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 847 records · Page 47Linked to original sources
PubMed2004

Effect of R(+)alpha-lipoic acid on pyruvate metabolism and fatty acid oxidation in rat hepatocytes.

R-(+)-alpha-lipoic acid (R-LA) is the naturally occurring enantiomer of LA. It is a strong antioxidant and cofactor of key metabolic enzyme complexes catalyzing the decarboxylation of alpha-keto acids. Racemic LA (rac-LA) has shown promise in treating diabetic polyneuropathy, and some studies suggest that it improves glucose homeostasis in patients with type 2 diabetes. We examined the effects of R-LA on pyruvate metabolism and free fatty acid (FFA) oxidation in primary cultured hepatocytes isolated from 24-hour fasted rats. After overnight culture in serum-free medium, cells were pre-exposed to R-LA for 3 hours before assays. R-LA (25 to 200 micromol/L) significantly increased pyruvate oxidation ( approximately 2-fold at the highest dose tested) measured as (14)CO(2) production from [1-(14)C]pyruvate by the cells over 1 hour post-treatment. These effects correlated with proportional, significant increases in the activation state of the pyruvate dehydrogenase (PDH) complex. R-LA treatment inhibited glucose production from pyruvate by approximately 50% at 50 micromol/L R-LA and approximately 90% at 200 micromol/L. Palmitate oxidation was measured in hepatocytes cultured in the presence of albumin and physiological (0.1 mmol/L) or high (1.5 mmol/L) concentrations of FFA. The latter markedly enhanced FFA oxidation. R-LA treatment significantly inhibited FFA oxidation in both media, but was more effective in high FFA, where it reduced FFA oxidation by 48% to 82% at 25 to 200 micromol/L, respectively. Identical doses of R-LA did not affect FFA oxidation by L6 myotubes (a cell culture model for skeletal muscle) in either high or low FFA medium, but enhanced pyruvate oxidation. In conclusion, 3-hour exposure of primary cultured rat hepatocytes to R-LA at therapeutically relevant concentrations increased pyruvate oxidation, apparently by activation of the PDH complex, and decreased gluconeogenesis and FFA oxidation. These features may prove useful in the control of type 2 diabetes.

Animals↗
PubMed1974

Differential effects of 2-oxo acids on pyruvate utilization and fatty acid synthesis in rat brain.

1. The effects of 2-oxo-4-methylpentanoate, 2-oxo-3-methylbutanoate and 2-oxo-3-methylpentanoate on the activity of pyruvate dehydrogenase (EC 1.2.4.1), citrate synthase (EC 4.1.3.7), acetyl-CoA carboxylase, (EC 6.4.1.2) and fatty acid synthetase derived from the brains of 14-day-old rats were investigated. 2. The pyruvate dehydrogenase enzyme activity was competitively inhibited by 2-oxo-3-methylbutanoate with respect to pyruvate with a K(i) of 2.04mm but was unaffected by 2-oxo-4-methylpentanoate or 2-oxo-3-methylpentanoate. 3. The citrate synthase activity was inhibited competitively (with respect to acetyl-CoA) by 2-oxo-4-methylpentanoate (K(i)~7.2mm) and 2-oxo-3-methylbutanoate (K(i)~14.9mm) but not by 2-oxo-3-methylpentanoate. 4. The acetyl-CoA carboxylase activity was not inhibited significantly by any of the 2-oxo acids investigated. 5. The fatty acid synthetase activity was competitively inhibited (with respect to acetyl-CoA) by 2-oxo-4-methylpentanoate (K(i)~930mum) and 2-oxo-3-methylpentanoate (K(i)~3.45mm) but not by 2-oxo-3-methylbutanoate. 6. Preliminary experiments indicate that 2-oxo-4-methylpentanoate and 2-oxo-3-phenylpropionate (phenylpyruvate) significantly inhibit the ability of intact brain mitochondria from 14-day-old rats to oxidize pyruvate. 7. The results are discussed with reference to phenylketonuria and maple-syrup-urine disease. A biochemical mechanism is proposed to explain the characteristics of these diseases.

Acetyl-CoA Carboxylase↗
PubMed1995

Ethanol as a xanthine dehydrogenase inhibitor.

In the present study, we investigated whether ethanol inhibits the activity of xanthine dehydrogenase. Ethanol and/or inosine were administered to normal subjects, and plasma concentration and urinary excretion of purine bases were measured together with blood concentrations of lactic acid and pyruvic acid. In addition, ethanol and pyrazinamide were administered to these subjects, and plasma concentration and urinary excretion of pyrazinamide and its major metabolites were measured. Increases in plasma concentration and urinary excretion of xanthine induced by a combination of ethanol and inosine were greater than the sums of increases induced separately by ethanol and inosine, although increases in plasma concentration and urinary excretion of uric acid induced by the combination of ethanol and inosine were not different from the sums of increases induced separately by ethanol and inosine. Ethanol increased the ratio of blood lactic acid to blood pyruvic acid and decreased plasma concentration and urinary excretion of 5-hydroxypyrazinamide and 5-hydroxypyrazinoic acid. These results suggest that ethanol inhibits xanthine dehydrogenase presumably by an ethanol-induced increase in the cytosolic concentration of NADH in the liver.

Acetates↗
PubMed1990

Acute effects of cadmium and selenium on glucose output from rat liver hepatocytes using various gluconeogenic precursors.

Male Sprague-Dawley rats (250-310 g) fasted for 24 h were injected i.p. with either sodium acetate (C2H3NaO2; 1.23 mg/kg, 15 mumol/kg), cadmium acetate (C4H6CdO4; 0.84 mg/kg, 3.6 mumol/kg), sodium selenite (Na2SeO3; 1.6 mg/kg, 9.2 mumol/kg) or cadmium acetate (0.84 mg/kg, 3.6 mumol/kg) and sodium selenite (1.6 mg/kg, 9.2 mumol/kg) simultaneously. Rats were sacrificed 180 min post-treatment and hepatocytes were isolated. An average of 85% cell viability was achieved. Hepatocyte suspension (50 mg cell wt/ml, 1 ml/tube) was incubated for 180 min at 37 degrees/C with 10 mM of one of the following substrates: beta-D(-)fructose, glycerol, DL-alanine, L(+)lactic acid or pyruvic acid. Glucose concentration of the supernatant was measured by a colorimetric method. Cadmium decreased glucose output significantly (P less than 0.05), when lactic acid or alanine was used as substrate, but did significantly (P less than 0.05) increase the output when pyruvic acid, glycerol or fructose was used. Selenium alone significantly increased (P less than 0.05) hepatic glucose output only when fructose was used as substrate. Selenium and cadmium concurrently administered significantly increased (P less than 0.05) hepatic glucose output when pyruvic acid, glycerol or fructose was used as substrate as compared to sodium acetate (control), cadmium or selenium alone. These findings suggest that cadmium and selenium affect the hepatic gluconeogenic pathway and that their effects depend on the gluconeogenic precursor used.

Animals↗
PubMed1998

Spectrophotometric and spectrofluorometric studies on interaction of cationic dyes with bacterial capsular polysaccharide.

Interaction of Klebsiella K14 capsular polysaccharide with cationic dyes pinacyanol chloride, acridine orange and phenosafranin has been studied by spectrophotometric and spectrofluorometric techniques. The polymer containing both glucuronic acid and pyruvic acid in its repeating unit behaved as a unique polyelectrolyte. It induced blue shift of the absorption band of pinacyanol chloride indicating strong metachromasy. Stoichiometry of the polyanion and the dye cations in the polymer-dye compound (1:2) indicated that both glucuronic acid and pyruvic acid acted as potential anionic sites for interaction with the cationic dye molecules. The stoichiometry of anionic site (of polyanion): cationic site (of dye) in the polymer dye compound was calculated as 1:1. Interaction of the polymer with acridine orange and phenosafranin dyes studied by fluorescence measurements demonstrated Stern-Volmer type of quenching. Equivalent weight of the polymer was determined by spectrophotometric and spectrofluorometric titrations. From the present studies chromotropic property of the polymer was established.

Acridine Orange↗
PubMed1996

Comparison of the effect of various chemical peeling agents in a mini-pig model.

BACKGROUND: With the advent of newer chemical peels, there is now a wide range of peeling agents that can be applied on specific patients. OBJECTIVE: The purpose of this study was to closely examine the more common chemical peeling agents at different concentrations. METHODS: The study methods were carried out by thoroughly cleansing the skin surface with acetone. Different concentrations of the chemical peels were applied on different skin areas (2 x 2 cm each) and left on the skin for 15 minutes: phenol-Bakers, 25%, 50%, 75%, 88%; trichloroacetic acid, 25%, 50%, 75%; glycolic acid, 50%, 70%; and pyruvic acid, 50%, 100%. Serial biopsies were taken from each peeling site at 1, 7, and 21 days post-peel. Biopsies were then evaluated for epidermal changes, inflammation, and collagen deposition. RESULTS: The results show that Bakers phenol peel caused the most inflammation and nonspecific reaction, and in addition, a proportionate amount of new collagen deposition. Plus, increasing concentrations of phenol and TCA caused increasing amount of epidermal sloughing and inflammation after 1 day post-peel. The extent of reaction from the phenol and TCA was directly proportional to the collagen deposition at 21 days. CONCLUSIONS: The glycolic acid and pyruvic acid caused minimal nonspecific reaction. However, the collagen deposition caused by the glycolic acid and pyruvic acid was disproportionately increased suggesting a direct stimulatory effect by the two agents.

Animals↗
PubMed2001

The effect of surfactants on the deliquescence of sodium chloride.

This study investigated the deliquescence of sodium chloride aerosol with surfactants at a retention time of 4.24 sec. Two surfactants used in this study, glutaric acid and pyruvic acid, are found in atmospheric aerosol and have a high hydrophile-lipophile balance (HLB) value. The experimental system consisted of a relative humidity conditioner, a tandem differential mobility analyzer (TDMA) and a scanning mobility particle sizing (SMPS) system. Results obtained from the observation of TDMA presented the deliquescence point of sodium chloride aerosol at 75% RH. In addition, the growth size of sodium chloride aerosol was observed to be 79.47 nm and the growth ratio was 77.94%, when the initial size of aerosol was 101.82 nm. Surfactants were internally mixed with sodium chloride at six different weight fractions, i.e. 2.5, 5, 10, 20, 40, and 60% by weight of surfactants in dry aerosol. Both surfactants apparently decreased the deliquescence point of sodium chloride, in which the lowest deliquescence point appeared at about 71% RH when the weight fraction of surfactants is 60% by weight of surfactants in dry aerosol. Moreover, the smallest size of sodium chloride aerosol with surfactants was 142.7 nm at 60% by weight of pyruvic acid in dry aerosol. Our results further demonstrate that the deliquescence point and size of sodium chloride aerosol with surfactants are related to the weight fraction of surfactants.

Aerosols↗
PubMedDate not supplied

An immobilized bienzyme system for assay of sialic acid.

Sialic acid has been assayed enzymatically by an immobilized two-enzyme system. The method includes cleavage of sialic acid to pyruvic acid by N-acetylneuraminic acid (NANA) aldolase and reduction of pyruvic acid by lactate dehydrogenase in the presence of NADH, which is followed photometrically at 349 nm. For the membrane preparation 5 units of lactate dehydrogenase and 1 unit of NANA-aldolase were used. The pH optimum of the reaction using potassium phosphate buffer was 7.0. This two-enzyme membrane remains 100% active for several weeks at 4 degrees C in the assay buffer and remains stable after performing experiments at 45 degrees C.

Animals↗
PubMed2003

[A case of mitochondrial myopathy with external ophthalmoplegia and ataxic neuropathy].

We report a 70-year-old woman with bilateral optic atrophy, external ophthalmoplegia, bilateral blepharoptosis, and sensory ataxic neuropathy. She had a visual disturbance since childhood. She had dysarthria and gait disturbance at 28 years old. She had bilateral blepharoptosis, marked gait disturbance and dysphagia at 50. On neurological examination, external ophthalmoplegia, bilateral blepharoptosis, mild weakness and muscular atrophy of promixal muscles, hyporeflexia, positive Romberg sign, glove and stocking type sensory disturbance including hypesthesia, hypalgesia, and bathyhypesthesia were found. She did not show pigmented retinopathy, cognitive dysfunctions, hearing loss, cerebellar ataxia, Hoffman reflex nor Babinski sign. She did not show increased lactic acid nor pyruvic acid in the cerebrospinal fluid but mild increase of pyruvic acid (1.0 mg/dl) in her serum. The conduction velocity and amplitude of CMAP of tibial nerve was 37.4 m/sec and 2.9 mV, respectively. The SNAP of ulner and sural nerve were not evoked. Brain MRI showed no pathological findings. Muscle biopsy from the biceps muscle showed many ragged-red fibers (5.3%) and some fibers with decreased or absent COX activity. Sural nerve biopsy showed a marked loss of large myelinated fibers with thin myelinated fibers, and onion-bulb formation. The clinical findings of our patient is similar to that of SANDO (the triad of sensory ataxic neuropathy, dysarthria, and ophthalmoparesis), however, large mtDNA deletion reported by Fadic in patients with SANDO was not found in our patient. It might be possible that her mtDNA deletion is small or point mutation is existed.

Aged↗
PubMed1990

[Biochemical changes in cervix mucus in stepwise malignant transformation of cervix epithelium].

The authors investigated 10 free amino acids, LDH, pyruvic acid and the levels of glucose in mucus of the cervix of patients in cases of gradually malignisation. We could show that the levels of all free amino acids are lower in cases of invasive carcinomas than in cases with dysplasias. LDH and pyruvic acid had an higher level in cases invasive carcinomas. We found no differences in cases of dysplasias and normal patients cervical mucus.

Amino Acids↗
PubMed1965

EFFECTS OF DIELDRIN, PICROTOXIN AND TELODRIN ON THE METABOLISM OF AMMONIA IN BRAIN.

1. Increases in the concentrations of lactic acid and pyruvic acid in rat brain during acute dieldrin poisoning are associated with hyperactivity of the brain, whereas an increase in the cerebral alanine concentration occurs before the convulsions. Throughout the dieldrin-induced seizure pattern, fluctuations in the concentration of brain ammonia are out of phase with the actual convulsions. 2. Increases in the concentrations of alanine, ammonia and lactic acid in rat brain accompany picrotoxin-induced seizures; there is no increase in the concentration of glutamine. These changes are consistent with the inhibition of glutamine synthesis. 3. In addition to previously reported changes in the concentrations of intermediary metabolites of the brain after the administration of Telodrin (Hathway & Mallinson, 1964), increases have now been found in the alanine and lactic acid concentrations. Since increases in the alanine and glutamine concentrations occur before the convulsions, liberation of ammonia also occurs before the onset of convulsions and throughout their course. Ammonia-binding mechanisms later become inadequate and free ammonia accumulates in cerebral tissues. 4. An increase in the pyruvic acid concentration of the brain after the intraperitoneal injection of either dieldrin or Telodrin is endogenous in origin. 5. The parenteral administration of a small dose of glutamine increases the cerebral concentrations of alanine and glutamic acid. Some animals previously treated with glutamine resisted Telodrin convulsions. 6. Mechanisms for the disposal of ammonia liberated in brain are discussed.

Alanine↗
PubMedDate not supplied

[Glucose tolerance test and some pathways of glucose metabolism in patients with craniocerebral trauma].

Intravenous glucose tolerance test was done and concentrations of lactic acid and pyruvic acid were determined together with the lactic acid/pyruvic acid index and lactic dehydrogenase activity in fasting venous blood and 35 and 90 min. after glucose load. The investigations were carried out in 30 patients with cerebral concussion and 20 patients with cerebral contusion on the 1st, 3rd and 7th days after trauma. Thirty healthy subjects served as controls. Presence of hyperglycaemia in fasting state and impairment of glucose tolerance were demonstrated in the first week of the disease. These disturbances were accompanied by significant decrease of the activity of lactic and pyruvic acid metabolism during the first three days after trauma. The values of lactic acid/pyruvic acid index and LDH activity were not changed significantly. Disturbances of carbohydrate metabolism persisted during the first week after trauma and were more frequent, more intense and persisted longer in patients with brain contusion than in those with brain concussion but showed no significant differences related to the degree of trauma.

Adolescent↗
PubMedDate not supplied

[Acid-base equilibrium of cerebrospinal fluid in inflammatory diseases of the central nervous system].

In 51 patients with meningoencephalitis the acid-base equilibrium of the cerebrospinal fluid (CSF) was assessed. In the fluid the following gasometry parameters were determined: pH, pCO2, pO2 and HCO3-, and also the levels of lactic acid, ATP, pyruvic acid, and sodium and potassium ion concentrations. The control group included 13 patients in whom on the basis of CSF examination, inflammatory disease of the central nervous system was ruled out. The results were analysed in groups of patients with purulent and lymphocytic meningitis. The changes were taken into account of the determined parameters in the course of the disease as well as their relationship with clinical condition of the patients. The differences were found in the values of acid-base equilibrium parameters of the CSF between purulent and lymphocytic meningitis. The differences of the values of the determined parameters between the patients in the group of purulent meningoencephalitis depended on their clinical condition and the outcome of the pathological process. In patients with purulent meningoencephalitis metabolic, lactic acidosis of the CSF occurred which was statistically significantly higher than in the group of patients with lymphocytic meningitis. The lowest values of pH and HCO3- concentration and the highest concentrations of lactic and pyruvic acids and potassium ion levels were found in the group of patients with purulent meningoencephalitis. The highest degree of acid-base equilibrium disturbances in the CSF was observed in the subgroup of patients with purulent meningoencephalitis who died.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Imbalance↗
PubMed1980

Inhibitors of polyamine biosynthesis VII: Evaluation of pyruvate derivatives as inhibitors of S-adenosyl-L-methionine decarboxylase.

The mechanism of the enzymatic decarboxylation of S-adenosyl-L-methionine catalyzed by S-adenosyl-L-methionine decarboxylase and its inhibition by methylglyoxal bis(guanylhydrazone) were investigated. The results indicate that the carbonyl group of the pyruvate cofactor does not form an azomethine bond with an amino group of the enzyme protein. The substrate and/or product forms an azomethine bond with the pyruvate cofactor, which can be reduced efficiently with sodium cyanoborohydride. Methylglyoxal bis(guanylhydrazone) appears to interfere with the formation of the enzyme--substrate complex by competing with the substrate for binding with the active enzyme site. The dimethylaminoethylhydrazone, semicarbazone, and guanylhydrazone derivatives of pyruvic acid, ethyl pyruvate, pyruvic acid amide, and pyruvyl glycineamide were synthesized. None of these compounds had significant inhibitory activity on the enzymatic decarboxylation of S-adenosyl-L-methionine by S-adenosyl-L-methionine decarboxylase from rat liver in vitro. These results indicate that the structural requirements for binding of methylglyoxal bis(guanylhydrazone) to the enzyme are strict and that structural modifications of this compound result in a dramatic loss of activity.

Adenosylmethionine Decarboxylase↗
PubMed1968

Fixation of carbon dioxide in the dark by the malic enzyme of bean and oat stem rust uredospores.

Malic enzyme was found in both bean rust and cat stem rust uredospores. In bean rust uredospores it was shown to catalyze the formation of pyruvic acid from l-malic acid and to synthesize malic acid from pyruvic acid and CO(2). The malic enzyme from bean rust uredospores was specific for NADP and dependent on manganous ions for activity. The specific activity of the bean rust malic enzyme in crude extracts of ungerminated uredospores was approximately 6 times greater than that found in crude extracts obtained from germinated uredospores. The malic enzyme was also found in extracts obtained from healthy and rust-infected bean leaves. The specific activity of the enzyme was approximately 2 to 5 times greater in partially purified extracts obtained from the infected bean tissue at 6 days after inoculation. The specific activity of the malic enzyme in crude extracts obtained from oat stem rust uredospores was 2 times greater than the specific activity of this enzyme in crude extracts obtained from bean rust uredospores. Phosphoenolpyruvate carboxylase activity could not be demonstrated in crude extracts obtained from the ungerminated uredospores of the bean rust fungus.

Journal Article↗
PubMed2006

Brain pyruvate and 2-oxoglutarate dehydrogenase complexes are mitochondrial targets of the CoA ester of the Refsum disease marker phytanic acid.

Pyruvate and 2-oxoglutarate dehydrogenase complexes are strongly inhibited by phytanoyl-CoA (IC(50) approximately 10(-6)-10(-7) M). Palmitoyl-CoA is 10-fold less potent. Phytanic or palmitic acids have no inhibitory effect up to 0.3 mM. At the substrate saturation, the acyl-CoA's affect the first and second enzymatic components of the 2-oxoglutarate dehydrogenase complex, while the third component is inhibited only at a low saturation with its substrate dihydrolipoamide. Thus, key regulatory branch points of mitochondrial metabolism are targets of a cellular derivative of phytanic acid. Decreased activity of the complexes might therefore contribute to neurological symptoms upon accumulation of phytanic acid in Refsum disease.

Animals↗
PubMed2003

Studies on structure-function relationships of indolepyruvate decarboxylase from Enterobacter cloacae, a key enzyme of the indole acetic acid pathway.

Enterobacter cloacae, isolated from the rhizosphere of cucumbers, produces large amounts of indole-3-acetic acid. Indolepyruvate decarboxylase, the key enzyme in the biosynthetic pathway of indole-3-acetic acid, catalyses the formation of indole-3-acetaldehyde and carbon dioxide from indole-3-pyruvic acid. The enzyme requires the cofactors thiamine diphosphate and magnesium ions for catalytic activity. Recombinant indolepyruvate decarboxylase was purified from the host Escherichia coli strain JM109. Specificity of the enzyme for the substrates indole-3-pyruvic acid, pyruvic acid, benzoylformic acid, and seven benzoylformic acid analogues was investigated using a continuous optical assay. Stopped-flow kinetic data showed no indication for substrate activation in the decarboxylation reaction of indole-3-pyruvic acid, pyruvic acid or benzoylformic acid. Size exclusion chromatography and small angle X-ray solution scattering experiments suggested the tetramer as the catalytically active state and a pH-dependent subunit association equilibrium. Analysis of the kinetic constants of the benzoylformic acid analogues according to Hansch et al. [Hansch, C., Leo, A., Unger, S.H., Kim, K.H., Nikaitani, D & Lien, E.J. (1973) J. Med. Chem.16, 1207-1216] and comparison with indole-3-pyruvic acid conversion by pyruvate decarboxylases from Saccharomyces cerevisiae and Zymomonas mobilis provided some insight into the catalytic mechanism of indolepyruvate decarboxylase.

Binding Sites↗