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PubMed1961

THIAMINE AND NICOTINIC ACID: ANAEROBIC GROWTH FACTORS FOR MUCOR ROUXII.

Bartnicki-Garcia, S. (Rutgers, the State University, New Brunswick, N. J.), and Walter J. Nickerson. Thiamine and nicotinic acid: Anaerobic growth factors for Mucor rouxii. J. Bacteriol. 82:142-148. 1961.-Mucor rouxii requires preformed thiamine and nicotinic acid for anaerobic growth. Such requirements are not manifested during aerobic incubation. Aerobically, the fungus was shown to be able to synthesize both vitamins. The yeastlike form and the filamentous form of anaerobically grown M. rouxii exhibit the same vitamin requirements. Thiamine can be substituted by its thiazole moiety. Under certain conditions, nicotinic acid was partly substituted by tryptophan, kynurenine, 3-hydroxykynurenine, and 3-hydroxyanthranilic acid.Anaerobically. the fungus (thiamine requiring) was about ten times more susceptible to pyrithiamine antagonism than the same organism grown aerobically (thiamine independent).

Journal Article↗
PubMed1988

Comparison of the biopotencies of nicotinic acid and nicotinamide for broiler chicks.

1. Two experiments were conducted with 1056 1-d-old Cobb x Cobb feather-sexed broiler chicks, to determine the relative nicotinic acid biopotencies of nicotinic acid (NA) and nicotinamide (NAm). 2. Two methods were used: the slope-ratio technique and the broken-line model. 3. In experiment 1, using the slope-ratio technique, NAm was 0.82 as active as NA in promoting growth to 21 d of age. In experiment 2 NAm was 0.96 as bipotent as NA. 4. Applying the broken-line model to the body weight data at 21 d of age for both NA and NAm in experiment 1, it was found that NAm had approximately 0.82 NA activity. The same analysis applied to the data of experiment 2 indicated that the biopotency of NAm was 1.09. 5. A t-test of the slope-ratio values obtained in both experiments indicated that the average (0.89) was not significantly different from 1.0. 6. It was concluded that the relative biopotencies of NA and NAm in broiler chicks fed a maize-soyabean meal diet were similar.

Animals↗
PubMed2006

[Nicotinic acid: an unjustly neglected remedy].

In human organism, the administration of nicotinic acid (niacin) leads to two types of effects. Within the physiological range (approximately = 20 mg/day), niacin has a vitamin-like role as pellagra preventing factor. The pharmacological dosage (approximately 0,5-4,5 g/day) substantially influences the plasma lipid and lipoprotein concentrations: decreases VLDL and LDL concentrations, changes the profile of LDL subfractions towards the larger particles as well as particles with lower density; it also profoundly increases the concentration of HDL-C in consequence of elevated concentration of HDL2 subfraction. Niacin as the only hypolipidemic drug reduces the lipoprotein(a) concentration. The hypolipidemic mechanism of niacin is different from that of other hypolipidemic drugs. On the basis of clinically controlled trials (both interventional epidemiological and angiographical), which satisfy the criteria of evidence-based medicine, it is possible to conclude that niacin falls unambiguously into the class of hypolipidemic drugs with proven beneficial effect not only on cardiovascular mortality and morbidity, but also on total mortality. Therefore, niacin should have an indisputable role in the pharmacological control of dyslipidemias. With the respect of basic mechanism (inhibition of the lipolysis of adipose tissue) with subsequent decrease in the concentration of free fatty acids and their flux to liver, niacin fulfils the criteria for pathogenetic treatment of atherogenic dyslipidemia in metabolic syndrome. The prerequisite condition for the niacin treatment is the respect for serious adverse effects and possible health hazards of administration (skin flush, hepatotoxicity and deterioration of glucose homeostasis). Recently discovered extrahypolipidemic effects of niacin (antioxidative activity, facilitation of reverse cholesterol transport, activation of PPAR-gamma, antithrombotic effects) and the introduction of drug forms with sustained (extended resp.) release of active compound (that minimizes the adverse effects and administration hazards) form together the basis for firm statement that the derivatives of nicotinic acid should be introduced to the clinical practice in Czech Republic.

Humans↗
PubMedDate not supplied

[Nicotinic acid metabolism in patients with non-coronarogenic heart diseases].

To study the supply with nicotinic acid, 74 patients with rheumatic fever of varying degree and circulatory disorders, 10 patients with infectious-allergic myocarditis, 15 with tonsilogenous myocardiodystrophy were examined. Seventy normal subjects served as control. The supply with vitamin PP was evaluated from the blood content of NAD, NADP and N'-methylnicotinamide and its excretion with urine. All the patients with myocarditis and rheumatic fever demonstrated a decrease in the nicotinic acid supply which became more marked as the degree of rheumatic fever rose and circulatory failure supervened. In patients with tonsilogenous myocardiodystrophy , the disturbance of the vitamin supply was less overt.

Adult↗
PubMed1995

Physiological and performance responses to nicotinic-acid ingestion during exercise.

The purpose of this study was to assess how selected physiological and performance responses are affected when the normal increase in plasma free fatty acid concentration during exercise is blunted by ingesting nicotinic acid. On four occasions, 10 subjects cycled at 68 +/- 1% VO2peak for 120 min followed by a timed 3.5-mile performance task. Every 15 min during exercise, subjects ingested 3.5 ml.kg LBM-1 of one of four beverages: 1) water placebo (WP), 2) WP + 280 mg nicotinic acid.l-1 (WP + NA), 3) 6% carbohydrate-electrolyte beverage (CE), and 4) CE + NA. Ingestion of nicotinic acid (WP + NA and CE + NA) blunted the rise in FFA associated with WP and CE; in fact, NA ingestion effectively prevented FFA from rising above rest values. The low FFA levels with NA feeding were associated with a 3- to 6-fold increase in concentrations of human growth hormone throughout exercise. The mean performance time for CE (10.7 min) was significantly less than for WP (12.2 min) and WP + NA (12.8 min), but did not differ from CE + NA (11.4 min). The results indicate that blunting the normal rise in FFA alters the hormonal response to exercise and reduces the capacity to perform high-intensity exercise.

Blood Glucose↗
PubMed1991

A comparison between nicotinic acid and acipimox in hypertriglyceridaemia--effects on serum lipids, lipoproteins, glucose tolerance and tolerability.

Serum and lipoprotein lipid levels, oral glucose tolerance and side-effects were compared in an open cross-over study of 31 non-diabetic patients with hypertriglyceridaemia (type II B and IV) before and after 6 weeks of treatment with nicotinic acid (3 g daily) and acipimox (0.75 g daily), a new nicotinic acid-like drug, respectively. Acipimox was about equally potent in reducing serum and VLDL lipid levels and in increasing HDL cholesterol levels. Acipimox had no significant negative effects on glucose metabolism measured by an oral glucose tolerance test compared with nicotinic acid, which decreased the late glucose tolerance as well as the area under the glucose curve (P less than 0.05 for the difference between the two treatments). The incidence and severity of flush or any other recorded side-effects was higher after nicotinic acid treatment than after acipimox. In addition, no effects on laboratory parameters such as liver enzymes and uric acid were seen after treatment with acipimox. The results of this study demonstrate that acipimox is a satisfactory alternative to nicotinic acid in patients with hypertriglyceridaemia.

Adult↗
PubMedDate not supplied

[Role of nicotinic acid and its derivatives in disorders of nervous system function].

Participation of nicotinic acid and its derivates in the functioning of nervous system is considered basing on the data from literature. It is supposed that the favourable therapeutic effects of nicotinamide, nicotinic acid and their active biological form--NAD are realized due to the mechanisms of their functioning in the nervous system, for treating schizophrenia, epilepsy and other diseases of the nervous system.

Humans↗
PubMed2005

Role of the nicotinic acid group in NAADP receptor selectivity.

Nicotinic acid adenine dinucleotide phosphate (NAADP) has been shown to be an intracellular Ca2+-releasing messenger in a wide variety of systems to date. Its actions are both potent and highly specific despite differing structurally from the endogenous cellular co-factor and its precursor, NADP, only in the substitution of a hydroxyl for the amine group at the 3' position of the pyridine ring. This substitution allows NAADP to bind to a membrane-localized binding site in sea urchin egg homogenates with an IC50 at least 1000-fold greater than that of NADP as measured by competition radioligand binding assays. This suggests that the NAADP receptor protein must include certain features in the NAADP binding site that regulate this specificity. In order to investigate this interaction, we synthesised a series of NAADP analogues differing from NAADP at the 3' position of the pyridine ring that included both simple carboxylic acid analogues as well as a series of chemical isosters. We then investigated both their affinity for the NAADP binding site in sea urchin egg homogenates and their ability to activate the NAADP sensitive Ca2+ channel. We hereby show that a negative charge at the 3' position is an important determinant of affinity but the protein displays a large tolerance for the size of the group. Furthermore, the protein does not easily accommodate multiple charged groups or large uncharged groups.

Animals↗
PubMed1994

Nicotinic acid hydroxylase from Clostridium barkeri: electron paramagnetic resonance studies show that selenium is coordinated with molybdenum in the catalytically active selenium-dependent enzyme.

Nicotinic acid hydroxylase from Clostridium barkeri contains selenium in an unidentified form that is dissociated as a low molecular weight compound upon denaturation of the enzyme. Other cofactors of this enzyme are molybdopterin, FAD, and iron-sulfur clusters. In the current study, we show that the enzyme, as isolated, exhibits a stable Mo(V) electron paramagnetic resonance (EPR) signal ("resting" signal) and that this signal is correlated with the selenium content and nicotinate hydroxylase activity of the enzyme. Substitution of 77Se for normal selenium isotope abundance results in splitting of the Mo(V) EPR signal of the native protein without affecting the iron signals of the FeS clusters. The Mo(V) EPR signal and nicotinic acid hydroxylase activity of enzyme isolated from cells grown in selenium-deficient medium are barely detectable. In contrast, the EPR signals of the FeS clusters, the electronic absorption spectrum, the NADPH oxidase activity, and the chromatographic behavior are changed little and are typical of active selenium-containing enzyme. An EPR signal indicative of the presence of molybdenum in the selenium-deficient enzyme also is exhibited. From these results, we conclude that a dissociable selenium moiety is coordinated directly with molybdenum in the molybdopterin cofactor and, moreover, this selenium is essential for nicotinic acid hydroxylase activity.

Bacterial Proteins↗
PubMed1990

The effects of nicotinic acid treatment on high density lipoprotein particle size subclass levels in hyperlipidaemic subjects.

Twenty-three consecutive hyperlipidaemic patients were treated with 4 g nicotinic acid daily for 6 weeks. The treatment resulted in the expected reduction of serum very low density (VLDL) and low density lipoproteins (LDL) and in the increase of high density lipoproteins (HDL). The cholesterol concentration of the latter fraction rose by 45%. The HDL fraction was isolated by ultracentrifugation and then subjected to gradient gel electrophoresis (gge), in order to determine the HDL particle size distribution, before and after treatment. The increase of HDL was almost exclusively confined to the largest HDL (gge) subclass HDL-2b, the protein content of which rose by 183%. In contrast, there was about a 25% decrease in the concentration of the smallest HDL(gge) subclasses, HDL-3b and HDL-3c. The levels of HDL-2b and VLDL triglycerides showed a significant inverse correlation before, as well as after, treatment. Multiple partial correlation analysis demonstrated, however, that the nicotinic acid induced increase in HDL-2b concentration showed a highly significant inverse correlation to the decrease in LDL cholesterol, but not to the decrease in VLDL triglyceride levels. Recent studies, in particular those regarding the negative correlation between both the degree and progression of coronary atherosclerosis and the HDL-2b concentration in young male myocardial infarct patients, suggest that the profound increase of HDL-2b levels by nicotinic acid treatment in hyperlipidaemic patients might be of considerable importance in the protection of coronary atherosclerosis.

Adult↗
PubMedDate not supplied

[Properties and biosynthesis of acetyl-CoA-carboxylase from chicken liver with administration of nicotinic acid during stimulation of lipogenesis].

Acetyl-CoA-carboxylase is isolated and purified to a homogeneous state from the chicken liver with alimentary lipogenesis stimulation. Under the action of nicotinic acid in vivo the specific enzyme activity is shown to decrease considerably followed by some variations in its properties. According to the results obtained during ultracentrifugation and PAAG electrophoresis nicotinic acid causes partial enzyme deaggregation with simultaneous increase of its phosphorylation. The latter is accompanied by a rise in the content of phosphate labile to alkali on acetyl-CoA-carboxylase subunits. Nicotinic acid in vivo has practically no effect on acetyl-CoA-carboxylase synthesis and decay rate. Its inhibiting action is induced by stimulation of enzyme phosphorylation.

Acetyl-CoA Carboxylase↗
PubMedDate not supplied

Synthesis and degradation of NAD in guinea pig cardiac muscle: I. Dependence upon the extracellular concentration of nicotinamide and nicotinic acid.

The NAD concentration as well as the 14C-incorporation in NAD and the disappearance of 14C-NAD were studied in spontaneously beating atria of guinea pigs at high and low concentrations of the precursors nicotinamide or nicotinic acid. Atria were incubated in Krebs-Henseleit solution containing 15 mM glucose and the appropriate precursors at 30 degrees C. The control NAD concentration (33 nMol/100 mg w.w.) remained unchanged during a 24-h-incubation time. -20 mM 14C-nicotinamide increased the total NAD about three-fold (90 nMol/100 mg w.w.) after an incubation period of 24 h, with positive effects on the performance. The incorporation rate in 14C-NAD was calculated to be 43.7 nMol/100 mg w.w. . 24 h. The ADPR moiety for the NAD synthesis stemmed from an endogenous pool. Between 5 and 20 mM nicotinamide the increase in the NAD concentration followed an apparent Michaelis-Menten kinetics with a Km of 6.1 mM nicotinamide and a Vmax of 70.92 nMol NAD/100 mg w.w. . 24 h. This can be explained as a new synthesis of NAD by a high concentration of nictoinamide and also by a decreased degradation of NAD, due to inhibition of the glycohydrolase by the high concentration of nicotinamide. The ratio of incorporation and disappearance of 14C-NAD during the 8th and 16th h incubation period was 2:1. After pre-incubation with 20 mM nicotinamide for an 8-h period the NAD concentration decreased to normal values after incubation for 8 h in a nicotinamide free medium. -20 mM 14C-nicotinic acid did not change the total NAD level and no significant incorporation in 14C-NAD could be detected, whereas negative effects on the performance occurred. -10 muM 14C-nicotinamide showed a slight increase in the total NAD concentration (39.7 nMol/100 mg w.w.) and in the 14C-incorporation (4.8 nMol/100 mg w.w.) within 24 h. -10 muM 14C-nicotinic acid seemed here to be the better precursor in this concentration. The NAD concentration increased to 49.8 nMol/100 mg w.w. after a 16 h incubation period and the incorporation in 14C-NAD was 12.1 nMol/100 mg w.w. after an incubation time of 24 h. As consequences of the observed different influences of each precursor on NAD turnover and NAD concentration the pathways of NAD synthesis and degradation must be studied. The importance of an increased NAD level for the energy metabolism of the cardiac muscle under aerobic and anaerobic conditions is discussed.

Animals↗
PubMed1992

[Mechanisms of hepatoprotective action of new nicotinic acid derivatives in experimental CCL4-induced liver injury].

New biologically active compounds (BAC) created on the basis of nicotinic acid possess hepatoprotective action. The preparations were introduced preventively in doses of 10 mg/kg during 14 days. Litonit and nicogamol increased survival of experimental animals by 36.8% and nicotinic acid by 26.8%. ALT, AST, GGT activity in the blood serum was reduced. The activity of the main antioxidant enzymes (SOD and catalase) grew in the rat liver tissue in parallel with inhibition of DK and MDA activity. Morphological picture of the rat liver, most evident after application of litonit improved. Hepatoprotective action of these BAC are attributed to their membrano stabilizing effects.

Animals↗
PubMed1996

Immune response and disease resistance of calves fed chromium nicotinic acid complex or chromium chloride.

Twenty-one Holstein bull calves (< 7 d of age at the initiation of the experiment) fed a milk replacer diet were used to assess the effects of supplemental Cr on immune response. Treatments consisted of milk replacer without supplemental Cr (control) or milk replacer with 0.4 ppm of supplemental Cr from CrCl3 or a Cr-nicotinic acid complex. On d 64, increases in skinfold thickness after an intradermal injection of phytohemagglutinin were measured to evaluate cell-mediated immune response. Calves supplemented with Cr-nicotinic acid complex had a greater response than did controls at 6, 12, 24, and 48 h after injection. Calves supplemented with CrCl3 had a greater response than did controls at 24 and 48 h after injection. In vitro blastogenic responses of lymphocytes to phytohemagglutinin or pokeweed mitogen and antibody response to porcine red blood cells were not affected by treatment. Following a disease challenge with an intranasal dose of infectious bovine rhinotracheitis on d 75, body temperature tended to be lower for calves supplemented with Cr-nicotinic acid complex than for control calves. Calves supplemented with either Cr source had lower serum cortisol concentrations at 5 d after challenge. Chromium supplementation enhanced cell-mediated immune function.

Animals↗