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At least 19 recordsLinked to original sources
PubMed2005

Removal of alpha-picoline, beta-picoline, and gamma-picoline from synthetic wastewater using low cost activated carbons derived from coconut shell fibers.

In the present study the ability of activated carbons developed from coconut shell fibers to remove alpha-picoline, beta-picoline, and gamma-picoline from aqueous solution in the broad range of concentrations (1-100 mg/L) is investigated. The derived carbons are designated as FAC (activated carbon derived from coconut shell fibers without any treatment) and ATFAC (activated carbon derived from acid treated coconut shell fibers). Systematic equilibrium and kinetic adsorption studies at different pH, temperatures, particle size, and solid-to-liquid ratio were carried out to determine various parameters necessary to establish the fixed bed reactors. The Langmuir and Freundlich models were applied and the data are not fitted well by the Freundlich and Langmuir equations, but the Langmuir model has an edge over Freundlich model. The monolayer adsorption capacity (Q0) as calculated using Langmuir adsorption isotherm of the activated carbons viz., FAC and ATFAC is found to increase with an increase in temperature confirming the endothermic process. The ATFAC has a higher sorption capacity than FAC. Overall the adsorption of alpha-picoline, beta-picoline, and y-picoline on FAC and ATFAC follow the order FACalpha-picoline < ATFACalpha-picoline < FAC gamma-picoline < ATFACbeta-picoline < FACbeta picoline < ATFAC gamma-picoline. The adsorption of alpha-,beta-, and gamma-picoline followed the pseudosecond-order rate kinetics. On the basis of these studies, various parameters such as effective diffusion coefficients, activation energy, and entropy of activation were evaluated to establish the mechanisms. It was concluded that the adsorption occurred through particle diffusion at low temperatures viz., 10 degrees C and 25 degrees C (except alpha-picoline where it was film diffusion), while at 40 degrees C it occurred through film diffusion. Similarly at concentrations of 25 and 50 mg/L the adsorption was particle diffusion controlled (except for alpha-picoline where it was film diffusion), while at > 50 mg/L it was film diffusion controlled.

Adsorption↗
PubMed2006

SanJ, an ATP-dependent picolinate-CoA ligase, catalyzes the conversion of picolinate to picolinate-CoA during nikkomycin biosynthesis in Streptomyces ansochromogenes.

Nikkomycins, a group of peptidyl nucleoside antibiotics, are competitive inhibitors of chitin synthase. The nikkomycin biosynthetic gene cluster has been cloned previously from Streptomyces ansochromogenes. The cluster contains 25 complete ORFs including sanJ. The sanJ gene was inactivated by the insertion of a kanamycin resistance gene and the resulting disruption mutants failed to produce nikkomycins. Moreover, the nikkomycin production was restored by complementation with a single copy of sanJ. The deduced product of sanJ bears striking sequence similarity with enzymes belonging to the adenylate-forming superfamily. sanJ was overexpressed as a His6-tagged fusion protein in Escherichia coli and purified to apparent homogeneity by affinity chromatography. The purified SanJ demonstrated adenylate ligase activity in the presence of picolinate or its analogs (benzoate, nicotinate, 4-methoxybenzoate, 4-hydroxybenzoate), ATP and Mg2+. SanJ was also found to catalyze the conversion of picolinate, benzoate, nicotinate to their corresponding CoA esters and 4-methoxybenzoate, 4-hydroxybenzoate to their respective AMP derivatives in vitro. This was unambiguously shown by using HPLC and electrospray ionization mass spectrometry (ESI-MS) or by comparing the reaction product with an authentic standard of benzoyl-CoA. These results indicated that sanJ encodes an ATP-dependent picolinate-CoA ligase which is essential for nikkomycin biosynthesis.

Adenosine Triphosphate↗
PubMed1984

Changes in streptonigrin lethality during adaptation of Escherichia coli to picolinic acid. Correlation with intracellular picolinate and iron uptake.

Uptake studies with [14C]picolinate and 55Fe3+ have provided an explanation for the change in streptonigrin killing on adaptation of Escherichia coli to picolinate, in terms of the available iron within the cell. When picolinic acid is added to a growing culture of E. coli an interval of bacteriostasis ensues; this adaptation period is followed by resumption of exponential growth. Addition of picolinate (4 mM) to a log phase culture of strain W3110 gave protection from the lethal action of streptonigrin (30 microM) when the two agents were added simultaneously. In contrast streptonigrin killed cells that had adapted to picolinate; however, a preincubation of adapted W3110 with phenethyl alcohol protected the cells from streptonigrin lethality. [14C]Picolinate uptake studies showed that initially picolinate entered the cells, but that it was excluded from adapted cells; addition of phenethyl alcohol permitted the entry of picolinate into adapted W3110. The changes in streptonigrin killing parallel the changes in concentration of intracellular picolinate, which can chelate the iron required by streptonigrin for its bactericidal action. 55Fe3+ uptake studies showed that initially picolinate prevented iron accumulation by strain W3110, whereas adapted cells did take up iron in the presence of picolinate. Addition of phenethyl alcohol prevented any observed uptake of iron by adapted W3110. This modulation of iron transport by picolinate also affects streptonigrin lethality. Experiments with iron transport mutants showed that picolinate acted on both the enterochelin and citrate routes of uptake. Therefore picolinate affects the concentration of available iron within the cell both by (a) its intracellular presence resulting in chelation of iron and (b) its action on iron uptake; these effects explain the change in streptonigrin killing on adaptation of E. coli to picolinate.

Escherichia coli↗
PubMed2006

Hydrogen-bonding patterns in trimethoprim picolinate and 2-amino-4,6-dimethylpyrimidinium picolinate hemihydrate.

In the title compounds, namely 2,4-diamino-5-[(3,4,5-trimethoxyphenyl)methyl]pyrimidin-1-ium pyridine-2-carboxylate, C14H19N4O3+.C6H4NO2-, (I), and 2-amino-4,6-dimethylpyrimidin-1-ium pyridine-2-carboxylate hemihydrate, C6H10N3+.C6H4NO2-.0.5H2O, (II), the trimethoprim and 2-amino-4,6-dimethylpyrimidin-1-ium cations are protonated at one of the pyrimidine N atoms. In (I), bifurcated hydrogen bonds are observed between a picolinate O atom, the protonated N atom and the 2-amino group; the graph-set designator is R2(1)(6). The pyrimidine moieties of the trimethoprim cations are centrosymmetrically paired through a pair of N-H...N hydrogen bonds. In addition to the base pairing, one of the picolinate O atoms bridges the 2- and 4-amino groups on either side of the paired bases, resulting in a complementary DADA array. In (II), the carboxylate group of the picolinate anion binds with the protonated pyrimidine N atom and the 2-amino group of the pyrimidine moiety through a pair of N-H...O hydrogen bonds, leading to the common ring motif R2(2)(8). The water molecule, which resides on a twofold rotation axis, bridges the carboxylate group of the picolinate anion via O-H...O hydrogen bonds.

Crystallography↗
PubMed2005

Experimental (FT-IR, FT-Raman, 1H NMR) and theoretical study of magnesium, calcium, strontium, and barium picolinates.

The experimental IR, Raman, and 1H NMR spectra of picolinic acid, as well as magnesium, calcium, strontium, and barium picolinates were registered, assigned and studied. Characteristic changes in the spectra of metal picolinates in comparison with the spectrum of ligand were observed, which lead to the conclusion that perturbation of the aromatic system of picolinates increases along with the series Mg-->Ca-->Sr-->Ba. Theoretical structures of beryllium and magnesium picolinates, as well as theoretical IR spectrum of magnesium picolinate were calculated in B3PW91/6-311++G(d, p) level. On the basis of calculated bond lengths in pyridine ring geometric, aromaticity indexes HOMA were calculated. The idea of these indexes is based on the fact that the essential factor in aromatic stabilization is the pi delocalization manifested in: planar geometry, equalization of the bond lengths and angles, and symmetry. The decidedly lower value of HOMA for magnesium picolinate (i.e. 0.545; 0.539) than that for beryllium picolinate (i.e. 0.998; 0.998) indicate higher aromatic properties of Be picolinate than of Mg picolinate. The comparison of theoretical and literature experimental structures of magnesium picolinate was done. The experimental structure contains two water molecules, so the calculations for hydrated magnesium picolinate were carried on, and the influence of coordinated water molecule on the structure of picolinates was discussed. The HOMAs for hydrated experimental and calculated Mg picolinate amount to 0.870; 0.743, and 0.900; 0.890, respectively, whereas for anhydrous structure, it is as described above, i.e. 0.545; 0.539. Thus, the calculations clearly showed that water molecules coordinated to the central atom weakens the effect of metal on the electronic system of ligand.

Barium↗
PubMed2006

Effect of chromium picolinate on modified forced swimming test in diabetic rats: involvement of serotonergic pathways and potassium channels.

Depression occurs frequently in patients with diabetes mellitus. Chromium picolinate, an essential trace element is recommended for diabetes and also has been reported to benefit depression, but its mechanism is still debated. To investigate the mechanism, we studied its effects on serum insulin, serum glucose and on modified forced swimming test, a behavioural paradigm for depression in rats. The study involving co-administration of sub-active doses of glimepiride, a K(+) channel blocker and chromium picolinate on blood glucose levels and modified forced swimming test was also performed to probe any role of K(+) channels in its antidiabetic and antidepressants effects. Streptozotocin (55 mg/kg, intraperitoneally) was injected in rats to induce diabetes (Type 1). After a week, chromium picolinate (8 microg/ml in drinking water) was administered for 4 weeks. Normal rats received similar drug treatment. The sub-active doses of chromium picolinate (4 microg/ml in drinking water) and glimeperide (2.5 mg/kg, orally) were co-administered and their effects on modified forced swimming test and on glucose levels were measured. Chromium picolinate (8 microg/ml in drinking water) produced hypoglycaemia in diabetic and normal rats. It had no effects on the streptozotocin-induced reduction in insulin levels. Chromium picolinate (8 microg/ml in drinking water) increased swimming with subsequent decrease in immobility. The sub-active doses of chromium picolinate and glimeperide showed significant additive effects in modified forced swimming test and reduction in serum glucose concentrations, though statistically insignificant. In conclusion chromium picolinate shows antidepressant action on modified forced swimming test affecting only swimming that suggests serotonergic pathways involvement. The additive effects on swimming in modified forced swimming test and reduction in serum glucose levels shows involvement of K(+) channels in antidiabetic and antidepressant actions of chromium picolinate.

Animals↗
PubMed1993

Transformation of 3- and 4-Picoline under Sulfate-Reducing Conditions.

A microbial population which transformed 3- and 4-picoline under sulfate-reducing conditions was isolated from a subsurface soil which had been previously exposed to different N-substituted aromatic compounds for several years. In the presence of sulfate, the microbial culture transformed 3- and 4-picoline (0.4 mM) within 30 days. From the amounts of ammonia released and of sulfide that were determined during the transformation of 3-picoline, it can be concluded that the parent compound was mineralized to carbon dioxide and ammonia. During the transformation of 4-picoline, a UV-absorbing intermediate accumulated in the culture medium. This metabolite was identified as 2-hydroxy-4-picoline by gas chromatography-mass spectrometry and nuclear magnetic resonance analysis, and its further transformation was detected only after an additional month of incubation. The small amount of sulfide produced during the oxidation of 4-picoline and the generation of the hydroxylated metabolite indicated that the initial step in the metabolic pathway of 4-picoline was a monohydroxylation at position 2 of the heterocyclic aromatic ring. The 3- and 4-picoline-degrading cultures could also transform benzoic acid; however, the other methylated pyridine derivatives, 2-picoline, dimethyl-pyridines, and trimethylpyridines, were not degraded.

Journal Article↗
PubMed2004

Insulin sensitising action of chromium picolinate in various experimental models of diabetes mellitus.

Although chromium is an essential element for carbohydrate and lipid metabolism, its effects in diabetic patients are still debated. We have studied the effect of 6 week treatment with chromium picolinate (8 microg/ml in drinking water) in streptozotocin (STZ)-induced type 1 and type 2 diabetic rat models. The mechanism of anti-diabetic action of chromium picolinate was studied using C2C12 myoblasts and 3T3-L1 adipocytes. Chromium picolinate significantly decreased the area under the curve over 120 min for glucose of both STZ-induced type 1 (40mg/kg, i.v. in adult rats) and type 2 (90 mg/kg, i.p. in 2 day old rat neonates) diabetic rats without any significant change in area under the curve over 120 min for insulin as compared to controls. The composite insulin sensitivity index and insulin sensitivity index (KITT) values of both type 1 and type 2 diabetic rats were increased significantly by chromium picolinate. Treatment with chromium picolinate produced a significant decrease in elevated cholesterol and triglyceride levels in both types of diabetic rats. In 3T3-L1 adipocytes, chromium picolinate (0-10 micromol) per se did not produce any effect, however, when co-incubated with insulin it significantly increased the intracellular triglyceride synthesis (EC50 = 363.7nmol/1). Similarly in C2C12 myoblasts, chromium picolinate alone did not produce any effect, however, it significantly increased insulin-induced transport of 14C-glucose. In conclusion, chromium picolinate significantly improves deranged carbohydrate and lipid metabolism of experimental chemically induced diabetes in rats. The mechanism of in vivo anti-diabetic action appears to be peripheral (skeletal muscle and adipose tissue) insulin enhancing action of chromium.

3T3 Cells↗
PubMed1999

Quinolinic acid, alpha-picolinic acid, fusaric acid, and 2,6-pyridinedicarboxylic acid enhance the Fenton reaction in phosphate buffer.

Quinolinic acid, alpha-picolinic acid, fusaric acid, and 2,6-pyridinedicarboxylic acid enhanced the Fenton reaction in phosphate buffer, respectively. The enhancement by quinolinic acid, alpha-picolinic acid, fusaric acid, and 2,6-pyridinedicarboxylic acid of the Fenton reaction may be partly related to their respective actions in the biological systems such as a neurotoxic effect (quinolinic acid), a marked growth-inhibitory action on rice seeding (alpha-picolinic acid and fusaric acid), and an antiseptic (2,6-pyridinedicarboxylic acid). The ultraviolet-visible absorption spectrum of the mixture of alpha-picolinic acid with ferrous ion showed a characteristic visible absorbance band with a lambda(max) at 443 nm, suggesting that alpha-picolinic acid chelate of Fe2+ ion forms in the solution. Similar characteristic visible absorbance band was also observed for the mixture of Fe2+ ion with quinolinic acid (or fusaric acid, or 2,6-pyridinedicarboxylic acid). The chelation seems to be related to the enhancement by quinolinic acid, alpha-picolinic acid, fusaric acid, and 2,6-pyridinedicarboxylic acid of the Fenton reaction. alpha-Picolinic acid was reported to be a toxic substance isolated from the culture liquids of blast mould (Piricularia oryzae CAVARA). On the other hand, it has also been known that chlorogenic acid protects rice plants from the blast disease. The chlorogenic acid inhibited the formation of the hydroxyl radical in the reaction mixture of alpha-picolinic acid, FeSO4(NH4)2SO4, and H2O2. Thus the inhibition may be a possible mechanism of the protective action of the chlorogenic acid against the blast disease.

Buffers↗
PubMed1990

Picolinic acid, a catabolite of tryptophan, as the second signal in the activation of IFN-gamma-primed macrophages.

We have studied the effects of picolinic acid, a product of tryptophan degradation, on the activation of mouse peritoneal macrophages (M phi). Picolinic acid acts synergistically with IFN-gamma in activating M phi from C57BL/6 mice. Moreover, M phi from C3H/HeJ mice and C3H/HeN that do not become cytotoxic in response to IFN-gamma alone could be fully activated by exposure to picolinate plus IFN-gamma. These results indicate that picolinic acid is a potent costimulator of M phi activation that functions as a second signal. Inasmuch as we have previously demonstrated that the activation of cytotoxic M phi correlates with specific changes in ribosomal RNA (rRNA), we investigated whether picolinic acid could modify M phi RNA metabolism. Picolinic acid inhibited the synthesis of total M phi RNA, the accumulation of newly synthesized 28S rRNA, and augmented the steady state levels of rRNA precursors (pre-rRNA). These changes in RNA metabolism were similar to those previously described in murine M phi activated in vitro or in vivo to express tumoricidal activity. These results demonstrate that picolinic acid is a potent, biologic M phi second signal, suggest that the changes in rRNA are causally connected with the expression of tumoricidal activity, and suggest the existance of an autocrine effect mediated by picolinic acid.

Animals↗
PubMed1993

Picolinic acid, a catabolite of L-tryptophan, is a costimulus for the induction of reactive nitrogen intermediate production in murine macrophages.

In this study we investigated the effects of picolinic acid, a catabolite of L-tryptophan, on the production of L-arginine-derived reactive nitrogen intermediates in the murine macrophage cell line ANA-1. ANA-1 macrophages did not produce nitrite (NO2-) constitutively, but accumulated detectable levels of NO2- on exposure to IFN-gamma. Picolinic acid, although ineffective by itself, augmented IFN-gamma-induced NO2- production. The activity of picolinic acid was evident at 1 mM and reached its maximum at 4 mM. Picolinic acid also augmented the IFN-gamma-dependent expression of TNF-alpha mRNA, but did not appreciably affect the secretion of the TNF-alpha protein. Neutralizing concentrations of anti-TNF mAb completely abrogated IFN-gamma- and IFN-gamma plus rTNF-alpha-induced NO2- production in ANA-1 macrophages, but only decreased by approximately 50% the synergistic interaction between IFN-gamma and picolinic acid. Although IL-4 inhibited the expression of IFN-gamma plus picolinic acid-induced TNF-alpha mRNA and protein, it only partially suppressed picolinic acid-dependent NO2- production. Therefore, picolinic acid may affect NO2- production via both TNF-alpha-dependent and TNF-alpha-independent pathways. Overall, this study suggests that amino acid catabolites may be important for the activation and the expression of effector functions by murine macrophages, and provides the first evidence of a possible connection between tryptophan and arginine metabolism.

Animals↗
PubMed1983

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↗
PubMed1993

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 microM). 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 microM) failed to influence kainic acid-induced release. Picolinic acid (100 microM) 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.

Animals↗