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Results for “NICOTINIC ACID”

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PubMed1996

The nadB gene of Salmonella typhimurium complements the nicotinic acid auxotrophy of Shigella flexneri.

Shigella species are characteristically nicotinic acid (NA) auxotrophs. The invasive S. flexneri strain M90T, transformed with the multicopy plasmid pZT349 encoding the nadB gene of Salmonella typhimurium, can grow in minimal glucose medium without exogenous NA, whereas, M90T containing the control vector, pUC18 does not, suggesting that this species lacks L-aspartic acid oxidase, the first enzyme in the de novo NAD biosynthetic pathway. The estimated growth rate of strain M90T (pZT349) in HeLa cells was identical to that of M90T (pUC18), indicating the available intracellular concentration of NA is not limiting for bacterial growth.

Humans↗
PubMed2000

Chromatographic and capillary electrophoretic methods for the analysis of nicotinic acid and its metabolites.

Methods for the assay of nicotinic acid (NiAc) and its metabolites in biological fluids using high-performance liquid chromatography (HPLC) and capillary electrophoresis (CE) are reviewed. Most of the references cited in this review concern HPLC methods. A few CE methods that have been recently reported are also included. As these compounds are relatively polar and have a wide range of physico-chemical properties, the sample pre-treatment or clean-up process prior to analysis is included. Most HPLC methods using an isocratic elution system allow determination of a single or few metabolites, but gradient HPLC methods enable simultaneous determination of five to eight compounds. Simultaneous determination of NiAc including many metabolites in a single run can be achieved by CE. We also discuss the pharmacokinetics of NiAc and some of its metabolites.

Chromatography, High Pressure Liquid↗
PubMed2004

Niaspan, the prolonged release preparation of nicotinic acid (niacin), the broad-spectrum lipid drug.

Niacin (nicotinic acid) is the broad-spectrum lipid drug, which lowers the concentration of all atherogenic plasma lipids/lipoproteins and at the same time raises the levels of the protective HDL (high-density lipoprotein). Niaspan is a prolonged release (PR) formulation of niacin, which has considerable advantages over both immediate release (IR) and slow release (SR) formulations of this drug. The major early side effect of IR niacin, the flush, is reduced with Niaspan. The hepatotoxic effects with SR niacin are not present with Niaspan. It is suitable for once daily prescription at bedtime. Niaspan is effective as monotherapy and in combination with other lipid-lowering drugs such as statins and fibrates. It is particularly useful for treatment of the dyslipidaemia of type 2 diabetes, where IR but not PR niacin may deteriorate the diabetic condition. Overall, niacin, now available as the well-tolerable drug formulation Niaspan, is the unique broad-spectrum lipid drug for the prevention and treatment of clinical atherosclerosis.

Arteriosclerosis↗
PubMed2002

Nicotinic acid adenine dinucleotide phosphate: a new intracellular second messenger?

Nicotinic acid adenine dinucleotide phosphate (NAADP) is one of the most potent stimulators of intracellular Ca2+ release known to date. The role of the NAADP system in physiological processes is being extensively investigated at the present time. Exciting new discoveries in the last 5 years suggest that the NAADP-regulated system may have a significant role in intracellular Ca2+ signaling. The NAADP receptor and its associated Ca2+ pool have been hypothesized to be important in several physiological processes including fertilization, T cell activation, and pancreatic secretion. However, whether NAADP is a new second messenger or a tool for the discovery of a new Ca2+ channel is still an unanswered question.

Animals↗
PubMed1990

[The effect of tocopherol and nicotinic acid on the microcirculation and blood coagulability in patients with ischemic heart disease].

Patients with ischemic heart disease were treated by routine techniques (53), using also tocopherol acetate (54) and combination of tocopherol with nicotinic acid (53). Changes of the microcirculatory bed of the bulbar conjunctiva was studied biomicroscopically and in the process of blood coagulation hemoelectrocoagulographically. Complex treatment using tocopherol acetate produced a positive effect on the coagulation properties of the blood and did essentially influence the fibrinolytic activity and microcirculation. Tocopherol plus nicotinic acid resulted in normalization of the blood coagulation process, favoured activation of fibrinolysis and improvement of the microcirculatory bed.

Adult↗
PubMed2002

Eptastigmine, nicotinamide and nicotinic acid determination using an inhibition enzyme sensor; application to pharmaceutical analysis.

An enzyme inhibition biosensor, developed in our laboratory and previously used for the analysis of compounds with anticholinesterase activity (e.g. physostigmine, neostigmine, pyridostigmine nicotine and organophosphorus compounds) has now been tested for the analysis of another recently synthesized cholinesterase inhibitor, i.e. eptastigmine. In addition nicotinic acid and nicotinamide, although displaying weaker inhibition properties, were also tested in pharmaceutical products using the same inhibition enzyme sensor. The biosensor consisted of a hydrogen peroxide amperometric electrode coupled to a functionalised nylon membrane chemically bonding both the enzymes butyrylcholinesterase and choline oxidase; a butyrylcholine standard solution in glycine buffer acted as substrate. The response of the system to all the inhibitors considered was characterised completely and the analysis of several pharmaceutical formulations containing nicotinamide or nicotinic acid was also performed.

Biological Assay↗
PubMed1996

Energy coupling in Salmonella typhimurium nicotinic acid phosphoribosyltransferase: identification of His-219 as site of phosphorylation.

Energy coupling between ATP hydrolysis and other enzyme reactions requires the phosphorylation of substrate-derived intermediates, or the existence of enzyme-derived intermediates capable of storage and transfer of energy. Salmonella typhimurium nicotinic acid phosphoribosyltransferase (NAPRTase, EC 2.4.2.11) couples net ATP hydrolysis to formation of NAMN and PPi from alpha-PRPP and nicotinic acid [Vinitsky, A., & Grubmeyer, C (1993) J. Biol. Chem. 268, 26004-26010]. In the current work, we have determined that the enzyme reacts with ATP to produce a covalently phosphorylated form of the enzyme (E-P), which is common to both the ATPase and NAMN synthesis functions of NAPRTase. We have isolated E-P and verified its catalytic competence. E-P showed acid lability and base stability, diagnostic of a phosphoramidate linkage. Pyridine and hydroxylamine-catalyzed hydrolysis of E-P gave second-order rate constants consistent with published values for phosphohistidine. Two-dimensional thin-layer chromatography of alkaline-hydrolyzed E-32P showed that the phosphorylated residue co-migrated with authentic 1-phosphohistidine. Chymotrypsin and trypsin proteolysis followed by HPLC and peptide sequencing localized the phosphopeptide to Ala-210 to Phe-222 of the 399-residue protein. This peptide contains a single histidine residue, His-219. NAPRTase phosphorylated at His-219 is an intermediate in the energy transduction mechanism of NAPRTase.

Adenosine Triphosphatases↗
PubMed2005

[Induction of nicotinic acid hydroxylase activity of Pseudomonas putida NA-1 and optimization of transformation conditions].

Some features of Pseudomonas putida NA-1 strain in cultivation and enzyme production were different from S. marcescens IFO 12648 and P. fluorescens TN5 stains which could transform nicotinic acid to 6-hydroxynicotinic acid reported by other scientists, such as optimal carbon and its optimal concentration, optimal inducer concentration, and optimal cultivation temperature. The ideal transformation condition was nicotinic acid 3%, temperature 35 degrees C and pH 7.0. Under an appropriate condition, in a 4 liter fermenter, production yield of 6-hydroxynicotinic acid by Pseudomonas putida NA-1 was 108.39 g/L.

Biotransformation↗
PubMed1983

Nicotinic acid and serum metabolite concentrations of lactating dairy cows fed supplemental niacin.

The effect of supplemental niacin on production and metabolite changes associated with early lactation were measured. Differences of milk production between treatments were not apparent, but serum nicotinic acid concentrations remained higher for those cows fed niacin (12 g/day). Changes of serum metabolites did occur when cows received a single oral dose of 12 or 120 g niacin. Significant alterations of nicotinic acid, free fatty acids, beta-hydroxybutyrate, blood urea nitrogen, serum glutamic-oxalacetic-transaminase, sodium, and chloride occurred within 24 h after initiation of treatment. These metabolites returned to basal concentrations within 60 h after administration.

3-Hydroxybutyric Acid↗
PubMed1992

Reversal of steroid-induced insulin resistance by a nicotinic-acid derivative in man.

A recent report suggested that the glucose-free fatty acid (FFA) cycle may contribute to steroid-induced insulin resistance in rats, and that glucose tolerance could be restored to normal when FFA levels were lowered with nicotinic acid. To test this hypothesis in man, we measured insulin sensitivity (by euglycemic insulin clamp in combination with indirect calorimetry and infusion of tritiated glucose) before and after short-term administration of a nicotinic-acid derivative (Acipimox) in 10 steroid-treated, kidney transplant patients with insulin resistance. Thirty-five healthy subjects served as controls. Six of them received Acipimox. Total body glucose metabolism was reduced in steroid-treated patients compared with control subjects (41.7 +/- 3.3 v 50.0 +/- 2.2 mumol/kg lean body mass [LBM].min, P less than .05). The reduction in insulin-stimulated glucose uptake was mainly due to an impairment in nonoxidative glucose metabolism (primarily glucose storage as glycogen) (18.3 +/- 2.8 v 27.2 +/- 2.2 mumol/kg LBM.min, P less than .01). Acipimox lowered basal FFA concentrations (from 672 +/- 63 to 114 +/- 11 mumol/L, P less than .05) and the rate of lipid oxidation measured in the basal state (1.5 +/- 0.2 to 0.6 +/- 0.1 mumol/kg LBM.min, P less than .01) and during the clamp (0.7 +/- 0.2 to 0.03 +/- 0.2 mumol/kg LBM.min, P less than .05). In addition, Acipimox administration normalized total glucose disposal (to 54.4 +/- 4.4 mumol/kg LBM.min), mainly due to enhanced nonoxidative glucose metabolism (to 28.9 +/- 3.9 mumol/kg LBM.min) in steroid-treated patients (both P less than .05 v before Acipimox).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex Hormones↗
PubMed1972

The oxidation of nicotinic acid by Pseudomonas ovalis Chester. The terminal oxidase.

In cell-free extracts of Pseudomonas ovalis nicotinic acid oxidase is confined to the wallmembrane fraction. It is associated with an electron-transport chain comprising b- and c-type cytochromes only, differing proportions of which are reduced by nicotinate and NADH. CO difference-spectra show two CO-binding pigments, cytochrome o (absorption maximum at 417nm) and another component absorbing maximally at 425nm. Cytochrome o is not reduced by NADH or by succinate but is by nicotinate, which can also reduce the ;425' CO-binding pigment. The effects of inhibitors of terminal oxidation support the idea of two terminal oxidases and a scheme involving the ;425' CO-binding pigment and the other components of the electron-transport chain is proposed.

Azides↗
PubMed2002

Nicotinic acid adenine dinucleotide phosphate mediates Ca2+ signals and contraction in arterial smooth muscle via a two-pool mechanism.

Previous studies of arterial smooth muscle have shown that inositol 1,4,5-trisphosphate (IP3) and cyclic ADP-ribose mobilize Ca2+ from the sarcoplasmic reticulum. In contrast, little is known about Ca2+ mobilization by nicotinic acid adenine dinucleotide phosphate, a pyridine nucleotide derived from beta-NADP+. We show here that intracellular dialysis of nicotinic acid adenine dinucleotide phosphate (NAADP) induces spatially restricted "bursts" of Ca2+ release that initiate a global Ca2+ wave and contraction in pulmonary artery smooth muscle cells. Depletion of sarcoplasmic reticulum Ca2+ stores with thapsigargin and inhibition of ryanodine receptors with ryanodine, respectively, block the global Ca2+ waves by NAADP. Under these conditions, however, localized Ca2+ bursts are still observed. In contrast, xestospongin C, an IP3 receptor antagonist, had no effect on Ca2+ signals by NAADP. We propose that NAADP mobilizes Ca2+ via a 2-pool mechanism, and that initial Ca2+ bursts are amplified by subsequent sarcoplasmic reticulum Ca2+ release via ryanodine receptors but not via IP3 receptors.

Animals↗