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PubMed1997

Peroxynitrite-mediated decarboxylation of pyruvate to both carbon dioxide and carbon dioxide radical anion.

There has been a recent renewal of interest in the antioxidant properties of pyruvate which are usually attributed to its capacity to undergo oxidative decarboxylation in the presence of hydrogen peroxide. The interaction of pyruvate with other oxidizing biological intermediates, however, has been scarcely considered in the literature. Here we report that peroxynitrite, the oxidant produced by the reaction between superoxide anion and nitric oxide, reacts with pyruvate with an apparent second-order rate constant of 88 +/- 7 M-1 s-1 at pH 7.4 and 37 degrees C. Kinetic studies indicated that pyruvate reacts with peroxynitrite anion (k = 100 +/- 7 M-1 s-1, peroxynitrous acid (k = 49 +/- 7 M-1 s-1, and a highly oxidizing species derived from peroxynitrous acid. Pyruvate decarboxylation was proved by anion exchange chromatography detection of acetate in incubations of peroxynitrite and pyruvate at pH 7.4 and 5.5. Formation of carbon dioxide radical anion was ascertained by EPR spin-trapping studies in the presence of GSH and the spin-trap 5,5-dimethyl-1-pyrroline N-oxide (DMPO). The use of pyruvate labeled with 13C at the 1-position led to the detection of the labeled DMPO carbon dioxide radical anion adduct. In the absence of GSH, oxygen consumption studies confirmed that peroxynitrite mediates the decarboxylation of pyruvate to free radical intermediates. Comparing the yields of acetate and free radicals estimated from the oxygen uptake studies, it is concluded that pyruvate is oxidized by both one- and two-electron oxidation pathways, the latter being preponderant. Hydrogen peroxide-mediated pyruvate oxidation does not produce detectable levels of carbon dioxide radical anion except in the presence of iron(II)-ethylenediamine-N,N,N',N'-tetraacetate (EDTA). The apparent second-order rate constant of the reaction between pyruvate and hydrogen peroxide was determined to be 1 order of magnitude lower than that of the reaction between pyruvate and peroxynitrite. The latter process may contribute to the antioxidant properties of pyruvate.

Anions↗
PubMed1955

Studies in cell permeability: the uptake of pyruvate by yeast.

The uptake of pyruvate by yeast was studied under a variety of conditions of temperature, extracellular concentration, O(2) pressure, and pH. It was shown that physical diffusion adequately explains the permeation of undissociated pyruvic acid into the outer and inner regions of the cell. The entrance of pyruvate ion into the outer region appears to take place by the same process. The passage of pyruvate ion across the membrane separating the outer from the inner region was found to occur only under conditions under which pyruvate is metabolized. The mechanism of the active process involved in the uptake of pyruvate is not known.

Permeability↗
PubMed1991

[The mechanisms of the development of tissue hypoxia and the criteria for its assessment in patients with hemorrhagic fever with renal syndrome].

Comparison of the parameters that characterize the activity of the sympathoadrenal system (urine adrenalin and noradrenalin) and the severity of hypoxia (lactic acid in blood and urine, pyruvic acid in blood and urine, lactate/pyruvate) in patients suffering from hemorrhagic fever with the renal syndrome (HFRS) showed them to be significantly and directly correlated. The time-course of changes in the study parameters mirrors the gravity of the pathological process. The authors hold that the sympathoadrenal system plays the leading role in the development of different types of tissue hypoxia in HFRS patients.

Adult↗
PubMed2004

Glutamic acid removal and PHB storage in the activated sludge process under dynamic conditions.

Glutamic acid removal in the activated sludge process is studied herein, primarily the formation of storage polymers under dynamic conditions. The activated sludge process was operated by using a sequencing batch reactor (sludge age of 6 d) fed with a synthetic mixture of readily available carbon sources, including glutamic acid. Removal of glutamic acid as the only carbon sources was studied in batch tests, along with oxygen consumption, ammonia uptake-release, and formation of storage polymers. It was found that poly-3-hydroxybutyrate (PHB) was stored and that the storage also occurred simultaneously to biomass growth. PHB storage accounted for 16% of the overall solids that were formed from glutamic acid, as the average value of nine batch tests. Neither other Polyhydroxyalkanoates nor polyglutamic acid were detected. Nuclear magnetic resonance analysis, performed on biomass extracts, allowed us to clarify the main metabolic pathways involved in glutamic acid removal and, in particular, the pathways involved in PHB storage. It was found that glutamic acid enters the Krebs cycle as alpha-ketoglutaric acid and exits to form pyruvic acid and then acetyl-CoA, which is the starting point of PHB production pathway.

Ammonia↗
PubMed1984

Weak acid-induced release of liposome-encapsulated carboxyfluorescein.

Leakage of the entrapped anionic fluorophore carboxyfluorescein was used as a measure of the permeability of liposomes to several different acids. Carboxyfluorescein leakage increased with increasing buffer concentration at a given pH and depended on its chemical nature: apolar weak acids such as acetic or pyruvic acids induced fast leakage at relatively high pH (4 to 5), while glycine, aspartic, citric and hydrochloric acids induced leakage only at lower pH. Fluorescence leakage measurements reflected the acidification of the liposomes' aqueous spaces, which was primarily caused by the diffusion of undissociated acid molecules across the lipid bilayer. A simple mathematical model in accord with this hypothesis and assuming that carboxyfluorescein leakage was directly related to the proportion of its neutral lactone form, described satisfactorily the carboxyfluorescein leakage kinetics and allowed rough estimation of permeability coefficients for carboxyfluorescein (neutral lactone form: 9 X 10(-9) cm X s-1), acetic acid (greater than 1 X 10(-7) cm X s-1) and glycine (cation: 6 X 10(-9) cm X s-1). These results are consistent with low effective proton permeability of liposomes (less than 5 X 10(-12) cm X s-1) and with the permeability coefficient of HCl (3 X 10(-3) cm X s-1) reported by Nozaki and Tanford ( (1981) Proc. Natl. Acad. Sci. U.S.A. 78, 4324-4328). Diffusion of weak acid molecules across lipid membranes has implications for drug encapsulation and delivery, and may be of biological significance.

Acids↗
PubMed1991

Inhibition of long-chain acyl-CoA synthetase by the peroxisome proliferator perfluorodecanoic acid in rat hepatocytes.

Perfluorodecanoic acid (PFDA) is a potent peroxisome proliferator and is known to affect hepatic lipid metabolism in rats. The effects of PFDA on fatty acid utilization were examined in isolated rat hepatocyte suspensions and in rat liver mitochondria and microsomes. PFDA inhibited the oxidation of palmitic acid but not octanoic or pyruvic acids when hepatocytes were incubated with 1 mM PFDA. At this PFDA concentration the esterification of palmitic acid into triacylglycerols was also reduced. The activity of long-chain acyl-CoA synthetase (ACS), an enzyme essential for both oxidation and esterification of fatty acids, was reduced in hepatocytes incubated with 1 mM PFDA. Carnitine palmitoyltransferase (CPT), an important enzyme for the oxidation of long-chain fatty acids, was not altered in hepatocytes incubated with this PFDA concentration. In rat liver mitochondria, palmitate oxidation and ACS activity were reduced significantly (P less than 0.01) at a PFDA concentration that had no effect on CPT activity. The inhibition of ACS by PFDA was similar in liver mitochondria and microsome preparations. In mitochondria incubated with PFDA, the inhibition of ACS appears to be noncompetitive for the substrates palmitic acid and CoA. However, the ACS inhibition by PFDA appeared to be competitive for the ATP binding site of the enzyme. Several chain length perfluorinated fatty acids were examined for their ability to inhibit mitochondrial ACS. Short-chain perfluorinated fatty acids (perfluoroproprionic and -butyric acid) did not inhibit ACS activity. However, medium-chain perfluorinated acids (perfluorooctanoic, -ananoic and -decanoic acid) were found to be potent inhibitors of ACS in isolated mitochondria. Whether ACS inhibition is causally related to PFDA-induced peroxisome proliferation and altered lipid metabolism seen in vivo is yet to be determined.

Animals↗
PubMed2002

Formation of kynurenic and xanthurenic acids from kynurenine and 3-hydroxykynurenine in the dinoflagellate Lingulodinium polyedrum: role of a novel, oxidative pathway.

The dinoflagellate Lingulodinium polyedrum (syn. Gonyaulax polyedra) was used as a model organism for studying the effects of high and low physiological oxidative stress on the formation of kynurenic and xanthurenic acids from kynurenine and 3-hydroxykynurenine. Cell were incubated with the precursors and exposed to light (high physiological stress due to photosynthetically formed oxidants) or kept in darkness (low stress). In cultures of less than 0.5 ml cell volume/l of medium, cells took up approximately one half of 0.1 mM extracellular kynurenine within 18 h. The amino acid was partially converted to kynurenic acid, most of which was released to the medium; however, intracellular concentrations of the product were by approximately 10-fold higher than extracellular levels. Rates of kynurenic acid release exceeded by far those explained by kynurenine and tryptophan aminotransferase activities, the latter representing an additional source of kynurenic acid formation via indole-3-pyruvic acid. Light enhanced the release of kynurenic acid by approximately 4-fold; these rates were further increased by exposure to continuous light. Diurnal rhythmicity of kynurenic acid release was clearly exogenous and did not match with the circadian pattern of kynurenine or tryptophan aminotransferase activities; no rhythm was detected in constant darkness. Similar findings were obtained on turnover of 3-hydroxykynurenine to xanthurenic acid and release of the product to the medium. However, light/dark differences were relatively smaller, and additional products were formed, according to HPLC data obtained with electrochemical detection. Results are most easily explained on the basis of a recently discovered pathway of kynurenic acid formation from kynurenine, involving either non-enzymatic oxidation by H(2)O(2) or, at higher rates, enzymatic catalysis by hemoperoxidase. A corresponding mechanism may exist for the hydroxylated analogue.

Animals↗
PubMed2001

Dysfunctional mitochondria, not oxygen insufficiency, cause cancer cells to produce inordinate amounts of lactic acid: the impact of this on the treatment of cancer.

It has been known for decades that cancer cells produce excessive amounts of lactic acid. The fact that most cancers have poor vascular systems has led cancer scientists to assume that such cells are deprived of a normal supply of oxygen. Researchers believe that without sufficient oxygen, cancer cells must revert to fermentation for their energy supply and this is what causes them to produce excessive lactic acid. I challenge this traditional assumption and suggest instead that cancer cells have dysfunctional mitochondria, which prevent their use of the citric acid or Krebs cycle. Consequently, pyruvic acid, the end product of glycolysis, which normally would enter the mitochondria for its total combustion into energy, is instead converted to lactic acid. Evidence exists to support this hypothesis which, when acknowledged, could dynamically impact both cancer research and the treatment of all forms of cancer.

Humans↗
PubMed1996

Two potential indole-3-acetaldehyde dehydrogenases in the phytopathogenic fungus Ustilago maydis.

The phytopathogenic basidiomycetc Ustilago maydis produces indole-3-acetic acid (IndCH2COOH) and indole-3-pyruvic acid (Ind-Prv) from tryptophan. Indole-3-acetaldehyde (IndCH2CH2O) is the common intermediate in the conversion of Ind-Prv and tryptamine to IndCH2COOH. We purified an enzyme (Iad1) from U. maydis that catalyzes the NAD(+)-dependent conversion of IndCH2CH2O to IndCH2COOH and isolated corresponding cDNA and genomic clones. The identity of the cDNA clone was confirmed by expression in Escherichia coli and demonstration of enzymatic activity. In U. maydis, iad1-null mutants were generated by gene replacement. The ability to convert IndCH2CH2O to IndCH2COOH was at least 100-fold reduced in U. maydis iad1-null mutants grown in medium with glucose as carbon source. However, the iad1-null mutants were not diminished in their capacity to produce IndCH2COOH from tryptophan, indicating that IndCH2COOH formation from tryptophan apparently proceeds in the absence of IndCH2CH2O dehydrogenase activity under these conditions. Iad1 expression was strongly induced during growth on ethanol while under these conditions iad1-null mutants were unable to grow. This reveals that iad1 is primarily engaged in the conversion of ethanol to acetate. In iad1-null mutants we detected an additional NAD(+)-dependent IndCH2CH2O dehydrogenase activity that was induced during growth on L-arabinose but repressed in the presence of D-glucose. In arabinose-containing medium the conversion of tryptophan to IndCH2COOH was approximately 5-fold reduced in wild-type strains but 10-15-fold reduced in iad1-null mutant strains compared to IndCH2COOH formation in glucose-containing medium. In addition, the formation of Ind-Prv from tryptophan was abolished in wild-type and iad1-null mutant strains. During growth on arabinose, the conversion of tryptamine to IndCH2COOH was strongly favored suggesting that the glucose-repressible IndCH2CH2O dehydrogenase is required to convert IndCH2CH2O derived from tryptamine to IndCH2COOH.

Aldehyde Dehydrogenase↗
PubMed1988

In vitro and in vivo Phlebovirus inhibition by ribavirin.

Ribavirin (1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide) was markedly inhibitory in vitro to Adames and Balliet strains of Punta Toro virus (PTV), a Phlebovirus related to Rift Valley fever and sandfly fever viruses. By using inhibition of viral cytopathic effect in LLC-MK2 cells with both virus strains, the 50% effective dose was 4 to 10 micrograms/ml and the virus rating was 1.3. The Adames strain of PTV infection in mice was established for evaluation of the in vivo antiviral efficacy of ribavirin. The drug was administered subcutaneously (s.c.) twice daily for 5 to 7 days beginning 4 h pre-virus inoculation, 24 h post-virus inoculation, or 36 h post-virus inoculation, with increased survivors, reduced hepatic icterus, reduction of serum glutamic oxalic acid transaminase and serum glutamic pyruvic acid transaminase, and inhibition of infectious virus from sera and livers of infected mice. The minimum effective dose was 4.7 mg/kg per day, with a maximum tolerated dose of 75 mg/kg per day. When the same treatment schedule beginning 4 h pre-virus inoculation, 4 h post-virus inoculation, or 24 h post-virus inoculation was used, orally administered ribavirin was effective at doses as low as 6.3 mg/kg per day. Single s.c. ribavirin treatments at doses of 175 to 700 mg/kg administered from 4 to 48 h post-virus inoculation were also effective. No effect was seen when ribavirin was administered s.c. to mice infected intracerebrally with the PTV strain Balliet, even though treatment was begun 36 h before virus exposure.

Animals↗
PubMed1987

A new low-molecular-weight component promoting adrenergic development in cultured chick sympathetic neurons.

A low-molecular-weight component present in medium conditioned by cultured chick liver cells (LCM) enhances the adrenergic properties of dissociated chick superior cervical ganglion (SCG) neurons in culture (Zurn and Mudry, 1986). This substance cannot replace NGF as a survival, growth, or differentiation factor. However, in the presence of NGF, it stimulates neuronal metabolism and catecholamine (CA), but not ACh production by the SCG neurons. The effect on transmitter production is greater than that on neuronal metabolism. Yet this is not due to an increase in the specific activity of tyrosine hydroxylase (TH), the rate-limiting enzyme in CA synthesis. Interestingly, the effect of LCM on CA and ACh production, but not on neuronal metabolism, is potentiated in the presence of a large excess of NGF. The active component(s) present in LCM has a molecular weight lower than 500 Da and is not inactivated by heat or pronase treatment. So far, none of the small molecules tested (ascorbic acid, pyruvate, glucose, L-glutamic acid, glutathione, etc.) were able to mimic the effects of LCM on the SCG neurons. Thus this report describes a novel low-molecular-weight component different from NGF that promotes metabolism and adrenergic development in cultured chick sympathetic neurons.

Acetylcholine↗
PubMed1978

A study on cerium-induced liver injury in rats after pretreatment with spironolactone, phenobarbital, pregnenolone-16 alpha-carbonitrile and nafenopin.

A number of drugs known to induce liver microsomal enzymes were studied with respect to their effect on the elevated liver triglyceride (TG) concentration and serum glutamic oxaloacetic acid transaminase (GOT) and glutamic pyruvic acid transaminase (GPT) activities induced by an i.v. injection of cerium in rats. Pretreatment with pregnenolone - 16 alpha - carbonitrile (PCN) and 2-methyl-2-[p-(1,2,3,4-tetrahydronaphth-1-yl)phenoxy]-propionic acid (nafenopin) decreased the liver TG concentration significantly. Spironolactone and phenobarbital pretreatment also decreased the TG level in comparison to controls, but the difference was not statistically significant. Both GOT- and GPT-activities in serum increased on the first day after cerium injection and reached a maximum after 3 days. All the drugs significantly reduced the elevated levels. After 7 days the activity was almost normal in all the surviving animals.

Alanine Transaminase↗
PubMedDate not supplied

Novel microbial inhibitors of ACE. Isolation and characterization.

Two novel microbial ACE-inhibitors BAY o 6997 and BAY q 1313 were detected in the fermentation broths of streptomyces spec. WS 464 and spec. WS 1065, respectively. Both were isolated and purified by ion exchange chromatography as initial steps, and final purification was achieved by HPLC or additional chromatography of the Cu-chelate (BAY q 1313). Both inhibitors are reversibly inactivated on chelation with Cu2+ or Zn2+. Irreversible inactivation occurs on standing in aqueous and acidic solution or in ammonium hydroxide at room temperature and more rapidly on heating. In 4 M sodium hydroxide solutions BAY o 6997 is completely stable, and BAY q 1313 still remarkably stable even on longer heating to 80 degrees C. Thus, BAY o 6997 was alternatively and advantageously isolated after heating of its solution in 4 M sodium hydroxide to 37 degrees C for 2 days and subsequent fractional precipitation with ethanol in a relatively pure state. Total hydrolysis yielded His, 2-methylamino-4-amino-butyric acid and alpha-keto butyric acid (BAY o 6997) and pyruvic acid (BAY q 1313) respectively. The unusual stability of both inhibitors in sodium hydroxide solution on the one hand and their instability on heating and storage in aqueous or acidic solutions on the other hand clearly prove that the constituents are not linked by amide bonds.

Ammonium Hydroxide↗
PubMed1975

Inhibition of pyruvate transport by fatty acids in isolated cells from rat small intestine.

1. A technique is described for the rapid separation of intestinal epithelial cells from the incubation medium by passage through a silicon-oil layer and collection in acid, in which their soluble constituents are released. 2. The inhibition by fatty acids of pyruvate oxidation is further studied. Measurement of pyruvate transport in epithelial cells at 0 degree C showed that short- and medium-chain fatty acids as well as ricinoleate inhibit this transport. Propionate inhibits pyruvate transport by another mechanism than octanoate. 3. Differences between pyruvate propionate and octanoate transport across the epithelial cell membrane were obtained in efflux studies. These studies revealed that acetate, propionate, butyrate and high concentrations of bicarbonate readily stimulate the efflux of pyruvate, probably by anionic counter-transport. No effects were seen with octanoate and hexanoate. The data obtained in these efflux studies suggest that lipophilicity and the pKa values of the monocarboxylic acids determine the contribution of non-ionic diffusion to overall transport. 4. Saturation kinetics, competitive inhibition by short-chain fatty acids and counter-transport suggest a carrier-mediated transport of pyruvate.

Animals↗
PubMed2002

Kinetic and mechanistic investigations on reductions of aflatoxins by lactic acid.

The kinetics of reduction of AFB(1) to AFB(2) and AFG(1) to AFG(2) by lactic acid has been investigated in dilute aqueous acidic solutions (pH 3.35-4.50) as a function of the concentrations of lactic acid, AFB(1), AFG(1) and hydrogen ion at 37 degrees C. The rate of the reaction was found to be first order with respect to the concentrations of lactic acid and aflatoxins and independent on hydrogen ion concentration. The experimental results are interpreted in terms of mechanisms involving an initial formation of transient oxonium intermediate, which tends to polarize the olefinic (C=C) carbon, which in turn causes the hydride abstraction from alpha-carbon atom of lactic acid in rate determining step. The proposed mechanisms involve an overall transfer of two protons and two electrons from lactic acid to AFB(1) and AFG(1) to give the corresponding reduced less toxic products AFB(2) and AFG(2) and the oxidised product pyruvic acid.

Aflatoxins↗
PubMed1991

[Biochemical and anatomic changes in the muscles after leg bone lengthening by the Ilizarov method].

In process of crus lengthening, following the method, given by Ilizarov G. A., with 22 adult patients have been studied the peculiarities of metabolic processes of muscle tissue of the lengthened segment as well as the muscle tissue structural changes. As the tests were used; determination of lactate dehydrogenase content and its isoenzymatic spectrum in the blood serum, the residual products of lactic and pyruvic acids glycolysis, relating to the higher indications of the internal medium of an organism; carboxylase activity detection. Energy provision of an organism was estimated according to the ATP content; anatomical state of muscles of the lengthened extremity segment and muscle tissue structure were estimated by means of contrast myography. Dynamics of biochemical indexes suggests that the sparing character of an operation, patient mobility from the first days, preservation of locomotive and supporting function contribute to prevention of metabolic disease and ensure earlier transformation of catabolic reaction to anabolic one. Carboxylase and lactate-dehydrogenase activity increase indicates the biochemical adaptation of an organism. Metabolic changes well correlate with the detected structural changes in the lengthened crus muscles.

Adenosine Triphosphate↗
PubMedDate not supplied

[The state of the microsomal oxidative system in the rat liver during fecal peritonitis].

Content and activity of cytochrome P-450, activity of main microsomal enzymes as well as content of glycogen, lactic and pyruvic acids were studied in liver tissue of rats within 24, 48 and 72 hrs after simulation of acute fecal peritonitis. Inhibition of the enzymatic activity of microsomal oxidative system correlated with hypoxia which developed in liver tissue within all the periods of acute fecal peritonitis studied. At the same time, catalytic activity of cytochrome P-450 was increased towards substrates of the I and II types. Endotoxemia and hypoxia of liver tissue, resulting in activation of phospholipases, appear to be mainly responsible for inhibition of microsomal enzymes activity in liver tissue under conditions of acute peritonitis.

Acute Disease↗