PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Acids”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1979

Conversion of 7-ketolithocholic acid to ursodeoxycholic acid by human intestinal anaerobic microorganisms: interchangeability of chenodeoxycholic acid and ursodeoxycholic acid.

Chenodeoxycholic acid, ursodeoxycholic acid and 7-ketolithocholic acid were incubated with human intestinal bacteria (source: 4 healthy males) at 37 degrees C for 72 hours in an anerobic condition. The bile acids of the products in culture medium were identified by three independent methods, thin layer chromatography, gas-liquid chromatography and GLC-mass spectrometry. Lithocholic acid, ursodeoxycholic acid and 7-ketolithocholic acid were observed in the culture of chenodeoxycholic acid. Lithocholic acid, chenodeoxycholic acid and 7-ketolithocholic acid were observed in the culture of ursodeoxycholic acid. Chenodeoxycholic acid and ursodeoxycholic acid were produced from 7-ketolithocholic acid. These data may suggest that chenodeoxycholic acid and ursodeoxycholic acid are interconvertible via 7-ketolithocholic acid by the mixed culture of human intestinal microorganisms under an anaerobic condition.

Anaerobiosis↗
PubMed1976

Biosynthesis of stizolobinic acid and stizolobic acid in higher plants. An enzyme system(s) catalyzing the conversion of dihydroxyphenylalanine into stizolobinic acid and stizolobic acid from etiolated seedlings of Stizolobium hassjoo.

It was demonstrated that an enzyme system(s) extracted from etiolated seedlings of Stizolobium hassjoo catalyzed the conversion of L-dihydroxyphenylalanine into stizolobinic acid, alpha-amino-6-carboxy-2-oxo-2H-pyran-3-propionic acid, and stizolobic acid, alpha-amino-6-carboxy-2-oxo-2H-pyran-4-propionic acid, in the presence of NADP+ or NAD+ under aerobic conditions. Enzymically synthesized radioactive stizolobinic acid and stizolobic acid isolated from the reaction mixtures were purified and confirmed to have constant specific radioactivities by cocrystallization with authentic samples. Maximal activity of the enzyme preparation was obtained by using an insoluble polyphenol adsorbent (Polyclar AT) and a reducing agent (araboascorbic acid) in the extraction medium and by subsequent fractionation of the extract with ammonium sulfate followed by Sephadex G-25 gel filtration. Catalytic activity of the enzyme preparation was more unstable under aerobic condition than anaerobic. Attempts to stabilise the enzyme activity were made by the use of many substances which are known to stabilise other enzymes or expected to arrest the inactivation. Evidence is provided in this paper that the previously proposed biosynthetic pathways of stizolobinic acid and stizolobic acid from dihydroxyphenylalanine proceeded in the cell-free system from etiolated seedlings of S. hassjoo.

Aerobiosis↗
PubMed1975

Enzymic reactions of fatty acid hydroperoxides in extracts of potato tuber. II. Conversion of 9- and 13-hydroperoxy-octadecadienoic acids to monohydroxydienoic acid, epoxyhydroxy- and trihydroxymonoenoic acid derivatives.

1. Crude extracts and partially purified enzyme preparations from potato tubers catalyse, at pH 5-7, the conversion of linoleic acid hydroperoxides to a range of oxygenated fatty acid derivatives. 2. 9-D- and 13-L-hydroperoxide isomers are converted at similar rates to equivalent (isomeric) products. 3. The major products from the 13-hydroperoxide isomer were identified as the corresponding monohydroxydienoic acid derivative, threo-11-hydroxy-trans12,13-epoxy-octadec-cis9-enoic acid and 9,12,13-trihydroxy-octadec-trans10-enoic acid. The corresponding products from the 9-hydroperoxide were the monohydroxydienoic acid, 9,10-epoxy-11-hydroxy-octadec-12-enoic acid and 9,10,13-trihydroxy-octadec-11-enoic acid. 4. No separation of activities forming the different products was achieved by partial purification of enzyme extracts. 5. Product formation was unaffected by EDTA, CN-, sulphydryl reagents or glutathione but was reduced by boiling the extracts. 6. This system is compared with the 9-hydroperoxide-specific enzymic formation of divinyl ether derivatives by potato extracts.

Fatty Acids, Unsaturated↗
PubMed1975

Pyridine-2, 6-dicarboxylic acid (dipicolinic acid) formation in Bacillus subtilis. II Non-enzymatic and enzymatic formations of dipicolinic acid from alpha, epsilon-diketopimelic acid and ammonia.

Non-enzymatic formation of dipicolinic acid (DPA) from diketopimelic acid and ammonia was clearly demonstrated using a new method for DPA analysis. The reaction rates of DPA formation were almost the same under aerobic and anaerobic conditions. Nearly equimolecular quantities of DPA and tetrahydrodipicolinic acid were detected in spontaneous reaction mixture. The spontaneous reaction seemed to be due to dismutation of dihydrodipicolinic acid, resulting in DPA and tetrahydrodipicolinic acid. The apparent optimum pH of the spontaneous reaction was 8.2 and the maximal rate of DPA formation was observed with a 1 : 4 molar ratio of diketopimelic acid to ammonia. The rate of the spontaneous reaction was stimulated by ferrous sulfate, FMN, and riboflavin. Dihydrodipicolinate reductase catalyzes the reduction of dihydrodipicolinate, prepared from pyruvate and aspartic beta-semialdehyde, with NADPH as reductant. The reductase was isolated from Bacillus subtilis, and found to stimulate DPA formation from diketopimelic acid and ammonia. The enzymatic DPA formation was absolutely dependent on oxygen, and optimum pH was 6.4. The catalytic action of the enzyme was similar to that of the oxidase. Possible mechanisms of DPA formation from diketopimelic acid and ammonia are proposed.

Aerobiosis↗
PubMed1979

Urinary excretion of conjugated homovanillic acid, 3,4-dihydroxyphenylacetic acid, p-hydroxyphenylacetic acid, and vanillic acid by persons on their usual diet and patients with neuroblastoma.

We report quantitative data on beta-glucuronidase- and sulfatase-hydrolyzable conjugates of homovanillic acid, 3,4-dihydroxyphenylacetic acid, p-hydroxyphenylacetic acid, and vanillic acid in the urine of 20 apparently normal and healthy control persons and of three patients with neuroblastoma. We used organic solvent extraction and capillary gas chromatography. There was considerable person-to-person variation in the conjugation percentages calculated. Mean conjugated percentages of the four compounds for 16 normal healthy persons 2.5--40 years of age were, respectively, 12%, 33%, 14%, and 35%. For newborns and patients with neuroblastoma, these percentages were somewhat different. Increased amounts of vanillic acid were found in the urine of the patients with neuroblastoma, but results of a small metabolic study in rats suggest that this increase most probably is of dietary origin.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1978

5-Methyltetrahydrofolic acid, 5-formyltetrahydrofolic acid (folinic acid), and folic acid requirements of normal and Rous sarcoma virus-infected chicken fibroblasts.

Normal and Rous sarcoma virus-infected chicken fibroblasts proliferate maximally in a culture medium containing a physiological (10 ng/ml) concentration of 5-methyltetrahydrofolic acid or folinic acid (5-formyltetrahydrofolic acid), while their maximal proliferation requires a hyperphysiological (1000 ng/ml) concentration of folic acid. The normal and Rous-infected fibroblasts do not differ in their requirements for 5-methyltetrahydrofolate, folinic acid, or folic acid.

Animals↗
PubMed1979

Pattern of aliphatic dicarboxylic acids in uremic serum including a new organic acid, 2,4-dimethyladipic acid.

(1) 2,4-Dimethyladipic acid was first identified in normal human urine using gas chromatography-mass spectrometry. Urinary excretion of 2,4-dimethyladipic acid in 7 healthy adults ranged from 4.9 mumol to 14 mumol per 24 h. (2) Succinic acid, adipic acid, 3-methyladipic acid, 2,4-dimethyladipic acid, pimelic acid and azelaic acid were identified in the ultrafiltrate of the blood obtained from a chronic uremic patient using a hemodialyzer. (3) Levels of succinic acid, adipic acid, 3-methyladipic acid, 2,4-dimethyladipic acid, pimelic acid and azelaic acid in uremic serum were determined using a mass fragmentographic technique. Concentration of succinic acid in uremic serum was comparable to that in normal serum, whereas concentrations of adipic acid, 3-methyladipic acid, 2,4-dimethyladipic acid, pimelic acid and azelaic acid were highly elevated in uremic serum.

Adipates↗
PubMed1977

Characterization of liver cholic acid coenzyme A ligase activity. Evidence that separate microsomal enzymes are responsible for cholic acid and fatty acid activation.

Investigations on the cholic acid CoA ligase activity of rat liver microsomes were made possible by the development of a rapid, sensitive radiochemical assay based on the conversion of [3H]choloyl-CoA. More than 70% of the rat liver cholic acid CoA ligase activity was associated with the microsomal subcellular fraction. The dependencies of cholic acid CoA ligase activity on pH, ATP, CoA, Triton WR-1339, acetone, ethanol, magnesium, and salts were investigated. The hypothesis that the long chain fatty acid CoA ligase activity and the cholic acid CoA ligase activity are catalyzed by a single microsomal enzyme was investigated. The ATP, CoA, and cholic (palmitic) acid kinetics neither supported nor negated the hypothesis. Cholic acid was not an inhibitor of the fatty acid CoA ligase and palmitic acid was not a competitive inhibitor of the cholic acid CoA ligase. The cholic acid CoA ligase activity utilized dATP as a substrate more effectively than did the fatty acid CoA ligase activity. The cholic acid and fatty acid CoA ligase activities appeared to have different pH dependencies, differed in thermolability at 41 degrees, and were differentially inactivated by phospholipase C. Moreover, fatty acid CoA ligase activity was present in microsomal fractions from all rat organs tested while cholic acid CoA ligase activity was detected only in liver microsomes. The data suggest that separate microsomal enzymes are responsible for the cholic acid and the fatty acid CoA ligase activities in liver.

Adenosine Triphosphate↗
PubMed1978

Metabolism of arachidonic acid by platelets: utilization of arachidonic acid by human platelets in presence of linoleic and dihomo-gamma-linolenic acids.

In vitro human platelet prostaglandin synthesis has been studied from added radioactive arachidonic acid (i) as function of substrate concentration, (ii) as function of platelet concentration and (iii) as function of pH. Platelets, as in platelet rich plasma when labelled with arachidonic acid, washed and treated with thrombin, released radioactivity mainly from phosphatidylcholine and phosphatidylinositol. The released radioactivity was mostly accounted for by the formation of the previously identified oxygenation products of arachidonic acid. Platelet utilization or arachidonic acid was also studied in presence of linoleic and dihomo-gamma-linolenic acids, the two essential fatty acids known for antithrombotic effect. At its high concentrations linoleic acid decreased platelet cyclo-oxygenase activity as seen by a decreased formation of endoperoxides from arachidonic acid. Dihomo-gamma-linolenic acid was found to be a mutually competitive substrate with arachidonic acid for the platelet prostaglandin synthetase thus causing reduced utilization of arachidonic acid as shown by measuring the various oxygenation products of arachidonic acid. These two acids were utilized differently by platelet prostaglandin synthetase.

8,11,14-Eicosatrienoic Acid↗
PubMed1978

D-Amino acids of the amino acid pool and occurrence of racemase and D-amino acid oxidase activities in Escherichia coli B.

Less than 20% of the amino acid content of the amino acid pool of Escherichia coli B exists in the D-form. Alanine, glutamic acid, and valine were shown by gas- chromatography to be partially in the D-form. Only D-alanine was formed by racemization in the crude extract of this organism. Alanine racemase was easily released from the membranes or vesicles but D-alanine oxidase activity remained firmly bound to the membrane. Most protein amino acids stimulated proline uptake into the vesicles, and the oxidative deamination activities were verified by the proline uptake stimulating amino acids. It is concluded that the obligatory pathway of L-amino acid--D-amino acid--oxo acid which exists in the oxidation of L-alanine does not exist with other L-amino acids. It is likely that other D-amino acids in the pool are formed in the presence of D-amino acid oxidase or D-amino acid aminotransferase.

Alanine Racemase↗
PubMed1976

Effect of treatment with exogenous interferon, polyinosinic acid-polyctyidylic acid or polyinosinic acid-polycytidylic acid-poly-L-lysine complex on encephalomyocarditis virus infections in mice.

The effect of treatment with exogenous interferon was compared with two interferon inducers, polyinosinic acid-polycytidylic acid [poly(I:C)] and [poly(I:C)]-poly-l-lysine complex (P-L-L complex), in two model encephalomyocarditis virus infections of mice. Although both inducers stimulated the production of interferon, the peak serum levels induced by P-L-L complex were five- to eightfold greater than those induced with poly(I:C). When encephalomyocarditis virus was inoculated by either the intraperitoneal or the intranasal route, interferon and both of the inducers protected mice against mortality and prolonged the mean day of death when the compounds were given prior to or immediately after viral challenge. In general, treatment with interferon was not as successful as treatment with poly(I:C) or P-L-L complex. In these infections, P-L-L complex appeared to be the most effective agent in that successful treatment resulted when drug therapy was initiated as late as 48 h after virus inoculation. An examination of the effect of treatment on the pathogenesis of the infection indicated that protection was associated with the prevention of viremia and subsequent seeding of target organs, particularly the central nervous system.

Animals↗
PubMed1978

Effects of dihydroxy bile acids and hydroxy fatty acids on the absorption of oleic acid in the human jejunum.

Perfusion studies of the normal human jejunum were performed to test whether dihydroxy bile acids and hydroxy fatty acids inhibit the absorption of oleic acid, since previous reports documented their inhibitory effects on the absorption of several other organic solutes. 3 mM deoxycholate and 7 mM glycodeoxycholate inhibited the absorption of 3 mM oleic acid in isotonic micellar solutions while inducing net fluid secretion. Similarly, fractional absorption of oleic acid decreased in the presence of hydroxy fatty acids. However, only the changes induced by 2 mM ricinoleic acid could be distinguished from changes induced by an increase in total fatty acid concentration. Under all experimental conditions, close linear relationships existed between net water movement and fractional absorption of glucose, xylose, and fatty acids, as well as between the absorption rates of these solutes. In contrast, net fluid secretion induced by hypertonic D-mannitol (450 mosmol/liter) had no effect on solute absorption. Our data and observations in the literature do not allow formulation of a hypothesis which would adequately define all effects of dihydroxy bile acids and fatty acids on intestinal transport processes. The observations help explain the malabsorption of fat and other nutrients in patients with the blind loop syndrome.

Adult↗
PubMed1979

[Protein digestibility and absorption of amino acids in various segments of the digestive tract of pigs. 2. Protein and amino acid balances at the end of the small intestine and of the whole digestive tract (apparent and true protein and amino acid digestibility)].

Growing pigs with ileum and ileocecal re-entrant canulae were given 5 different rations (pig fattening feed 1 and 2, rations with dried skim milk, wheat gluten + lysine and wheat + wheat gluten + lysine). The crude protein and amino acid excretion was quantitatively determined with ileum chyme and feces. The calculation of the amino acid balances (apparent and true digestibility) at the end of the small intestine, at the end of the wholedigestive tract and the isolated colon showed characteristic differences for the individual amino acids. On ileum level the amino acids with relatively high endogenous quotas, threonine, tryptophane, alanine, aspartic acid and glycine showed a distinctly lower, the amino acids arginine, methionine, phenylalanine, glutamic acid, proline and tyrosine a distinctly higher digestibilityhan crude protein. In comparison of the values on the feces level, including the true digestibility, these differences are largely balanced out. At the end of the small intestine the absorption of the amino acids is in the main completed. The disappearance rate of amino acids from the colon shows large differences with reference to the different rations as well as the individual amino acids. They were particularly high for various rations as far as proline, tryptophane, glycine and cystine are concerned. If wheat gluten + lysine rations were given, a net synthesis of methionine in the colon could be proved.

Amino Acids↗
PubMed1978

Micelle and acid-soap formation of linoleic acid and 13-L-hydroperoxylinoleic acid being substrates of lipoxygenase-1.

Surface tension measurements of linoleic acid solutions in 0.1 M sodiumborate buffer pH 10 at 23 degrees C showed that at increasing the linoleic acid concentration a sharp transition from monomers to micelles occurs at 167 micrometer. At pH 9 and 8 formation of acid-soap dimers from monomers starts at 60 micrometer and 21 micrometer respectively. The concentration range at which only monomers exist is therefore markedly reduced. For 13-L-hydroperoxylinoleic acid at pH 10 acid-soap formation still takes place, starting at approx. 220 micrometer. The total lipid concentration at which acid-soap or micelle formation starts in mixtures of linoleic acid and 13-L-hydroperoxylinoleic acid has been determined in relation to the molar ratio of both acids.

Kinetics↗
PubMed1975

Accumulation of 3-hydroxyisobutyric acid, 2-methyl-3-hydroxybutyric acid and 3-hydroxyisovaleric acid in ketoacidosis.

1. Urine and serum samples from patients with ketoacidosis of varying degree and etiology have been examined by gas chromatography and mass spectrometry. 2. In addition to 3-hydroxyisovaleric acid, relatively high concentrations of two analogous hydroxy acids, 3-hydroxyisobutyric acid and 2-methyl-3-hydroxybutyric acid, were found in the urine. 3. There were highly significant positive correlations between the excreted amounts of the three acids. 4. Experiments on rats with isotope-labelled compounds revealed that the acids were formed by the degradation of leucine, isoleucine and valine. 5. The accumulation of the hydroxy acids during ketoacidosis is probably caused by a similar derangement of the metabolism of all three branched-chain amino acids.

Acetates↗
PubMed1979

Faecal bile acid loss and bile acid pool size during short-term treatment with ursodeoxycholic and chenodeoxycholic acid in patients with radiolucent gallstones.

Twelve non-obese patients with radiolucent gallstones were fed on a standard diet. After 10 days (period A), six patients received 15 mg/kg/day of ursodeoxycholic acid (UDCA) (group I) and the other six (group II) the same dose of chenodeoxycholic acid (CDCA) for 15 days (period B). An intravenous injection of 20 micro Ci of 14C-UDCA and of 14C-CDCA was given on the 11th day of period B to the patients of group I and II respectively. Stools were collected at the end of period A and B and one bile sample was collected on the 12th day of period B. The faecal bile acid loss was higher during chenotherapy (36.12 mumol/kg/day) than during ursotherapy (23.94 mumol/kg/day), as was the proportion of lithocholic acid (73% vs 43%) in the faeces. Decay constant rate of faecal radioactivity was 0.365 day-1 in group I and 0.642 in group II. The results indicate that faecal bile acid excretion and turnover rate are greater during CDCA than UDCA, while UDCA increases the bile acid pool size to an even greater extent than does CDCA (150.2 vs 94.9 mumol/kg). This is probably because the former is more slowly degraded to poorly reabsorbable compounds. In fact, the bile saturation index was 0.66 in group I and 1.05 in group II, even though biliary CDCA in the latter had risen to 69.6%.

Bile Acids and Salts↗
PubMed1975

The estimation of 3,4-dihydroxyphenylacetic acid, homovanillic acid and homo-isovanillic acid in nervous tissue by gas-liquid chromatography and electron capture detection.

1 A gas chromatographic method using electron capture detection is described for the estimation of three acidic metabolites of dopamine, 4-hydroxy-3-methoxyphenylacetic acid (homovanillic acid, HVA), 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-hydroxy-4-methoxyphenylacetic acid (homo-isovanillic acid, iso-HVA). The method is based on the formation of the trifluoroacetyl-hexafluoroisopropyl derivatives of the three acids. 2 The method has been applied to the estimation of DOPAC, HVA and iso-HVA in tissues from the central and peripheral nervous systems.

3,4-Dihydroxyphenylacetic Acid↗