Disease relevance of pyruvic acid

• Topical application of sodium pyruvate (20 mM) significantly attenuated the decline in superfusate glucose during ischemia and enhanced the levels of both glucose and lactate during reperfusion [1].
• Effect of ferrous sulfate, sodium metabisulfite, and sodium pyruvate on survival of Campylobacter jejuni [2].
• The E. coli parental strains reached the non-culturable state in 33 days when the plate counts were evaluated on Luria-Bertani agar containing sodium pyruvate, whereas cells of the rpoS mutants lost their culturability in only 21 days [3].
• Heat-injured C. jejuni repaired (regained dye and bile tolerance) in brucella broth supplemented with Na2S2O3, FeSO4 X 7H2O, and sodium pyruvate within 4 h [4].
• Thirty minutes after the induction of a 240-min controlled arterial hemorrhage targeted at 40 mmHg, hypertonic sodium pyruvate (0.5 g. kg(-1). h(-1)) was infused to achieve an arterial concentration of 5 mM [5].

High impact information on pyruvic acid

• When transiently expressing, MnSOD inhibited AP-1 but increased NF-kappaB transactivation, which can be abolished by sodium pyruvate, a hydrogen peroxide scavenger [6].
• Pyruvate (1 ml/min of 150 mM sodium pyruvate, pH 7.4) was infused directly into the LAD prior to and 30 minutes after a 10 minute LAD occlusion [7].
• A simple modification of the Leibovitz medium by increasing the concentrations of glutamine, lysine, isoleucine, leucine, sodium pyruvate, galactose, and vitamins resulted in over 100% increase in cell growth yield [8].
• Glucose deprivation caused cell death, which was consistent with increased accumulation of H(2)O(2), since three distinct H(2)O(2)-detoxifying systems (N-acetyl-L-cysteine, sodium pyruvate, and catalase) rescued cells against cytotoxicity [9].
• We examined whether or not a mixture of vitamin E (as alpha-tocopherol), sodium pyruvate and phosphatidyl choline (PC), a mixture that promotes wound healing in non-neuronal systems, would provide neuroprotection beyond that observed with vitamin E alone [10].

Chemical compound and disease context of pyruvic acid

• The campylobacter supplement ferrous sulphate, sodium metabisulphite, sodium pyruvate (FBP) (Oxoid) was inhibitory for some isolates; the inhibitory component was found to be sodium metabisulphite [11].
• We conclude that sodium pyruvate is better than sodium chloride as a resuscitation solution in a model of profound hemorrhagic shock [12].
• The exogenous addition of catalase (500-2000 U) or sodium pyruvate (0.05-5%) to a nonselective recovery medium resulted in enhanced detection (12- to 465-fold) of AMW-stressed E. coli as compared with recovery on the medium lacking these supplements, whereas addition of 3,3'-thiodipropionic acid failed to improve recovery [13].
• A resuscitation medium consisting of a trypticase soy broth base supplemented with 0.5% yeast extract, 0.25% sodium pyruvate, 0.01% sodium thioglycollate, and 0.1% chicken fat was used in the resuscitation of heat-injured and freeze-injured cells of Listeria monocytogenes [14].
• METHODS: Sprague-Dawley rats were rendered diabetic by intravenous (i.v.) injection of streptozotocin (55 mg/kg body weight (b.w.)) and treated with sodium pyruvate (2%) in drinking water [15].

Biological context of pyruvic acid

• 3. The kinetics of the inactivating phosphorylation were investigated by measuring inactivation of the complex with MgATP2-. The apparent Km for the Mg complex of ATP was 25.5 microM; ADP was a competitive inhibitor (Ki 69.8 microM) and sodium pyruvate an uncompetitive inhibitor (Ki 2.8 microM) [16].
• Addition of catalase or sodium pyruvate to the surfaces of agar plates increased enumeration of TCE-injured cells by as much as 100-fold, indicating that the TCE-injured cells were ultrasensitive to oxidative stress [17].
• Treating intoxicated rats with sodium pyruvate, we hypothesized, would bypass the putative neurotoxin-induced blockade in glycolysis, thus ameliorating neurobehavioral and morphologic measures of neurotoxicity [18].
• Midway through each study, higher culturable cell counts began to be observed on plates containing catalase or sodium pyruvate; during the latter stages of the study, the plate counts on such media were up to 1,000-fold higher than those on unsupplemented plates [19].
• MEASUREMENTS AND MAIN RESULTS: The intravenous infusion of calcium and sodium pyruvate resulted in increased cardiac output, left ventricular contractility, and mixed venous oxygen saturation values in the experimental group compared with the control group of four dogs [20].

Anatomical context of pyruvic acid

• Effects of sodium pyruvate in nonserum maturation medium on maturation, fertilization, and subsequent development of bovine oocytes with or without cumulus cells [21].
• These results indicate that sodium pyruvate promotes nuclear maturation of bovine CDOs and that a continuing presence of cumulus cells during maturation is important for subsequent development of zygotes to the blastocyst stage [21].
• In 82 tissues with microscopic granulomas and acid-fast bacilli, a significantly greater number of isolates were obtained on Middlebrook 7H10 medium with sodium pyruvate than on Stonebrink medium, Herrold egg yolk agar medium, or Lowenstein-Jensen medium (P=0.01) [22].
• DOs, obtained by mechanically removing cells from cumulus-oocyte complexes (COCs) with a small-bore pipette, were cultured for 45 h in TCM199 supplemented with sodium pyruvate, gonadotropins, estradiol, and 10% porcine follicular fluid, with or without cysteamine (150 microM) [23].
• Hog carotid artery segments were allowed to replete glycogen stores to over 6 micromol/g of new 13C-labeled glycogen by incubation at 37 degrees C with 5 mM [1-13C]glucose for 6-16 h and then were isometrically contracted for 3 h with 80 mM KCl in the presence of 5 mM [2-13C]glucose and either 2 mM sodium acetate or 5 mM sodium pyruvate [24].

Associations of pyruvic acid with other chemical compounds

• These results suggest that the acute toxic effects of commercially available PD on the integrity, proliferation and IL-1 ra production of MC can be avoided by the use of sodium pyruvate instead of sodium lactate [25].
• Cytomix increased the permeability of Caco-2 monolayers to fluorescein isothiocyanate-labeled dextran (FD4; average molecular mass 4 kDa), but this effect was inhibited by adding 0.1 to 10 mM EP (but not similar concentrations of sodium pyruvate) to the culture medium [26].
• 3. Cell extracts also catalyzed the exchange of sodium [14C]formate into sodium pyruvate at an apparent pH optimum of 7.3 to 7.5, but only about 2.5 micronmol of acetylphosphate was produced at this lower pH value [27].
• We observed that inclusion of sodium pyruvate at between 5 and 20 mM in the labeling medium produced a dramatic decrease in incorporation of myristic acid radiolabel into vimentin [28].
• In tests, the adduct prepared with immobilized nicotinamide and sodium pyruvate bound specifically to lactate dehydrogenase (EC 1.1.1.27), whereas the adduct prepared with alpha-ketoglutarate bound to glutamate dehydrogenase (EC 1.4.1.3) [29].

Gene context of pyruvic acid

• Catalase and the intracellular hydrogen peroxide scavenger sodium pyruvate decreased, while hydrogen peroxide increased HUVEC proliferation, migration and activity of eNOS [30].
• Supplementation of the PPIX-based growth media with catalase or sodium pyruvate resulted in normal growth of the H. influenzae oxyR mutant [31].
• In contrast, sodium pyruvate appeared to antagonize D-glucose-induced TGF-beta 1 and MCP-1 secretion [32].
• To test the hypothesis that EP can ameliorate gut barrier dysfunction induced by other forms of inflammation, we incubated Caco-2 monolayers for 24 to 48 h with cytomix (a mixture of interferon-gamma, tumor necrosis factor-alpha, and interleukin-1beta) in the presence or absence of graded concentrations of EP or sodium pyruvate [26].
• Because autoclaving is known to generate hydrogen peroxide in rich media, and because catalase and sodium pyruvate are known to eliminate hydrogen peroxide, it appears that the conditions of the experiments led to the selection of a hydrogen peroxide-sensitive culturable cell subpopulation [19].

Analytical, diagnostic and therapeutic context of pyruvic acid

• The protocol includes: (i) seeding the cells in medium supplemented with sodium pyruvate, alpha-thioglycerol and bathocuproine disulfonate; (ii) delaying the onset of dominant marker selection to improve recovery of the cells after electroporation [33].
• Supplementation of the culture medium with sodium pyruvate favored the culturability and resuscitation of the two A. hydrophila strains at low temperatures (6 and 16 degrees C) [34].
• Improved membrane filtration method incorporating catalase and sodium pyruvate for detection of chlorine-stressed coliform bacteria [35].
• Sodium pyruvate protected cells significantly (P<0.05) against apoptosis in a dose dependent manner as assessed for cell viability by dye exclusion method and apoptosis by TUNEL [36].
• Oral administration of sodium pyruvate at three different dose levels of 125, 250 and 500 mg/kg body weight significantly inhibited the carrageenan induced acute paw edema in a dose dependent manner [37].

References