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At least 1,135 records · Page 63Linked to original sources
PubMed2000

Production of B-group vitamins by two Azotobacter strains with phenolic compounds as sole carbon source under diazotrophic and adiazotrophic conditions.

Azotobacter vinelandii strain ATCC 12837 and A. chroococcum strain H23 (CECT 4435) were able to grow on N-free or NH4Cl-amended chemically-defined (Burk's) media, with protocatechuic acid (1-2 mmol 1(-1)) or sodium p-hydroxybenzoate (1-10 mmol 1(-1)) as sole carbon (C) sources. At a concentration of 2 mmol 1(-1), both substrates supported nitrogen fixation (acetylene reduction assay) at similar or higher rates than bacteria grown in control media amended with 2 mmol 1(-1) sodium succinate as C source. The two strains produced the B-group vitamins niacin, pantothenic acid, thiamine, riboflavin and biotin after 72 h of growth in chemically-defined media with 2 mmol 1(-1) protocatechuic acid, sodium phydroxybenzoate or sodium succinate as sole C source, either in N-free media or in media amended with 0.1% NH4Cl. Quantitative production of all vitamins was affected by the use of the different C and N substrates.

Ammonium Chloride↗
PubMed1978

GABA transaminase provides an alternative route of beta-alanine synthesis in Aspergillus nidulans.

Three unlinked genes where mutation can lead to D(+)-pantothenic acid auxotrophy in Aspergillus nidulans have been identified. pantoA is probably the structural gene for pantothenate synthetase (EC 6.3.2.1) whilst pantoB and pantoC are involved in the syntheses of D-pantoic acid and beta-alanine, respectively. A pantoC- mutant is tentatively considered to be blocked in conversion of 5,6-dihydrouracil to beta-ureidopropionate. An alternative route of beta-alanine biosynthesis occurs by the transamination of malonic semialdehyde, catalysed by GABA transaminase. The possibility that beta-alanine can be replaced by certain structurally related compounds and yet nevertheless yield biologically active coenzyme A analogues is discussed.

4-Aminobutyrate Transaminase↗
PubMed2002

The alanine racemase gene alr is an alternative to antibiotic resistance genes in cloning systems for industrial Corynebacterium glutamicum strains.

The potential of the alanine racemase gene alr from Corynebacterium glutamicum ATCC 13032 to substitute for antibiotic resistance determinants in cloning systems has been investigated. The alr gene was identified by a PCR technique and its nucleotide sequence was determined. The deduced protein revealed the highest amino acid sequence similarity to the Alr protein from Mycobacterium smegmatis with 45% identical and 58% similar amino acids. A defined alr deletion mutant of C. glutamicum displayed a strict dependence on the presence of D-alanine for growth on complex and minimal medium. The alr gene was placed on a novel C. glutamicum vector which is completely free of antibiotic resistance genes. In vivo complementation of the chromosomal alr deletion with alr-carrying vectors permitted growth of the mutant strain in the absence of external D-alanine and provided strong selective pressure to maintain the plasmid. The alr gene enabled the selection of C. glutamicum transformants with a similar efficiency as the tetracycline resistance gene tetA(33). These data provided experimental evidence that the alr gene can be applied as an alternative selection marker to antibiotic resistance genes in industrial C. glutamicum strains. In an application example, the novel deltaalr host-alr(+) vector-system for C. glutamicum was used to overproduce the vitamin D-pantothenic acid.

Alanine Racemase↗
PubMed1986

Acute encephalopathy with hyperammonemia and dicarboxylic aciduria during calcium hopantenate therapy: a patient report.

We report a 3-year-old Japanese girl who developed acute encephalopathy while receiving calcium hopantenate (Calcium D-(+)-4-(2, 4-dihydroxy-3,3-dimethylbutyramido) butyrate hemihydrate). She had hyperammonemia, elevated CPK, lactic acidemia and pyruvic acidemia, however, she did not show elevated SGOT or SGPT. Calcium hopantenate has been used in Japan for the treatment of mental retardation with behavior abnormalities. Recently there have been three reports on the occurrence of Reye-like syndrome in patients receiving this drug. Clinical signs and laboratory data of these patients are similar to those of Reye syndrome. Calcium hopantenate causes pantothenic acid deficiency in the young rat, which may reduce the content of coenzyme A. If this drug decreases coenzyme A biosynthesis, it may reduce beta-oxidation of fatty acids and levels of dicarboxylic acids would increase because of increasing omega-oxidation. We suspect that there is a possible relationship between the occurrence of acute encephalopathy and calcium hopantenate therapy.

Acute Disease↗
PubMed1984

[Electrocardiogram changes in the rat by coenzyme A action].

The authors, having in a previous series of experiments observed that coenzyme A, administered intravenously in doses from 200 to 500 U.L., causes an immediate and transient decrease of the sinus rate, wanted to study to which part of the complex molecule of coenzyme A such effect is due. That's why they studied the action, intravenously, of pantothenic acid (200-400 mg/Kg), of cysteine (40-80 mg/Kg), of pantethein (40-100 mg/Kg) and of adenosine (4-10 mg/Kg). The results of the experiments demonstrate that the former bradycardia is due to adenosine, whereas the other substances have not this effect.

Adenosine↗
PubMed2001

CJ-15,801, a novel antibiotic from a fungus, Seimatosporium sp.

A novel antibiotic, CJ-15,801 (I), was isolated from the fermentation broth of a fungus, Seimatosporium sp. CL28611. The structure was determined to be a pantothenic acid analog having an alpha,beta-unsaturated carboxylic acid moiety by spectroscopic analyses. The compound inhibits the growth of multi-drug resistant (MDR) Staphylococcus aureus strains with MIC ranging from 6.25 to 50 microg/ml.

Anti-Bacterial Agents↗
PubMed1989

Problems in estimating the extent of coprophagy in the rat.

The quantity of re-ingested faeces was calculated by comparing faecal dry matter of unrestricted rats and coprophagy-restricted rats after correcting for differences in food intake. Due to high day-to-day variations of produced and re-ingested faeces it was not possible to calculate precisely the extent of coprophagy of an individual rat at a particular day with this difference method. Reliable quantitative estimates require at least two rats and a collection period of 7 d. When fed on a nutritionally complete diet, rats re-ingested 0-11% of their faeces. When fed on low-protein diets (66 g egg albumin/kg) or diets diluted with 200 g cellulose/kg, coprophagy was not significantly increased. A high re-ingestion rate (6-25%) was observed with thiamin and pantothenic acid deficiencies. After re-ingestion of faeces had been prevented for 1 week, the amount of faeces re-ingested during the subsequent week without tail-cups was increased twofold. It is concluded that rats are able to regulate the amount of faeces eaten precisely according to their requirements.

Animals↗
PubMed1983

Altered coenzyme A and carnitine metabolism in pressure-overload hypertrophied hearts.

Changes in the total content and acylation state of coenzyme A (CoA) and carnitine in the heart result in alterations in fatty acid metabolism that may be associated with ventricular dysfunction. The present study was undertaken to determine whether abnormal myocardial CoA and carnitine metabolism occur in pressure-overload hypertrophy and congestive heart failure. Right ventricular hypertrophy was induced in cats by pulmonary artery (PA) banding. Total tissue CoA was reduced by 50% in the hypertrophied right ventricle and 25% in the nonhypertrophied left ventricle of PA-banded cats in the presence or absence of heart failure. No alterations were observed in long-chain fatty acyl CoA levels in either ventricle of PA-banded cats. In addition, a 20% reduction in total CoA was also observed in hypertrophied hearts of rats subjected to aortic banding. Although the CoA content was reduced in hypertrophied cat hearts, myocardial tissue levels of its precursor, pantothenic acid, were unaltered. Total tissue carnitine and long-chain fatty acyl-carnitine levels were unchanged in both ventricles of PA-banded cats; however, total carnitine was reduced by 25% in hypertrophied rat hearts. This study establishes a marked reduction in myocardial CoA content in pressure-overload hypertrophy.

Animals↗
PubMed2003

The optimization of HPLC-UV conditions for use with FTIR detection in the analysis of B vitamins.

The water-soluble vitamins thiamine (B(1)), riboflavin (B(2)), pantothenic acid (B(5)), and pyridoxine (B(6)) are separated by high-performance liquid chromatography. The mobile phase, column temperature, and flow rate are optimized so that the chromatograph can be used with a Fourier-transform infrared (FTIR) detector. Reproducibility, linearity, and detection limits are evaluated for method validation. Finally, this method is successfully transferred to liquid chromatography-FTIR with a standard mixture.

Chromatography, High Pressure Liquid↗
PubMed1981

Regulation of coenzyme A synthesis in heart muscle: effects of diabetes and fasting.

Regulation of coenzyme A (CoA) synthesis was studied in the isolated perfused rat heart. Incorporation of [14C]pantothenic acid ([14C]PA) into CoA was determined to estimate rates of CoA synthesis. Although CoA levels were elevated in hearts removed from fasted and diabetic animals, in vitro rates of CoA synthesis were not elevated. The presence of 1.2 mM palmitate, 5 mM pyruvate, or 10 mM beta-hydroxybutyrate in the perfusate-reduced PA incorporation into CoA in control hearts by 40, 60, and 80%, respectively. Insulin (25 mU/ml) reduced incorporation by 90%. The alterations in CoA synthesis in hearts perfused with buffer containing palmitate, pyruvate, beta-hydroxybutyrate, and insulin were associated with no change in myocardial PA uptake. Data indicate that these substrates and insulin inhibit the first step in the pathway of CoA synthesis, pantothenate kinase. Because insulin is a strong inhibitor of CoA synthesis in vitro, decreased circulating levels of insulin in fasted and diabetic animals may account for the increased levels of CoA in vivo.

Alloxan↗
PubMed1976

Regulation of phosphatidylcholine synthesis in rat liver endoplasmic reticulum.

The biosynthesis of phosphatidylcholine in rat liver microsomal preparations catalysed by CDP-choline-1,2-diacylglycerol cholinephosphotransferase (EC 2.7.8.2) was inhibited by a combination of ATP and CoA or ATP and pantetheine. ATP alone at high concentrations (20 mM) inhibits phosphatidylcholine formation to the extent of 70%. In the presence of 0.1 mM-CoA, ATP (2 mM) inhibits to the extent of 80% and in the presence of 1 mM-pantetheine to the extent of 90%. ADP and other nucleotide triphosphates in combination with either CoA or pantetheine are only 10-30% as effective in inhibiting phosphatidylcholine synthesis. AMP(CH2)PP [adenosine 5'-(alphabeta-methylene)triphosphate] together with CoA inhibits to the extent of 59% and with pantetheine by 48%. AMP-P(CH2)P [adenosine 5'-(betagamma-methylene)triphosphate] together with either CoA or pantetheine had no significant effect on phosphatidylcholine formation. Other closely related derivatives of pantothenic acid were without effect either alone or in the presence of ATP, as were thiol compounds such as cysteine, homocysteine, cysteamine, dithiothreitol and glutathione. Several mechanisms by which this inhibition might take place were ruled out and it is concluded that ATP together with either CoA or pantetheine interacts reversibly with phosphatidylcholine synthetase to cause temporarily the inhibition of phosphatidylcholine formation.

Acetyl Coenzyme A↗
PubMed2006

Allergic contact dermatitis to panthenol and cocamidopropyl PG dimonium chloride phosphate in a facial hydrating lotion.

Dexpanthenol is the alcohol corresponding to pantothenic acid (the water-soluble vitamin B(5)). Although it is a common ingredient in many pharmaceuticals and cosmetics, contact allergy is relatively uncommon. Cocamidopropyl PG dimonium chloride phosphate is a phospholipid complex derived from pure coconut oil, and contact allergy is rare. We report a case of allergic contact dermatitis to panthenol and cocamidopropyl PG dimonium chloride phosphate in a facial hydrating lotion.

Administration, Cutaneous↗
PubMedDate not supplied

[Differentiated approaches to the treatment of nonstabilized primary open-angle glaucoma with normalized intraocular pressure considering its pathogenic features].

Clinical efficiency of dedystrophic treatments for nonstabilized primary open-angle glaucoma (POAG) in the presence of normalized intraocular pressure is compared in 168 patients (246 eyes). In one group of patients ischemic angiopathy and hyperreactivity of optic vessel adrenoreceptors associated with hypokinetic central hemodynamics and constitutional metabolic status of the organism was corrected by cinnarisin and riboxin. Patients with predominating congestive angiopathy symptoms, hyper- or eukinetic circulation and "slow" acetylation were treated by pantothenic acid, endotelon, and hyperbaric oxygenation. In both groups epithalamine, eiconol, and magnetic laser therapy were used, if indicated. This helped stabilize the process in 91% patients with initial POAG, in 87.5% with well-developed condition vs. 66.1% and 38.2% patients treated by traditional therapy (period of observation 3 years).

Aged↗
PubMed2002

Synthesis of a rabbit polyclonal antibody to the human sodium-dependent multivitamin transporter.

In mammalian cells, biotin is covalently attached to carboxylases and histones and is required for cell proliferation and function. Cellular uptake of biotin (as well as pantothenic acid and lipoic acid) is mediated by the sodium-dependent multivitamin transporter, SMVT. Studies of cellular biotin homeostasis have been hampered by the lack of an antibody to SMVT. Here, we describe the synthesis of a rabbit polyclonal antibody to human SMVT. Using this antibody, SMVT has been identified in human peripheral blood mononuclear cells, Caco-2 cells, and HepG2 cells. Moreover, we observed that cells respond to proliferation with increased synthesis of SMVT.

Animals↗
PubMedDate not supplied

[Mechanism of pantogam potentiation of certain effects of hexobarbital and sodium barbital and inhibition of phenamine hyperactivity].

Experiments on albino mice and rats have shown that pantogam, a derivative of pantothenic acid, potentiates the hypnotic effects of hexobarbital and barbital and enhances the effect of subthreshold doses of hexobarbital. The drug inhibits the amphetamine action in the amphetamine hyperaction test without affecting hexobarbital and amphetamine metabolism, or without increasing the blood-brain barrier permeability for these compounds and barbital. Pantogam does not influence the intensity of ethylmorphine N-demethylation in liver homogenates and the content of cytochrome P 450 and b5 in liver microsomes.

Amphetamine↗
PubMed1980

Coenzyme A-synthesizing protein complex of Saccharomyces cerevisiae.

The coenzyme A-synthesizing protein complex (CoA-SPC) is a multienzyme complex of Saccharomyces cerevisiae (Bakers' yeast), which has a molecular weight in excess of 200,000 as determined by Sephadex G-200 column chromatography. This multienzyme complex, which is insoluble in the crude yeast cell lysate, has been purified 229-fold. A cellular component of the yeast cell lysate, referred to as t-Factor, with a molecular weight of 400-1000 and chloride ion are involved in the solubilization of CoA-SPC. The CoA-SPC requires L-cysteine, D-pantothenic acid and ATP as substrates. The terminal CoA-SPC-bound intermediate is dephospho-CoA, which is subsequently phosphorylated and released from the complex as CoA. The sequence of reactions for the synthesis of CoA by the CoA-SPC differs significantly from those previously proposed for other systems. It could be that the reaction sequence is unique for the yeast cell.

Adenosine Triphosphate↗
PubMed1987

[Decrease in the concentration of leukocyte acetylation coenzyme associated with vitamin precursor deficiency in patients with alcoholic delirium].

Sixty-three patients with the typical variant of delirium tremens were examined. The results showed a marked reduction (by 8.7 times) in levels of coenzyme A (CoA) in leukocytes, which was indicative of deficiency of the coenzymic form of pantothenic acid (PA). Changes in CoA concentrations in leukocytes observed at the height of psychosis in patients with alcoholic delirium as compared to other parameters of PA metabolism have great significance for the assessment of vitamin metabolism. PA deficiency was more expressed in cases of long-standing and massive alcoholization which induces an earlier development of psychosis. CoA levels in leukocytes may be used as a parameter of detoxication processes in patients with delirium tremens. The data obtained are considered as indication for administration of PA drugs in combined detoxifying therapy of alcoholic psychoses.

Adult↗