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PubMedDate not supplied

The effect of amino acid derivative of clofibric acid (WKLB-5), and theophylline monoester of nicotinic acid (ME1) on the development of experimental atherosclerosis in rabbits.

In order to determine the efficacy of new compounds--an amino acid derivative of clofibric acid (WKLB-5), and a theophylline monoester of nicotinic acid (ME1)--a high fat diet (HFD) was applied to rabbits for 3 months, with or without the above mentioned compounds. The HFO included coconut oil, cholesterol and cholic acid. A substantial hypolipemic activity of those compounds was demonstrated; however, the studied lipid fractions did not undergo normalization, except FFA whose level after ME1 administration was distinctly lower than in control animals. Sudanophilic changes were found on 83% of surface of the interior membrane of aorta in rabbits kept on the HFD only, on 35% of surface--in rabbits treated with the HFD + WKLB-5, and on 75% of surface--in rabbits treated with the HFD + ME1. Thus in those animals no parallelism between the hypolipemic and antiatherosclerotic activities was observed.

Animals↗
PubMed2004

Crystallization and preliminary X-ray crystallographic analysis of nicotinic acid mononucleotide adenylyltransferase from Pseudomonas aeruginosa.

The enzyme nicotinic acid mononucleotide adenylyltransferase (NaMN AT; EC 2.7.7.18) is essential for the synthesis of nicotinamide adenine dinucleotide and is a potential target for antibiotics. It catalyzes the transfer of an adenyl group from ATP to nicotinic acid mononucleotide to form nicotinic acid adenine dinucleotide. NaMN AT from Pseudomonas aeruginosa was overexpressed in Escherichia coli and crystallized at 291 K using 100 mM bis-Tris propane pH 7.0, 700 mM trisodium citrate and 15%(v/v) glycerol. X-ray diffraction data have been collected to 1.70 A. The crystals are tetragonal, belonging to space group P4(1)22 (or P4(3)22), with unit-cell parameters a = b = 65.02, c = 109.80 A. The presence of one monomer in the asymmetric unit gives a reasonable V(M) of 2.15 A(3) Da(-1), with a solvent content of 42.7%.

Amino Acid Sequence↗
PubMed1984

Influence of nicotinic acid on cerebroside synthesis in the brain of developing rats.

The effect of nicotinic acid on synthesis of cerebroside was studied during brain development. Nicotinic acid concentration in the whole brain and liver of rats fed on nicotinic acid-deficient diet for 10 days after weaning was lower than that of animals fed on nicotinic acid-supplemented diet. The cerebroside concentration was markedly lower and the total lipid concentration was slightly lower in the brain of nicotinic acid-deficient animals than in those receiving nicotinic acid-supplemented diet. Therefore, the ratio of cerebrosides to total lipids of nicotinic acid-deficient rats was significantly lower than that of nicotinic acid-supplemented rats. In nicotinic acid-deficient rats, the ratio of long-chain to short-chain fatty acid (C20-24/C14-18) was decreased in the nonhydroxy fatty acid fraction. Moreover, the ratio of synthesis of cerebrosides with hydroxy fatty acid to nonhydroxy fatty acid of nicotinic acid-deficient rats was higher than that of rats fed on nicotinic acid-supplemented diet. These observations suggest that nicotinic acid affects the synthesis of cerebrosides with nonhydroxy fatty acid.

Animals↗
PubMed1965

Spectral and biological changes induced in nicotinic acid and related compounds by ultraviolet light.

1. Irradiation of nicotinic acid, nicotinamide, nicotinamide N-oxide, N'-methyl-4-pyridone-3-carboxamide, reduced nicotinamide-adenine dinucleotide and pyridine with ultraviolet light at 253.7mmu leads to striking spectral changes. 2. Nicotinic acid and nicotinamide are broken down to photosensitive intermediates which in turn undergo photodecomposition. 3. A major photoproduct of [7-(14)C]nicotinic acid is radioactive and absorbs ultraviolet light, but is inactive as a growth factor for Candida pseudotropicalis. 4. Irradiation of nicotinamide gives rise to small quantities of a biologically active photoproduct having the same R(F) as nicotinic acid. A second photoproduct is also formed, but its identity has not yet been established. 5. Irradiation of nicotinamide N-oxide leads to the formation of several photoproducts, one of which has the same R(F) as nicotinamide, absorbs ultraviolet light, and is biologically active. 6. Evidence is presented that irradiation of ethanolic solutions of N'-methyl-4-pyridone-3-carboxamide gives rise to acetaldehyde. 7. Irradiation of reduced nicotinamide-adenine dinucleotide in the presence of acetaldehyde leads to the formation of oxidized nicotinamide-adenine dinucleotide, which in turn can break down to nucleotide and/or nucleoside (depending on the conditions of the reaction). 8. The quantum yields of photolysis and the molar photosensitivities have been determined for N'-methyl-4-pyridone-3-carboxamide and nicotinamide N-oxide. 9. The possible biological significance of these photoreactions is discussed in relation to photosynthesis, visual-pigment metabolism and ultraviolet-light-induced cell damage. 10. A four-step theory is presented for the biochemical evolution of oxidation-reduction systems, involving photoactivated transformations of pyridine derivatives.

Chromatography↗
PubMed1995

Nicotinic acid decreases serum thyroid hormone levels while maintaining a euthyroid state.

OBJECTIVE: To evaluate the effects of nicotinic acid on serum thyroid hormone levels in the absence of systemic illness or hepatic dysfunction. DESIGN: We determined the effect of treatment with nicotinic acid on serum thyroid hormone levels in one female and four male patients (mean age, 44.4 years) with hyperlipidemia. MATERIAL AND METHODS: In the five study patients, we measured serum lipids in conjunction with serum thyroxine (T4), triiodothyronine (T3) resin uptake, T3, free T4, thyroid-stimulating hormone (TSH), and thyroxine-binding globulin before, during, and after treatment with nicotinic acid. RESULTS: Serum lipid levels responded appropriately to nicotinic acid treatment. Thyroid function studies done a mean of 1.3 years (range, 0.5 to 3.5) after initiation of nicotinic acid therapy (mean daily dose, 2.6 +/- 0.7 g) revealed significant decreases in serum levels of total T4 (21%), free T4 index (16%), T3 (13%), and thyroxine-binding globulin (23%) (P < 0.02), whereas no significant changes were noted in free T4, T3 resin uptake, and TSH levels. During the course of treatment, the patients, who were carefully questioned, had no symptoms of hypothyroidism. Hypothyroidism was further excluded in three patients who had a normal serum TSH response to administration of thyrotropin-releasing hormone. In two patients, measurements of thyroid function returned to pretreatment levels after discontinuation of nicotinic acid therapy. No patient had significant abnormalities in liver-associated enzymes or evidence of systemic illness during the course of treatment. CONCLUSION: These results suggest that nicotinic acid decreases serum thyroid hormone concentrations while maintaining a euthyroid state. This effect may be mediated through reduction in thyroxine-binding globulin, but other mechanisms may also be involved.

Adult↗
PubMed1978

Effect of nicotinic acid on vascular permeability after thermal trauma in the rat.

Nicotinic acid has been suggested to decrease plasma volume loss after thermal injury. However, conflicting data have recently appeared, in reports of laboratory measurements of major derangements in cardiovascular function after large third-degree thermal injury. We investigated the microvascular effect of nicotinic acid on water and albumin leakage after a small second-degree thermal burn in the rat. No effect of nicotinic acid on albumin leakage was observed at 1/2 hour, 3 hours, or 6 hours; a minimal but significant (p less than 0.05) decrease in water content of burned tissue was observed 1/2 hour postinjury. Our studies confirm in rats previous work with sheep and dogs demonstrating that nicotinic acid has slight, if any, effect on fluid and protein loss after thermal injury.

Albumins↗
PubMed1997

The role of adrenal hormones in the activation of tryptophan 2,3-dioxygenase by nicotinic acid in rat liver.

In this study, our previous finding that nicotinic acid activates tryptophan 2,3-dioxygenase as strongly as tryptophan was investigated in further detail. This study focused on the role of the adrenals in the activation process. Adrenalectomy abolished the activation due to nicotinic acid, but not the activation caused by tryptophan. The role of corticoids and/or adrenomedullary hormones in the enzyme activation was studied, by supplementing these hormones in adrenalectomized rats using minipumps implanted under the skin. The results showed that the enhanced activity of tryptophan 2,3-dioxygenase caused by nicotinic acid was partly restored by adrenaline following adrenalectomy but not by corticosterone supplementation. The results were supported by further experiments in which the rats were treated with adrenaline or corticosterone intraperitoneally before nicotinic acid administration. The conclusion that adrenaline participates in the regulation of tryptophan 2,3-dioxygenase should promote further study to determine whether adrenaline is a general modulator of this enzyme. This experimental model generated new information on the activation mechanism of tryptophan 2,3-dioxygenase by nicotinic acid.

Adrenalectomy↗
PubMed1983

Nicotinic acid action on gastrointestinal smooth muscle.

The mechanism of nicotinic acid action in smooth muscle was studied by testing the drug in rat stomach fundus and descending colon using either the superfusion or perfusion technique. In the rat stomach strips nicotinic acid (or Na-nicotinate) induces concentration-dependent contractions that are drastically antagonized by indomethacin but not by the other inhibitors tested (scopolamine, phenoxybenzamine, propranolol, methysergide, pyrilamine, imidazole, anacardic acid). Reduced glutathione, on the contrary, clearly potentiates the contractile effect of nicotinic acid in the tissue. The response of the rat stomach strips to different prostanoids (PGE1, PGE2 alpha, PGF2 alpha, and PGI2) shows that only PGE2 (at a very low concentration: 14 nM) induces muscle contraction similar to that evoked by Na-nicotinate (34.4 nM). In segments of rat descending colon Na-nicotinate induces concentration-dependent contractions that are abolished by scopolamine, by hemicholinium-3 or incubation at low temperature (20 degrees C). These results provide evidence that nicotinic acid influences gastrointestinal smooth muscle by indirect mechanisms, i.e. by release of endogenous autacoids, namely prostaglandins in the stomach fundus and cholinergic transmitter in the descending colon.

Animals↗
PubMed1978

Efficacy of hypolipidemic treatment in inhibition of experimental atherosclerosis: the effect of nicotinic acid and related compounds.

The hypolipidemic and antiatherogenic effects of different nicotinic acid derivatives were studied. Five rabbit groups maintained on an atherogenic diet were given simultaneously various nicotinic acid derivatives (50 mg/kg body weight/day): nicotinic acid, Xantinol-nicotinate, beta-pyridylcarbinol or Pirozadil (bis-3,4,5-trimethoxybenzoate, 2,6-pyridindiyldimethylene). All 4 compounds showed a clear hypocholesterolemic and antiatherogenic effect, as measured by serum cholesterol, and by planimetric evaluation of the aortic lesions in terms of percent surface area affected in the aortas and coronary lumen. The simultaneously observed elevation of the HDL/LDL cholesterol ratio of the aortic tissue possibly indicates an antiatherogenic effect of these changes.

Animals↗
PubMed1975

Autoradiographic studies of nicotinic acid utilization in human-mouse heterokaryons and inhibition of utilization in newly-formed hybrid cells.

Although most mammalian cell lines can utilize either nicotinic acid or nicotinamide for the biosynthesis of nicotinamide adenine dinucleotide (NAD), thymidine kinase-deficient, mouse 3T3-4F cells are unable to utilize nicotinic acid. When 3T3-4E cells were fused with human D98/AH2 cells, autoradiography showed that the resultant heterokaryons synthesized NAD from nicotinic acid at rates comparable to the human parental cell. The rate of nicotinic acid utilization in heterokaryons remained unchanged over the four-day period of study following cell fusion. In contrast to the results observed with heterokaryons, nicotinic acid utilization was markedly reduced in hybrid cells. Of 100 hybrid clones examined at four or five days following cell fusion, 60 utilized nicotinic acid at rates less than one tenth that of the parental human cell. Similar results were observed in hybrid clones at nine or ten days following fusion. Uniformly high rates of NAD biosynthesis were observed in hybrid clones with nicotinamide as the precursor. This excludes the possibility that the reduction in nicotinic acid utilization in hybrid cells is due to a general metabolic dysfunction. The biochemical mechanism by which nicotinic acid utilization is markedly reduced has not been determined with certainty, however, several observations suggest genetic suppression.

Aminopterin↗
PubMed2005

Solubility of nicotinic acid in polyamidoamine dendrimer solutions.

In the present study we investigated the effect of ethylenediamine (EDA) core polyamidoamine (PAMAM) dendrimers on the aqueous solubility of nicotinic acid. The aqueous solubility of nicotinic acid was measured in the presence of dendrimers at room temperature in distilled water. The effect of variables, such as pH condition, concentration, surface functional group and generation (molecule size) of dendrimer, has been investigated. Results showed that the solubility of nicotinic acid in the dendrimer solutions was proportional to dendrimer concentration, both amine and ester-terminated dendrimers caused the higher increase in nicotinic acid solubility at higher pH conditions. The order in which the dendrimers increased the solubility at a constant pH condition was G4>G3>G2>G1. In addition, at each pH, the solubility of nicotinic acid was greater in the presence of amine-terminated dendrimers compared to the amine ester-terminated dendrimers possessing the same number of surface functional groups. Under suitable conditions PAMAM dendrimers can be highly effective used to enhance the solubility of nicotinic acid.

Dendrimers↗
PubMed1968

Mode of action of melinacidin, an inhibitor of nicotinic acid biosynthesis.

Melinacidin, a new antibacterial agent, blocked the synthesis of nicotinic acid and its amide in Bacillus subtilis cells. The inhibitory activity of the agent was reversed by nicotinic acid, its amide, or nicotinamide adenine dinucleotides, but not by l-kynurenine, l-3-hydroxykynurenine, l-hydroxyanthranilic acid, or quinolinic acid. These properties indicated that the antibiotic interferes with the conversion of quinolinic acid to nicotinate ribonucleotide by the enzyme quinolinate phosphoribosyl-transferase. However, the activity of a purified preparation of this enzyme derived from a Pseudomonas strain was not impaired by the antibiotic. This suggested that, in B. subtilis, melinacidin interferes with a reaction which occurs before the formation of quinolinic acid in the biosynthetic pathway leading to nicotinic acid. Failure of quinolinic acid to reverse melinacidin inhibition in B. subtilis cultures might be due to insufficient penetration of the cell membranes by quinolinate.

Anti-Bacterial Agents↗
PubMed1980

Effect of nicotinic acid on cholera-induced fluid movement and unidirectional sodium fluxes in rabbit jejunum.

Cholera toxin produces intestinal secretion and elevation of intestinal cyclic AMP. Nicotinic acid has been shown to prevent these responses. The effect of nicotinic acid on cholera toxin-induced secretion could be caused by decreased plasma-to-lumen flux, increased lumen-to-plasma flux, or a combination of both. The purpose of this study was to define the effects of nicotinic acid on net fluid movement and unidirectional sodium fluxes in rabbit jejunal loops exposed to cholera toxin. In the untreated animals receiving no nicotinic acid, the cholera toxin-exposed loops secreted 0.91 ml/cm/4h above the control loops receiving no cholera toxin (p < 0.01). On the other hand, pretreatment with 100 mg/kg nicotinic acid caused a striking decrease in secretion in the cholera toxin loop, so that the cholera toxin loop was not significantly different from the control loop. Unidirectional sodium fluxes in untreated animals showed that cholera toxin caused an increase in the plasma-to-lumen flux and a decrease in the lumen-to-plasma flux. Both effects were abolished by pretreating the animals with nicotinic acid. These studies indicate that nicotinic acid prevents cholera toxin-induced secretion by restoring the unidirectional fluxes to control levels.

Animals↗
PubMed1986

The metabolism of high intakes of tryptophan, nicotinamide and nicotinic acid in the rat.

1. The metabolic fate of high dietary intakes of nicotinamide, nicotinic acid and tryptophan, and of acute doses of nicotinamide and nicotinic acid, has been studied in the rat. A new high-pressure liquid chromatography method for measurement of the principal urinary metabolites of niacin is described. 2. Administration to rats of a single oral dose of nicotinamide or nicotinic acid (up to 100 mg/kg body-weight), or maintenance for 3 weeks on diets providing 150 mg nicotinamide or nicotinic acid/kg diet, resulted in only a small increase in the liver content of nicotinamide nucleotide coenzymes (NAD and NADP). The quantitative metabolism of nicotinamide and nicotinic acid differed, suggesting that intestinal bacterial deamidation is not the major fate of nicotinamide. 3. A high dietary intake of tryptophan (5.9 g/kg diet) led to a considerable increase in liver NAD(P) and also in urinary excretion of niacin metabolites. The results suggest that, as indicated by enzyme kinetic studies (Bender et al. 1982), the utilization of nicotinamide and nicotinic acid for nucleotide synthesis is limited, while there is little or no limitation of NAD(P) synthesis from the tryptophan metabolite quinolinic acid.

Animals↗