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PubMed1983

Modulation of Bordetella pertussis by nicotinic acid.

Growth of Bordetella pertussis in a high concentration of nicotinic acid (NA) had a modulating effect on several properties and activities of the bacteria. Compared with normally grown cells, those grown in a high concentration of NA had reduced capacity for taking up both NA and nicotinamide (ND); they had reduced adenylate cyclase activity and showed loss of agglutinogen factors 2 and 3, but an increase in factor 1. By contrast, cells grown in a high concentration of ND showed only a slightly decreased capacity for uptake of ND and none of the other changes. Modulation of B. pertussis by NA varied with the strain and culture conditions and appeared to be distinct from the antigenic modulation induced by high Mg2+ in the culture medium. Evidence is presented for the association of a small proportion of the extracytoplasmic adenylate cyclase with the outer membrane of B. pertussis.

Adenylyl Cyclases↗
PubMed1990

Determination of urinary tryptophan and its metabolites along the nicotinic acid pathway by high performance liquid chromatography with ultraviolet detection.

A fast and sensitive method is given for analysing urinary tryptophan and six of its metabolites on the nicotinic acid pathway. Kynurenine, tryptophan, 3-hydroxykynurenine, anthranilic acid, 3-hydroxyanthranilic acid, kynurenic acid and xanthurenic acid were isocratically eluted and completely resolved with a mobile phase of acetonitrile + sodium acetate buffer, pH 4.76 (4:96, v/v). The flow rate was 0.8 mL/min at the beginning and was then linearly increased to 1.2 after 6 min; after 14 min the flow was augmented from 1.2 to 2 mL/min. The effluent was monitored with a variable UV detector set at 254 nm for the first five peaks and at 280 and 325 nm for the penultimate peak and final peak. Analytical recoveries of the compounds after deproteinization varied between 64% and 98%. The reported method should enable one to examine easily, extensively, quantitatively and routinely urinary tryptophan and the most important metabolites of the nicotinic acid pathway.

Chromatography, High Pressure Liquid↗
PubMed1977

PH metric method for the determination of nicotinic acid in plasma.

The acidimetric method for the determination of nicotinic acid (NA) using Lactobacillus plantarum ATCC 8014 (Lactobacillus arabinosus 17-5) has been simplified and thus made less time consuming, and the sensitivity has been increased fivefold by replacement of the titration by a pH determination. As the regression of the decrease in pH on the amount of NA was found linear within a range of 1 to 4 ng of NA per ml, the calculations were performed according to the slope-ratio principle. The NA concentration of plasma was determined with a coefficient of variation of 5 to 7%, which rose to about 10% at low NA concentrations. Assays of fasting plasma samples from 13 hyperlipidemic male patients showed a group mean NA concentration of 80 +/- 55 ng/ml (mean +/- 2 standard deviation), before treatment, and 705 +/- 544 ng/ml (mean +/- 2 standard deviation) during therapy with sustained release NA preparations, of which a single dose, ingested during steady-state conditions, doubled or tripled the plasma concentration within 1 to 3 h.

Biological Assay↗
PubMed2001

The structure of Escherichia coli nitroreductase complexed with nicotinic acid: three crystal forms at 1.7 A, 1.8 A and 2.4 A resolution.

Escherichia coli nitroreductase is a flavoprotein that reduces a variety of quinone and nitroaromatic substrates. Its ability to convert relatively non-toxic prodrugs such as CB1954 (5-[aziridin-1-yl]-2,4-dinitrobenzamide) into highly cytotoxic derivatives has led to interest in its potential for cancer gene therapy. We have determined the structure of the enzyme bound to a substrate analogue, nicotinic acid, from three crystal forms at resolutions of 1.7 A, 1.8 A and 2.4 A, representing ten non-crystallographically related monomers. The enzyme is dimeric, and has a large hydrophobic core; each half of the molecule consists of a five-stranded beta-sheet surrounded by alpha-helices. Helices F and F protrude from the core region of each monomer. There is an extensive dimer interface, and the 15 C-terminal residues extend around the opposing monomer, contributing the fifth beta-strand. The active sites lie on opposite sides of the molecule, in solvent-exposed clefts at the dimer interface. The FMN forms hydrogen bonds to one monomer and hydrophobic contacts to both; its si face is buried. The nicotinic acid stacks between the re face of the FMN and Phe124 in helix F, with only one hydrogen bond to the protein. If the nicotinamide ring of the coenzyme NAD(P)H were in the same position as that of the nicotinic acid ligand, its C4 atom would be optimally positioned for direct hydride transfer to flavin N5. Comparison of the structure with unliganded flavin reductase and NTR suggests reduced mobility of helices E and F upon ligand binding. Analysis of the structure explains the broad substrate specificity of the enzyme, and provides the basis for rational design of novel prodrugs and for site-directed mutagenesis for improved enzyme activity.

Amino Acid Sequence↗
PubMed1996

Cerebral blood flow effects of piracetam, pentifylline, and nicotinic acid in the baboon model compared with the known effect of acetazolamide.

In normal aging humans there is a progressive decrease of oxygen and glucose consumption with a reduction of cerebral blood flow (CBF), which could be responsible for age-related changes in cognitive functions. A baboon model under anaesthesia using single photon emission computed tomography (SPECT) of the brain and the radiopharmaceutical hexamethylpropylene amine oxime (99mTc-HMPAO) has been developed and found to be sensitive to the effects of drugs that are known to increase CBF. In the present study, the effect of two haemorrheologically active drugs, viz a combination of pentifylline (CAS 1028-33-7) and nicotinic acid (CAS 59-67-6) vs. piracetam (CAS 7491-74-9) were compared with the known effect of acetazolamide (CAS 59-66-5) on CBF in the baboon model using the 99mTc-HMPAO split dose method. Acetazolamide (p < 0.05) and the combination of pentifylline and nicotinic acid (p < 0.01) increased the CBF when compared with the control baseline. The CBF was not significantly increased upon treatment with piracetam, pentifylline alone and nicotinic acid alone, when compared with the control values for total brain ratios (p > 0.05). However, an increased regional effect was observed for piracetam. These results indicate that the above haemorrheologically active drugs exhibit specific but different effects on cerebral blood flow with possible clinical implications.

Acetazolamide↗
PubMed1992

Effects of nicotinic acid treatment on fatty acid composition of plasma lipids and adipose tissue in hyperlipidaemia.

Effects of 6-week treatment with 4 g daily of nicotinic acid on fatty acid composition in different serum lipids and in adipose tissue glycerides were studied in 31 hyperlipidemic patients. The percentages of eight fatty acids in triglycerides, phospholipids and cholesteryl esters of whole plasma as well as in subcutaneous adipose tissue glycerides were measured. Nicotinic acid treatment produced decreases in triglyceride and total cholesterol concentrations of VLDL and LDL, whereas HDL total cholesterol levels in serum increased after drug therapy, all p less than 0.01. There were reductions in the relative contents of myristic acid in plasma phospholipids (from 0.4% to 0.3%; p less than 0.05) and cholesteryl esters (from 0.9% to 0.7%; p less than 0.001). There were decreases in the percentages of stearic acid in plasma phospholipids (from 17.0% to 15.0%) and cholesteryl esters (from 1.2% to 1.0%; both p less than 0.001). The relative contents of polyunsaturated fatty acids, mainly linoleic acid, in plasma phospholipids were increased (from 32% to 33.5%; p less than 0.05). There were reductions in the linolenic acid contents of adipose tissue (from 1.5% to 1.1%) and plasma triglycerides (from 1.1% to 0.8%), both p less than 0.05, possibly indicating increased conversion of linolenic acid to prostaglandins. There was no relationship between changes in the percentages of individual fatty acids and changes in triglyceride or total cholesterol levels of whole serum and its VLDL, LDL and HDL fractions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1990

[Nicotinic acid in dust-gas emissions from the biochemical industrial plants producing yeast for animal feed].

The presence of nicotine acid in the dustgaseous pollution from biochemical plants producing fodder yeast has been shown. Its allergic and sensitizing role compared to the same properties of protein-containing dust has been pointed out. It has been suggested that MAC of nicotine acid should be established for the sanitary-protective zone of microbiological industry enterprises.

Air Pollutants↗
PubMedDate not supplied

[Level of nicotinic acid and NAD in the organs of rats during complete starvation].

In the liver, heart, brain and pancreas of control rats and of test animals fasting for 2, 4, 7 and 11 days the content of nicotinic acid in the organs was determined by the microbiological method and that of NAD- biochemically. After 2, 7 and 11 days of fasting a statistically significant increase in the level of nicotinic acid per 1 g of tissue was ascertained in all the organs. After 4 days of fasting an increase in the vitamin content proved insignificant. With the calculation covering the entire organ the fall of the PP level in the liver proceeded uniformly and after the 11th day of fasting it amounted to 46 per cent, whereas in the heart the decline was insignificant, the content of the vitamin in the brain, however, rose by 21 per cent. The NAD level in the organs, calculated to 1 g of the tissue, changed but little and with the estimates covering the whole of the organ there could be noted its substantial drop in the liver, especially after 11 days of fasting (by as much as 62 per cent), and to a lesser degree--in the heart and pancreas and rise in the brain (by 13 per cent).

Animals↗
PubMed1984

[Comparative study of the effect of prolonged administration of nicotinic acid, nicotinamide and diethylnicotinamid (Cordiamin) on the rat liver monooxygenase system].

Nicotinic acid (50 mg/kg), nicotinamide (50 mg/kg) administered to rats intragastrically for 45 days do not exert any effect on the activity and the content of liver microsomal monooxygenase. Diethylnicotinamide (cordiamine) given in an equimolar dose (73 mg/kg) increases the microsomal content of cytochromes P-450 and b5, activates oxidoreductase of the components of the NADP X H-dependent redox-chain of the microsomal membranes, speeds up N-demethylation of amidopyrine and p-hydroxylation of aniline.

Animals↗
PubMed1971

End-product regulation of the tryptophan-nicotinic acid pathway in Neurospora crassa.

The regulation of the tryptophan-nicotinic acid pathway in Neurospora crassa was examined with mutants (nic-2, nic-3) which require nicotinamide for growth. The accumulation of N-acetylkynurenin and 3-hydroxyanthranilic acid by these mutants served to estimate the level of function of the early reactions in the pathway. In still cultures, maximal accumulation occurred with media containing growth-limiting amounts of nicotinamide; the accumulation of intermediates was almost negligible with nicotinamide in excess. Only nicotinamide and closely related compounds which also supported the growth of these mutants inhibited the accumulation of intermediates. The site of inhibition was assessed to be between tryptophan and kynurenin (or N-acetylkynurenin). The synthesis of N-acetylkynurenin was examined in washed germinated conidia suspended in buffer; the level of N-acetylkynurenin-synthesizing activity was inversely related to the concentration of nicotinamide in the germination medium. The addition of large amounts of nicotinamide to suspensions of germinated conidia did not affect their N-acetylkynurenin-synthesizing activity. Formamidase activity, kynurenin-acetylating activity, and gross tryptophan metabolism in germinated conidia was not influenced by the concentration of nicotinamide in the germination medium. The results obtained indicate that the site of inhibition by nicotinamide is the first step in the pathway, the tryptophan pyrrolase reaction. The data are interpreted as nicotinamide or a product thereof, such as nicotinamide adenine dinucleotide, acting as a repressor of the formation of tryptophan pyrrolase in N. crassa.

Arylformamidase↗
PubMed1982

Effect of nicotinic acid on myelin lipids in brain of developing rat.

Weanling rats (weaned 12 days after birth) were fed on nicotinic acid-deficient and on nicotinic acid-supplemented diet separately for 7 and 21 days. The yield of myelin in the brain of rat fed on the nicotinic acid-deficient diet was lower than that in the case of receipt of the nicotinic acid-supplemented diet at 19, 26 and 33 days of age. Despite the changing yield of myelin, the proportion of protein and total lipids, and the percentage composition of lipid were not changed between the groups fed on the nicotinic acid-deficient and the nicotinic acid-supplemented diet. Moreover, the ratio of long chain fatty acid (C20-23/C14-18) was markedly decreased in the nicotinic acid-deficient rats. These findings imply that nicotinic acid may play an important role in myelination associated with the synthesis of cerebrosides which contain high levels of long chain fatty acid.

Aging↗
PubMed1977

[Portal blood flow in minipig and its change by nicotinic acid (author's transl)].

The chronic double catheterisation of portal vein permits estimation of portal flow by dye dilution for example, the withdrawal of blood from the mesenteric vein and proximal portal vein, the injection of drugs into the portal circulation and measurement of portal pressure simultaneously. Beside the well known diminution of portal flow by vasopressin, which is extreme in anaesthetised minipig, there could be shown a remarkable diminution by high intravenous doses of nicotinic acid too without significant changes of systemic blood pressure and heart rat. Nicotinic acid causes also a diminution of pH in portal and venous blood.

Animals↗
PubMed1994

Biocidal action of chlorhexidine is annulled by nicotinic acid.

An analytical system comprising a bacterium and a protozoan was used to pinpoint the metabolic lesion whereby chlorhexidine (CLX) produced cell death. Nicotinic acid but not nicotinamide annulled the biocidal action of CLX. The results suggest that CLX may not permit bioconversion of nicotinamide to nicotinic acid to annul the growth inhibition induced by CLX.

Animals↗