Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Pyruvic Acid”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 37 records · Page 2Linked to original sources
PubMed1994

Pyruvic acid production by an F1-ATPase-defective mutant of Escherichia coli W1485lip2.

An F1-ATPase-defective mutant, TBLA-1, was constructed by the transduction of a defective gene for the alpha subunit of F1-ATPase, atpA401, into Escherichia coli W1485lip2, a lipoic acid-requiring pyruvic acid producer. The pyruvic acid production of the strain TBLA-1 was found to be improved markedly compared with that of strain W1485lip2. In cultures using a jar fermentor, the strain W1485lip2 consumed 50 g/liter of glucose and produced 25 g/liter of pyruvic acid after culture for 32h, while strain TBLA-1 consumed the same amount of glucose, and produced more than 30 g/liter of pyruvic acid in a 24-h culture. A revertant, No. 63-1, derived from the strain TBLA-1, had a normal level of F1-ATPase activity, and showed a similar pattern of pyruvic acid production to that of strain W1485lip2.

Escherichia coli↗
PubMed1987

Formation of a beta-carboline (1,2,3,4-tetrahydro-1-methyl-beta-carboline-1-carboxylic acid) following intracerebroventricular injection of tryptamine and pyruvic acid.

Tritium labelled 1-carboxy-tetrahydroharman was identified in rat brain following i.c.v.-injection of [3H]tryptamine and pyruvic acid. The animals had been treated with the MAO inhibitor pargyline (40 mg/kg) 30 min before i.c.v. injection. Under these conditions, only trace amounts of [3H]indole acetic acid could be detected in the brain. The formation of 1-CTHH was time-dependent. Five minutes following the i.c.v. injection, approximately 0.45% of the administered tryptamine was converted into 1-CTHH and 23% were still unchanged. The amount of the radioactive 1-CTHH increased slightly within 1 h (0.8%; [3H] tryptamine: 6%). Pretreatment of the rats with high doses of pargyline (75 mg/kg; 90 min before i.c.v. injection) prevented the formation of both [3H]1-CTHH and [3H]indole acetic acid (IAA) suggesting that high doses of pargyline inhibit the formation of 1-CTHH. As control for a possible non-enzymatic formation of 1-CTHH, [3H]tryptamine and various concentrations of pyruvic acid were incubated in phosphate buffer at pH 7.4. 1-CTHH was not detected under these conditions. However, the formation of 1-CTHH was observed at high pyruvic acid concentrations (final concentration = 100 mM) and low pH values (less than pH4). To support the assumption that the observed condensation of both precursors to 1-CTHH occurred intracellularly, the metabolism of tryptamine was studied. Two minutes after i.c.v. injection of [3H]tryptamine approximately 4% of the injected dose remained unchanged and 10% were metabolized to [3H]IAA. These findings suggest a rapid disappearance of [3H]tryptamine from the cerebrospinal fluid as well as a rapid penetration into the cerebral tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1979

Use of p-aminophenyl D and L-lactic acids and p-aminophenyl pyruvic acid as effectors in the affinity chromatography of lactate dehydrogenase.

p-Aminophenyl pyruvic acid and D-p-amino-phenyllactic acid were immobilized on a new synthetic acrylic carrier bearing acylating N-succinimidyl ester groups. The derivatives obtained were used successfully to purify lactate dehydrogenase (LDH) by affinity chromatography, the elution being carried out by means of NADH or preferably L-phenyllactic acid. Moreover, the specific activity of the LDH contained in a human blood serum was increased 270 times, using L-p-aminophenyllactic acid immobilized on a mixed polyacrylic agarose carrier.

Animals↗
PubMed1984

Enzymatic synthesis of [1-11C]pyruvic acid, L-[1-11C]lactic acid and L-[1-11C]alanine via DL-[1-11C]alanine.

L-[1-11C]Lactic acid was prepared enzymatically from [1-11C]pyruvic acid by way of DL-[1-11C]alanine, using remote, semiautomated procedures. The DL isomers of alanine were prepared by a modification of the Bucherer-Strecker reaction from no-carrier-added (NCA) hydrogen [11C]cyanide. The enantiomer mixture was transformed to [1-11C]pyruvic acid by successive elution through columns of (a) immobilized D-amino acid oxidase (D-AAO)/catalase and (b) immobilized L-alanine dehydrogenase (L-AID) or L-amino acid oxidase (L-AAO/catalase). [1-11C]-Pyruvic acid was subsequently converted to L-[1-11C]lactic acid by passage through a L-lactic dehydrogenase (L-LDH) column. L-[1-11C]Alanine and [1-11C]-pyruvic acid were separated chromatographically by way of a cation-exchange column (AG50W-X2, H+ form). Typically the synthesis time was 35-40 min after cyclotron production of hydrogen [11C]cyanide (400 mCi), with radiochemical yields of 25 mCi (25%) for L-[1-11C]lactic acid, 35 mCi (29%) for [1-11C]pyruvic acid, and 20 mCi (20%) for L-[1-11C]alanine. The use of immobilized enzymes eliminates the possibility of protein contamination and assures the production of sterile, pyrogen-free products, allowing for rapid and effective regio- and stereo-specific transformations.

Alanine↗
PubMed1992

Gluma shear bond strength to enamel and dentin treated with pyruvic acid and glycine.

The purpose of this study was to determine the effect of pyruvic acid and glycine on the shear bond strength (SBS) of the Gluma Bonding System to dentin and enamel. Forty-five mandibular and maxillary permanent first and second molars and 45 maxillary permanent central incisors were used in the study. Fifteen test specimens were prepared with each of the following procedures. Dentin: using the conventional Gluma Bonding System (A); the Gluma 2 Cleanser was replaced with 10% pyruvic acid containing 10% glycine with pH 2.8 (B); or the dentin was etched with 10% pyruvic acid (pH 1.5) followed by the application of 10% glycine with pH adjusted to 9.0 (C). Enamel: etched with Gluma 1 Etchant (D); etched with 10% pyruvic acid containing 10% glycine (E); or etched with 10% pyruvic acid followed by the application of 10% glycine (F). The test specimens were disassembled 15 minutes after cure, stored in physiological saline at 37 degrees C for 24 hours, and the SBS determined in an Instron machine at a crosshead speed of 0.5 mm.min.-1 The SBS was expressed in MPa. The data were analyzed by ANOVA and the Student-Newman-Keuls test. The mean +/- SD of the SBS in MPa were: A: 8.7 +/- 5.2; B: 14.7 +/- 4.6; C: 12.8 +/- 4.8; D: 19.8 +/- 3.8; E: 18.0 +/- 3.1; F: 17.6 +/- 3.5. The application of 10% pyruvic acid containing 10% glycine, and 10% pyruvic acid followed by 10% glycine, resulted in a significant increase in SBS to dentin. The SBS to enamel treated with the three procedures were not significantly different.

Acid Etching, Dental↗
PubMed1990

Effects of indole-pyruvic acid on sleep and food intake in the rat.

Indole-pyruvic acid was studied for its short- and long-term effects on electroencephalographic sleep and on food intake in rats implanted with cortical and muscular electrodes. Following a single injection, indole-pyruvic acid (10-50 mg kg-1 i.p.) reduced by 16-23 min (range) the latency of the first slow-wave episode in a dose-related fashion and produced a significant increase in slow-wave sleep time (12-40%) in doses of 10-30 mg kg-1. Rapid eye movement sleep latency and rapid eye movement sleep time were increased (by 23-37 min) and reduced (57-71%) respectively. The effects of indole-pyruvic acid on slow-wave sleep time were still present after 3, 7 and 14 days of chronic administration (10 mg kg-1 day-1), whereas tolerance to the effect of indole-pyruvic acid on rapid eye movement sleep was observed. Daily food consumption was reduced (20-28%) by acute administration of indole-pyruvic acid (15-30 mg kg-1 i.p.), but tolerance developed after 5 days of repeated injections. These findings are in accordance with previous evidence suggesting that indole-pyruvic acid effects may be related to the activation of central serotonin neurons, which are involved in the inhibitory control of sleep and food intake.

Animals↗
PubMed1988

Pyruvic acid protects against the lethality of sulfide.

The efficacy of pyruvic acid in protecting mice against the lethal effects of sodium sulfide was examined. Pyruvic acid (1 g/kg, i.p.) reduced the mortality of sodium sulfide (100 mg/kg, i.p.) from 100% to 5% when administered 15 min prior to the sulfide. The protective effect of pyruvic acid decreased over time but was still present at 20 min and 30 min, with 40% and 50% mortality, respectively. The lethality of sulfide in larger mice was less than that in smaller mice when the doses were normalized for body weight, but the protection factor of the pyruvic acid, approximately 2.0, was the same for both sizes.

Animals↗
PubMed1991

Use of pyruvic acid in the treatment of actinic keratoses: a clinical and histopathologic study.

Twelve patients with multiple actinic keratoses were treated with either 5-fluorouracil and pyruvic acid or pyruvic acid alone. Three patients were treated with 5 percent 5-fluorouracil cream for one to three weeks for comparison. Exposure time to alpha-hydroxy acids varied between one and ten minutes. Biopsy specimens were taken at times varying from immediately after treatment to eight weeks after treatment. The results show that the combination of 5-fluorouracil and pyruvic acid is an effective treatment for actinic keratoses. In addition, the exposure time to 5-fluorouracil is decreased and therefore this treatment is better tolerated than prolonged treatment with 5-fluorouracil alone.

Administration, Cutaneous↗