The mechanism of the formation of organic acids by mould fungi; the formation of acetic and pyruvic acids in Aspergillus niger growing in glucose media.
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The lactic acid/pyruvic acid quotient of rat anterior pituitary varies betweeen 30 and 80. The dominance of lactic acid is in accordance with the earlier observation that pituitary lactate dehydrogenase isoenzymes in rat are made up, in majority, of M subunits. The pituitary lactic acid concentration in female and male animals shows no appreciable difference and does not change 2 and 4 weeks after castration. In males the pituitary pyruvic acid concentration was almost double of that in females. Pyruvic acid content increases after ovariectomy and decreases after orchidectomy. The sexual differences having been observed in lactic acid/pyruvic acid quotient are in correlation with the discrepancy of pyruvic acid concentration.
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Etching of enamel surfaces produces a marked increase in the bond strength of dental materials to tooth structure. The results of recent studies have indicated that pyruvic acid may be used in preference to phosphoric acid, because of its milder etching effect on enamel surfaces, without adversely affecting the bond strength. The pulpal responses elicited by 10% pyruvic acid applied for 90 seconds to freshly prepared cavities in monkey teeth, were examined after 4, 14 and 42 days. The differences between some of the ariteria used to evaluate the pulpal responses in acid-treated and control teeth at the three post-operative time intervals were statistically significant. These results suggest that exposed dentin should be protected with a lining before etching adjacent enamel surfaces with 10% pyruvic acid.
The methyl ester of pyruvic acid (methyl pyruvate) stimulated a dose-dependent increase in insulin secretion from isolated perifused rat islets. The threshold level for release was about 10 mM, and at 20 mM the addition of MP to perifused islets resulted in a large first phase of secretion followed by an insulin-secretory response that was sustained for at least 40 min. When compared to the effects of 20 mM glucose, peak first-phase release rates in response to 20 mM methyl pyruvate were comparable, but the second phase of release was only about 10-15% of that observed with an equimolar level of the hexose. The stimulatory effects of 20 mM methyl pyruvate on secretion were abolished by the K1+-ATP channel blocker diazoxide (200 microM) and by the calcium channel antagonist nitrendipine (500 nM). The glucokinase inhibitor mannoheptulose (20 mM) had no adverse effect on the secretory response to 20 mM methyl pyruvate, whereas 10 microM forskolin amplified the insulinotropic action of MP. Sodium pyruvate alone or in combination with 10 microM forskolin had no insulinotropic effect. In additional experiments islet phosphoinositide pools were labeled with myo-2-[3H]inositol, and the subsequent accumulation of labeled inositol phosphates was used to monitor the activation of phospholipase C. Methyl pyruvate stimulated a dose-dependent increase in inositol phosphate levels when measured after a 30-min incubation period with a maximal increase of about 300% at 20 mM methyl pyruvate. The increase in phosphoinositide hydrolysis caused by methyl pyruvate (20 mM) was, like insulin secretion, reduced by both diazoxide and nitrendipine but was immune to inhibition by mannoheptulose. Pyruvate (20 mM) had no effect on inositol phosphate accumulation. Prior short-term exposure to methyl pyruvate sensitized islets to subsequent stimulation with 15 mM glucose. Sodium pyruvate did not sensitize islets. These findings support the concept that the mitochondrial metabolism of nutrient molecules is an event sufficient to acutely augment insulin release from the beta cell, to increase phospholipase C-mediated phosphoinositide hydrolysis, and to induce time-dependent potentiation of insulin secretion.
The lambda > 300 nm photolysis of h4- or d4-pyruvic acid aqueous glasses at 77 K yields identical electron magnetic resonance (EMR) spectra arising from distant (r greater or similar 0.5 nm) triplet radical pairs. Spectra comprise: (1) well-resolved quartets, X, at g approximately ge, that closely match the powder spectra of spin pairs interacting across r approximately 1.0 nm with D approximately 3.0 mT, E approximately 0 mT zero field splittings (ZFS), and (2) broad signals, Y, centered at g approximately 2.07 that display marked g-anisotropy and g-strain, exclude D greater or similar 20.0 mT values (i.e., r less or similar 0.5 spin nm separations), and track the temperature dependence of related g approximately 4 features. These results imply that the n-pi excitation of pyruvic acid, PA, induces long-range electron transfer from the promoted carbonyl chromophore into neighboring carbonyl acceptors, rather than homolysis into contact radical pairs or concerted decarboxylation into a carbene. Since PA is associated into hydrogen-bonded dimers prior to vitrification, X signals arise from radical pairs ensuing intradimer electron transfer to a locked acceptor, while Y signals involve carbonyl groups attached to randomly arranged, disjoint monomers. The ultrafast decarboxylation of primary radical ion pairs, 3[PA+* PA-*], accounts for the release of CO2 under cryogenic conditions, the lack of thermal hysteresis displayed by magnetic signals between 10 and 160 K, and averted charge retrotransfer. All EMR signals disappear irreversibly above the onset of ice diffusivity at approximately 190 K.
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BACKGROUND: Acne is one of the most common dermatological diseases, affecting about 50% of adolescents. Different chemical peelings are used in local treatment, either alone or in association with other therapies. OBJECTIVE: To evaluate the efficacy and tolerability of chemical peeling with pyruvic acid for treatment of mild to moderate papulo-pustular acne. METHODS: We conducted an open-label study in which patients affected by mild to moderate papulo-pustular acne were treated with 40-50% pyruvic acid every 2 weeks for a total of 3-4 months. Forty patients (26 women and 14 men), ranging in age from 18 to 30 years, were enrolled in the study. Evaluations of sebum production and skin hydration were performed before and after treatment in 24 patients. RESULTS: Complete remission was observed in 16 patients (40%), partial remission was detected in 20 patients (50%), and no improvement was seen in four patients (10%). No side-effects were observed during or after treatment. Post-treatment evaluation of sebum production in 24 patients revealed a reduction in sebum levels in all patients. Post-treatment values of cutaneous hydration did not vary significantly from pretreatment values in the 24 patients evaluated. CONCLUSIONS: The results of our study indicate that peeling with pyruvic acid can be considered an effective, safe and well-tolerated procedure in the treatment of patients affected by mild to moderate papulo-pustular acne.
We isolated the ipdc gene coding for indole-3-pyruvic acid decarboxylase (IPDC), a key enzyme in the indole-3-pyruvic acid pathway for indole-3-acetic acid biosynthesis, in the plant growth-promoting rhizobacterium Azospirillum lipoferum FS. Gel mobility-shift assay showed the presence of two DNA-binding proteins that might be involved in regulation of the ipdc gene expression.
The authors studied the effect of chlorfenvinphos on the pyruvic acid level in the liver and cardiac muscle of male Wistar rats. The animals were intoxicated with chlorfenvinphos in a single oral dose of 5 mg/kg (0.5 LD50). The pyruvate was assayed spectrophotometrically after 2, 4 and 24 hours following administration of the insecticide. The results obtained indicate that after intoxication with chlorfenvinphos there are no changes in the pyruvic acid level in the liver, but in the heart muscle, two hours after administration of insecticide, a significant decrease of this keto acid was observed. No alterations were found 4 and 24 hours after intoxication with chlorfenvinphos.
The carbonyl-amine reaction between pyruvic acid and alpha-amino alcohols was monitored by Fourier transform infrared spectroscopy at a temperature range between 20 and 100 degrees C and under acidic and basic conditions. To avoid interference, the reactions were conducted in the absence of solvent using liquid reactants such as methyl pyruvate, pyruvic acid, ethanolamine, and 1-amino-2,3-propanediol. Analysis of the time- and temperature-dependent spectra indicated that under basic conditions and at room temperature, the initial imine formation and its subsequent isomerization through a 1,3-prototropic shift occur very rapidly and the reaction goes to completion within 12 min. Interestingly, the isomerization product of the initial imine is the so-called Schiff base intermediate formed when the corresponding amino acid and the reducing sugar react during a typical Maillard reaction. Furthermore, the detailed studies also indicated that during the first 30 s, the rate of formation of the initial imine was faster than the rate of its isomerization; however, after 60 s, its rate of isomerization becomes faster than the rate of its formation. The data also indicated that under acidic conditions, this isomerization was prevented from occurring and the reaction was terminated at the initial imine formation stage. In addition, temperature-dependent spectra indicated that the isomerization of the Schiff's base into eneaminol can be achieved at or above 60 degrees C and its subsequent rearrangement into Amadori product can be attained at temperatures above 80 degrees C even under basic conditions, thus providing a novel route to Maillard reaction products starting from a keto acid and an amino alcohol. This observation was also confirmed through identification of the common Amadori product in both keto acid/amino alcohol and sugar/amino acid mixtures, by the application of tandem mass spectrometry and chemical ionization techniques.
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Hydralazine is an antihypertensive vasodilator agent. Lack of specific assay techniques for its measurement have delayed elucidation of its pharmacokinetic profile. This study compares the plasma profiles of hydralazine, measured both by a specific and by a previously published nonspecific assay and of a major plasma metabolite, hydralazine pyruvic acid hydrazone. After po and iv administration of hydralazine, peak hydralazine levels were lower (7-33%) and plasma half lives were shorter (15-31%) when measured by the specific technique. The mean plasma half life of the pyruvic acid hydrazone was 156 min and mean urinary clearance, 28 ml/min. The plasma profile of hydralazine and of the major metabolite, the pyruvic acid hydrazone, do not appear to correspond to the duration of antihypertensive effect of administered hydralazine.
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