[Content of pyruvic acid and lactic acid in the intraocular fluids. Further contribution to the study of the metabolism in vivo of retinal tissue].
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Aqueous Humor↗
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In vitro kinetic studies of the reaction of hydralazine and its acetone hydrazone with pyruvic acid.
To understand the reaction between hydralazine (HP) or its acetone hydrazone (HAH), a metabolite of HP and pyruvic acid, a new selective HPLC method for simultaneous determination of HP, HAH, and hydralazine pyruvic acid hydrazone (HPH) was developed. In vitro degradation of HAH and formation of HP and HPH were investigated at pH 7.4 and 37 degrees C in the presence or absence of pyruvic acid. Hydralazine degraded slowly according to an apparent first-order rate (7.46 x 10(-2)h-1). The degenerative reaction of HAH, accompanied by simultaneous hydrolysis to the parent drug HP, was also subject to apparent first-order loss (3.00 x 10(-1)h-1). In addition, HAH was partly converted to HP and HPH in the presence of pyruvic acid. For the formation pathway of HPH, a model that included the direct reaction of HAH with pyruvic acid and the secondary formation mediated by back-conversion to HP gave a better fit to the experimental data than the model consisting of the latter reaction only. About 10% of the HPH formed was generated by the direct reaction of HAH with pyruvic acid, based on the rate constants estimated. These results suggest that the formation of HPH is not all accomplished through back-conversion to HP.
Chemical Phenomena↗
[Effect of nutritional conditions on the fermentative production of pyruvic acid by Torulopsis glabrata].
The effects of some nutritional conditions, such as peptone concentration, feeding glucose as well as oxygen supply manner and ratio of C/N in batch culture, on the fermentative production of pyruvic acid by Torulopsis glabrata WSH-IP12 were investigated. In shaking-flask culture: (1) peptone of more than 20 g/L inhibited the accumulation of pyruvic acid; (2) production of pyruvic acid was increased from 23.5 g/L to 30.2 g/L by simply feeding glucose. In 5 L jar-fermentor batch culture: (1) high level of dissolved oxygen and (2) increasing the concentration of glucose and peptone proportionally with constant C/N ratio(26:1) improved the production of pyruvic acid. It was also found that, glucose consumption and pyruvic acid production almost stopped under the condition of nitrogen difficiency while recovered by adding peptone and (NH4)2SO4. By using ammonia water instead of potassium hydroxide for the control of pH, the cells kept stronger ability for synthesizing pyruvic acid within the whole process, 57.3 g/L pyruvic acid with the yield of 0.498 g/g was achieved at 55 h of fermentation.
Candida↗
Pyruvic acid as an etching agent in clinical dentistry.
The objective of this study was to evaluate the use of pyruvic acid as an alternative etching agent to phosphoric acid (H3PO4). Solutions containing 5, 10, 15, 20, 25, and 30 m/m % pyruvic acid and 50% m/m H3PO4 were prepared. The tensile bond strengths of a composite resin to enamel surfaces etched with the respective etching agents were determined. The rates of etching of enamel surfaces by each of the etching solutions were evaluated. Unground and polished enamel surfaces were etched with the respective etching solutions and the surfaces examined by scanning electron microscopy. The tensile bond strengths of the resin to enamel surfaces etched with 10-30% pyruvic acid exceeded those obtained on enamel surfaces etched with 50% H3PO4. The rates of etching of all the pyruvic acid solutions were significantly less than of H3PO4. Well-defined etching patterns were observed on the enamel surfaces etched with all the etching solutions. The results of this laboratory study suggest that pyruvic acid may be a suitable alternative to phosphoric acid as an etching agent in clinical dentistry.
Acid Etching, Dental↗
Occurrence of pyruvic acid in capsular polysaccharides from various Klebsiella species.
Capsular polysaccharide materials from several different klebsiella serotypes were demonstrated to contain an alpha-keto acid characterized as pyruvic acid. Linkage to the capsular polysaccharides was shown to be acid labile and alkali stable, suggesting ketosidic rather than ester linkages.
Amino Acids↗
Study of blood pyruvic acid levels in pellagrins with and without neurological manifestations and response to nicotinic acid therapy.
In 25 cases of pellagra and 10 healthy controls, the blood pyruvic acid levels in the fasting stage and after 60 and 90 minutes of glucose load were estimated by the technique of Friedmann & Haugen (1943). The blood pyruvic acid levels after 60 and 90 minutes of glucose load were significantly higher in pellagrins as compared to controls. The following conclusions were drawn from this study: (i) that there is impairment of pyruvic acid metabolism in cases of pellagra, which is more marked in pellagrins with neurological manifestations than in those without; (ii) that after administration of nicotinic acid alone for 15 days the pyruvic acid levels returned to normal, thereby indicating that nicotinic acid deficiency is the cause of deranged pyruvate metabolism; (iii) that there is significant improvement in neurological status after nicotinic acid therapy.
Adolescent↗
Effect of acephate (orthene) on tissue levels of thiamine, pyruvic acid, lactic acid, glycogen and blood sugar.
Effect of Acephate, an organophosphorus insecticide, on tissue levels of thiamine, pyruvic acid, lactic acid, glycogen and blood sugar, has been studied. The albino rats, injected subcutaneously with Acephate (25 mg/10 gm body wt./day) for 4 weeks and 8 weeks, showed appreciable depletion of thiamine in liver, heart, kidney, brain and blood. The depletion of thiamine was found to be more after 8 weeks of Acephate injection. There was concomitant increase in pyruvic acid and lactic acid in various tissues. There was enormous depletion of glycogen in liver and slight rise in blood sugar concentration. The animals injected thiamine (120 micrograms/100 gm body wt./day) along with Acephate, showed more or less normal levels of thiamine, pyruvic acid, lactic acid, liver glycogen and blood sugar. The increase in pyruvic acid and lactic acid in tissues has been attributed to depletion of thiamine which is required of pyruvic acid oxidation. The increase in blood sugar has been attributed to the excess breakdown of glycogen.
Animals↗
Aminopyrazine analogues as chemiluminescence derivatization reagents for pyruvic acid.
Aminopyrazine analogues were studied as sensitive and selective chemiluminescence derivatization reagents for pyruvic acid. These analogues reacted with pyruvic acid under acidic conditions at 100 degrees C to produce Cypridina luciferin derivatives, which exhibit chemiluminescence by reaction with hydrogen peroxide in the presence of potassium t-butoxide in dimethylformamide. Of the four aminopyrazine analogues (2-amino-5-phenylpyrazine, 2-amino-5-(4-hydroxyphenyl)pyrazine, 2-amino-5-(3,4, 5-trimethoxyphenyl)pyrazine, and 2-aminoquinoxaline), in the present test 2-amino-5-(3,4,5-trimethoxyphenyl) pyrazine was the most sensitive for pyruvic acid, and the chemiluminescence intensity was about four times higher than that obtained with aminopyrazine.
Indicators and Reagents↗
[The important role of vitamins in the over-production of pyruvic acid].
The effect of nicotinic acid, thiamine, pyridoxine, biotin and riboflavin on the production of pyruvic acid by Torulopsis glabrata WSH-IP303 with glucose as carbon source and NH4Cl as sole nitrogen source was investigated. By using orthogonal experiment method, thiamine was confirmed to be the most important factor affecting the production of pyruvic acid. Based on a certain concentration range of thiamine (0.01-0.015 mg/L), glucose consumption rate can be enhanced by increasing the concentration of nicotinic acid. When the concentration of nicotinic acid, thiamine, pyridoxine, biotin and riboflavin were 8, 0.015, 0.4, 0.04 and 0.1 mg/L, respectively, the concentration and yield to glucose of pyruvic acid reached 52.4 g/L and 0.525 g/g at 48 h in flask culture, respectively. Batch culture was conducted in a 2.5 L fermentor with initial glucose concentration of 120 g/L. By adopting the optimal concentration combination of vitamins, the concentration and yield to glucose of pyruvic acid reached 69.4 g/L and 0.593 g/g at 57.5 h, which were increased by 32.4% and 13% than the best results in flask culture, respectively.
Ammonium Chloride↗
Indole-pyruvic acid treatment reduces damage in striatum but not in hippocampus after transient forebrain ischemia in the rat.
The effects of treatment with indole-pyruvic acid, an endogenous metabolite of tryptophan converted into kynurenic acid in the brain, were studied in rats after transient forebrain ischemia induced by the 4-vessel occlusion procedure. The histological analysis showed a significant protective effect of indole-pyruvic acid treatment on striatal ischemic lesions assessed by the extent of regional atrophy and the area of neuronal disappearance 14 days after ischemia. Striatal neurons were labelled by dopamine and adenosine 3':5' monophosphate regulated phosphoprotein-32 immunoreactivity. Conversely, increased neuronal loss, regional atrophy and glial fibrillary acidic protein immunoreactivity, an index of post-injury astroglial activation, were observed in the hippocampal formation, especially the CA3 field, of indole-pyruvic acid-treated rats when compared with vehicle-treated ischemic rats. The treatment with indole-pyruvic acid did not produce any improving effects in a test assessing short-term impairments after transient ischemia (motor test score at 24 h and 48 h post-ischemia). Furthermore, no significant effects of indole-pyruvic acid treatment were found on performance in water T-maze studied at 7 and 14 days post-ischemia. The opposite effects of indole-pyruvic acid on ischemic lesion in different brain regions may be related to its multiple neurochemical actions in the brain. The protective effect of indole-pyruvic acid on ischemic damage in striatum may be due to its conversion into kynurenic acid, a broad spectrum glutamate receptor antagonist. At hippocampal level, where glutamate receptor antagonists have been proved ineffective in the present lesion model, indole-pyruvic acid-induced changes in monamine availability may lead to a worsening of neuronal damage.
Animals↗
Angiogenic activity of pyruvic acid in in vivo and in vitro angiogenesis models.
The excessive growth of a tumor requires high rates of glucose uptake and glycolysis and continuous recruitment of new blood vessels. Here, we provide several lines of evidence showing that pyruvic acid, the end product of glycolysis, exhibits strong angiogenic activity. Pyruvic acid promoted angiogenesis in chorioallantoic membrane assay and in vivo mouse Matrigel plug assay. Pyruvic acid also positively affects angiogenic cascade, DNA synthesis, migration, and tube formation in bovine aortic endothelial cells. Furthermore, mRNA expression of fibroblast growth factor receptor-2 and vascular endothelial growth factor was enhanced by pyruvic acid. These results strongly suggest that pyruvic acid plays an important role in angiogenesis for tumor growth and metastasis.
Allantois↗
In vitro correlation between two colorimetric assays and the pyruvic acid consumption by fibroblasts cultured to determine the sodium laurylsulfate cytotoxicity.
The target of this research was to determine the cytotoxicity of sodium laurylsulfate on single-layer cultures of human fibroblasts, using two colorimetric methods (neutral red and MTT tests) and the evaluation of the pyruvic acid consumption by the cells. For the determination of the cytotoxicity by colorimetric tests, we have determined the absorbance at 540 nm using a spectrophotometer. Pyruvic acid, present in the culture medium, is the mitochondria's C3 energetic metabolite. So, a measure of the cell's consumption of pyruvic acid was developed. The reaction is as follows: Pyruvic acid + NADH --> Lactic acid + NAD+ and the enzyme employed is the LDH (lactate dehydrogenase). This method can be used to measure cytotoxicity, proliferation, and the cell's activation. The method is rapid, precise, and lacks any toxic byproduct. The absorbance was measured using a spectrophotometer at 340 nm. The consumption of pyruvic acid follows upon the fibroblast's growth. Sodium laurylsulfate cytotoxicity test after 24 h shows that the NR colorimetric test and the pyruvic acid consumption are correctly correlated (r = 0.91, alpha = 0.05). This dosage can be used to study the barrier properties of the corneocyte layer without destroying the artificial skin.
Cells, Cultured↗
[Effect of heavy mechanical trauma on content of lactic and pyruvic acids in rat brain].
The content of lactic and pyruvic acids in the brain was studied as affected by heavy mechanical trauma. It was established that under the trauma effect the content of lactic acid in the brain tissue increases and phase changes are observed in the content of pyruvic acid and in the value of the lactate pyruvate ratio. Lactic acid accumulates most intensively in the cerebellum, cortex and subcortical areas of the brain, and less intensively--in medulla oblongata and spinal cord.
Animals↗
[Evaluation of pyruvic acid concentration in blood of patients with ischemic stroke in the earliest stage of the disease].
The aim of the study was the assessment of concentrations of pyruvic acid in the blood of patients with mild course and severe course of ischaemic stroke in the earliest stage of the disease. The subject of the study were 20 patients with a mild ischaemic stroke and 20 patients with a severe one on its 1st, 3rd and 7th day. Enzymatic method for determining pyruvic acid content in the blood was used (ready made reagents Test-Combination Pyruvate by Boerhinger Mannheim). In the group of patients with mild ischaemic stroke the concentrations of pyruvic acid were increased on all days of the disease, compared with controls, but the differences were statistically insignificant. In the group of patients with severe ischaemic stroke the concentrations of pyruvic acid were higher than the ones in control group, but only on the 1st and 3rd day of the disease the differences were statistically significant. The results of determinations indicate that there is a positive correlation between levels of pyruvic acid and severity of the clinical course of the disease.
Cerebral Infarction↗
Synthesis, formulation, and clinical pharmacological evaluation of hydralazine pyruvic acid hydrazone in two healthy volunteers.
Hydralazine pyruvic acid hydrazone [2-(phthalazin-1-yl hydrazono)propionic acid; 1] is a major plasma metabolite of hydralazine in humans. A number of in vitro and animal studies have suggested that this hydrazone may have cardiovascular activity and could account for the prolonged antihypertensive effect of hydralazine in humans in the absence of detectable plasma levels of the parent drug. To study this possibility, the soluble sodium salt of hydralazine pyruvic acid hydrazone (2) was synthesized, its chemical purity and stability was checked, and an intravenous formulation was prepared. Isomeric forms were identified. Doses of 0.3, 0.6, and 1.1 mumol/kg of 2 were administered intravenously to one slow and one heterozygous fast acetylator of sulfamethazine. The slow acetylator received two additional doses of 0.06 and 0.14 mumol/kg. Peak plasma levels of 1 of 18 mumol/L were attained without tachycardia or hypotension in either subject. There was no evidence of nonlinearity in kinetics over the dose range studied and clearance remained constant in both subjects (0.517 +/- 0.033 mL/min/kg in the slow acetylator and 0.744 +/- 0.058 mL/min/kg in the fast acetylator). The distribution of 1 varied unpredictably with dose, and changes were reflected in the terminal half-life (3.47-5.97 h in the slow acetylator and 2.06-5.33 h in the fast acetylator). Only traces of the acetylated metabolite of hydralazine, 3-methyl-s-triazolo[3,4-a]phthalazine (3), were detected in the plasma of the subjects, suggesting that significant metabolism via this route was unlikely. An established and specific assay for hydralazine was further modified to allow measurement of levels as low as 1 nmol/L (0.2 ng/mL).(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylation↗
Cytoprotection of pyruvic acid and reduced beta-nicotinamide adenine dinucleotide against hydrogen peroxide toxicity in neuroblastoma cells.
Elevated production of hydrogen peroxide (H2O2) in the central nervous system has been implicated in the pathogenesis of several neurodegenerative diseases, including Parkinson's disease, ischemic reperfusion, stroke, and Alzheimer's disease. Pyruvic acid has a critical role in energy metabolism and a capability to nonenzymatically decarboxylate H2O2 into H2O. This study examined the effects of glycolytic regulation of pyruvic acid on H2O2 toxicity in murine neuroblastoma cells. Glycolytic energy substrates including D-(+)-glucose, D-(-) fructose and the adenosine transport blocker dipyridamole, were not effective in providing protection against H2O2 toxicity, negating energy as a factor. On the other hand, pyruvic acid completely prevented H2O2 toxicity, restoring the loss of ATP and cell viability. H2O2 toxicity was also attenuated by D-fructose 1,6 diphosphate (FBP), phospho (enol) pyruvate (PEP), niacinamide, beta-nicotinamide adenine dinucleotide (beta-NAD+), and reduced form (beta-NADH). Both FBP and PEP exerted positive kinetic effects on pyruvate kinase (PK) activity. Interestingly, only pyruvic acid and beta-NADH exhibited powerful stoichiometric H2O2 antioxidant properties. Further, beta-NADH may exert positive effects on PK activity. Subsequent pyruvic acid accumulation can lead to the recycling of beta-NAD+ through lactate dehydrogenase and beta-NADH through glyceraldehyde-3-phosphate dehydrogenase. It was concluded from these studies that intracellular pyruvic acid and beta-NADH appear to act in concert through glycolysis, to enhance H2O2 intracellular antioxidant capacity in neuroblastoma cells. Future research will be required to examine whether similar effects are observed in primary neuronal culture or intact tissue.
Animals↗
Effect of dapsone on blood lactic and pyruvic acids in leprosy.
The effect of leprosy and dapsone (DDS) on the basal levels of blood lactic and pyruvic acids has been studied. In untreated tuberculoid and lepromatous leprosy patients both of the acids were found to be significantly raised. The rise in lactic acid was relatively more in tuberculoid patients; whereas pyruvic was relatively more elevated in lepromatous cases. Both the acids showed a tendency to increase with the duration of the disease in lepromatous leprosy. Statistically no significant differences were observed in lactic acid levels between untreated and treated cases of both forms of leprosy, suggesting that DDS was not effective in controlling the conditions responsible for the increased lactic acid. On the other hand, pyruvic acid showed a further increase in cases who were on DDS therapy, particularly in lepromatous cases. This indicated that DDS affects pyruvic acid metabolism. Whether DDS disturbs the normal degradative pathway of pyruvic acid or affects pathways of pyruvic acid production is not clear.
Dapsone↗
Interactions between grape anthocyanins and pyruvic acid, with effect of pH and acid concentration on anthocyanin composition and color in model solutions.
The formation of vitisin A, an anthocyanin formed naturally in small quantities in maturing port wines, was studied in model wine solutions at a range of pH values (2.0-4.5) and pyruvate concentrations [molar ratios of pyruvic acid to total anthocyanins (PA/TA) ranging from 12.20 to 172.40]. Additionally, the effect of vitisin A formation on the color changes of these model wines was evaluated. Vitisin A was formed through the interaction between malvidin 3-glucoside and pyruvic acid, and vitisin A in acylated forms, having the 6-position of the sugar acylated with acetic acid (3-acetylvitisin A) and p-coumaric acid (3-p-coumarylvitisin A), formed through the interaction between pyruvic acid and malvidin 3-acetylglucoside and malvidin 3-p-coumarylglucoside, respectively; their identities were confirmed by spectral analysis and FABMS. The maximum formation of these new anthocyanin derivatives was at pH 2. 7-3.0, at the higher pyruvic acid concentration (PA/TA of 172.40 units). The vitisins A caused changes in the color of the solution and expressed about 11 times (pH 3) to 14 times (pH 2) more color than the normal anthocyanins. On aging, the model solutions changed from a bluish red, attributable to the main anthocyanins present, to a slightly more orange red, attributable to the vitisin compounds. The aged models containing vitisins A were all much redder than the more red-brown color of the models aged without pyruvic acid.
Anthocyanins↗