pigs fed the two organic Zn sources, with those fed ZnMet w/PA showing the better gains and feed conversion. However, neither organic Zn source resulted in pig performance that was different from either the diet with no supplemental Zn or the diets supplemented with Zn from ZnSO4. In the second experiment the same dietary Zn sources and treatments were fed as in Exp. 1 except that corn oil was deleted as a variable. No differences in ADG, ADFI, feed/gain (F/G) or in changes in serum Zn or Cu were observed among treatments during either the 21-d nursery or the 56-d growing periods. During the subsequent 56-d finishing period ADG and ADFI were greater (P less than .01) for pigs fed the Zn-supplemented diets than for those fed the diets without supplemental Zn. There were no differences among treatments in F/G during the finishing period. Zn content of bone ash was lower (P less than .01) in the non-Zn-supplemented pigs. These data suggest that the Zn sources used are of similar biological value and do not support the theory that picolinic acid aids Zn absorption.

Amino Acids↗
PubMed1982

Tissue uptake of zinc in rats following the administration of zinc dipicolinate or zinc histidinate.

Tissue uptake of zinc was determined in rats fed a low zinc diet (less than 1 ppm Zn) and an adequate zinc diet (20 ppm Zn) following the intramuscular injection of either zinc dipicolinate (ZnPA2) or zinc histidinate (ZnHis). Significant differences were observed when dietary and treatment effects on zinc uptake were compared in pancreas, duodenum, jejunum, ileum, kidney, and liver. Zinc uptake by the pancreas was higher in rats fed adequate zinc than in rats fed low zinc regardless of which zinc complex was injected, suggesting that the pancreas has a role in zinc excretion. Since ZnHis was more readily taken up than ZnPA2 by the pancreas of rats on the zinc-adequate diet, zinc chelated by histidine may be more readily excreted than zinc chelated by picolinic acid. No differences in zinc uptake were observed in the intestinal segments from rats fed low zinc compared to rats fed adequate zinc. However, in rats fed low zinc, ZnPA2 was more readily taken up than ZnHis by all intestinal segments implying that zinc chelated by picolinic acid may be more available for storage or utilization by the small intestine than zinc chelated by histidine. Also, the ileum had the highest zinc uptake regardless of which zinc complex was injected. Since the ileum has the largest population of Paneth cells, and high zinc uptake observed in this segment of the small intestine suggests a role for Paneth cells in zinc homeostasis.

Animals↗
PubMed1984

Regulation of transferrin receptors in human hematopoietic cell lines.

Cells grown in the presence of ferric ammonium citrate or hemin exhibited a concentration and time-dependent decrease in 125I-transferrin (Trf) binding. In contrast, cells grown in the presence of protoporphyrin IX or picolinic acid (an iron chelator) exhibited a marked increase in Trf binding. The decrease or increase in binding activity observed under these different conditions of culture reflected, respectively, a reduction or increase in receptor number rather than an alteration in ligand receptor affinity. Growth of the cells in the presence of saturating concentrations of apotransferrin only induced a slight reduction in receptor number. Investigation of the Trf receptors' turnover and biosynthesis clearly showed that iron and hemin decreased the synthesis of Trf receptors without any modification of the receptor turnover; in contrast, protoporphyrin IX and picolinic acid markedly increased the synthesis of Trf receptors. Our results suggest that hemin, iron, and protoporphyrin IX may represent the main molecules involved in the regulation of Trf receptors.

Antibodies, Monoclonal↗
PubMed1984

[Antihypertensive effect of trifluoropentoxypicolinic acid: a pharmacokinetic study].

Two drugs, trifluoropentoxypicolinic acid (TFP) and 5-butoxypicolinic acid, which are composed of a picolinic acid skeleton and an alkoxyl group, were studied to determine characteristics of their antihypertensive effect. The study was carried out using normotensive rats and experimental hypertensive rats (DOCA type hypertensive, one-kidney type hypertensive and spontaneous hypertensive), and effects of these drugs were compared with those of fusaric acid (5-butylpicolinic acid), which is known as a hypotensive agent inhibiting dopamine beta-hydroxylase. The hypotensive effect of the drugs (10, 30 and 100 mg/kg, p.o.) on normotensive rats was weaker than on hypertensive rats. TFP showed a dose-dependent hypotensive effect which was not influenced by reserpine pretreatment. Though TFP showed the same inhibitory effect on serum dopamine beta-hydroxylase as fusaric acid, it had only approximately 0.5 times the inhibitory activity. However, TFP had a hypotensive effect which was 1.4 times stronger than that of fusaric acid. According to pharmacokinetic analysis based on the determination of blood drug concentration, the transfer rate of fusaric acid from the digestive tract to the blood was much higher than TFP by 1.6 X 10(4) times. Moreover, fusaric acid had a 4.5 times greater disappearance rate than TFP. From the above results, first of all, it is supposed that the antihypertensive effect of TFP is related to inhibition of dopamine beta-hydroxylase. In addition, it is suggested that prolonged presence of unchanged TFP in the blood increases its immediate depressive effect on the cardiovascular system, thereby causing a strong hypotensive effect.

Animals↗
PubMed2002

The clinical significance of cerebrospinal fluid levels of kynurenine pathway metabolites and lactate in severe malaria.

A retrospective study of 261 Vietnamese adults with severe malaria was conducted to determine the relationship between cerebrospinal fluid (CSF) levels of metabolites of the kynurenine pathway, the incidence of neurologic complications, and the disease outcome. Three metabolites were measured: the excitotoxin quinolinic acid (QA); the protective receptor antagonist kynurenic acid (KA); and the proinflammatory mediator picolinic acid (PA). These measurements were related prospectively to CSF lactate levels. QA and PA levels were elevated, compared with those of controls. There was no difference in the levels of KA between these groups. Although >40% of malaria patients had QA CSF concentrations in the micromolar range, there was no association with convulsions or depth of coma. Levels of QA and PA were associated significantly with death, but a multivariate analysis suggested that these elevations were a consequence of impaired renal function. CSF lactate remained an independent and significant predictor of poor outcome.

Adolescent↗
PubMed2002

Tryptophan-derived catabolites are responsible for inhibition of T and natural killer cell proliferation induced by indoleamine 2,3-dioxygenase.

Macrophages exposed to macrophage colony-stimulating factor acquire the capacity to suppress T cell proliferation; this effect is associated with de novo expression of the tryptophan-catabolizing enzyme indoleamine 2,3-dioxygenase (IDO). We have purified IDO and tested its activity in in vitro models of T cell activation. IDO was able to inhibit proliferation of CD4(+) T lymphocytes, CD8(+) T lymphocytes, and natural killer (NK) cells; proliferation of B lymphocytes was not affected. The inhibitory role of tryptophan and of its catabolites was then tested. In the presence of tryptophan, only L-kynurenine and picolinic acid inhibit cell proliferation. In a tryptophan-free medium cell proliferation was not affected. In the absence of tryptophan inhibition induced by L-kynurenine and picolinic acid was observed at concentrations below the lowest concentration that was effective in the presence of tryptophan, and quinolinic acid acquired some inhibitory capacity. Inhibition of cell proliferation induced by the tryptophan catabolites resulting from IDO activity was selective, applying only to cells undergoing activation. Resting cells were not affected and could subsequently activate normally. We suggest that IDO exerts its effect on cell proliferation by (i) starting the cascade of biochemical reactions that produce the three catabolites and by (ii) enhancing their inhibitory potential by depriving the extracellular microenvironment of tryptophan.

Animals↗
PubMed1980

[Effect of kynurenine and its metabolites on the vascular effects of serotonin, noradrenaline, and acetylcholine].

In female albino rats anesthetized with urethane, the depressor effect of serotonin was basically diminished by kynurenine, 3-hydroxyanthranilic acid (3-HAA), and anthranilic acid and was potentiated by quinolinic and picolinic acids (PA). All kynurenines were injected in a dose of 200 micrograms. 3-Hydroxykynurenine and nicotinic acid (NA) had a dual action. The pressor effect of noradrenaline was largely diminished by 3-HAA, PA and NA. Each of the rest kynurenines exerted an opposite action in different experiments. The pressor effect of acetylcholine was not affected by kynurenines.

3-Hydroxyanthranilic Acid↗