Oxidation Product Of Glucose Research Articles

Detection of Glucose Oxidation Products in Chilled Fresh Meats Undergoing Spoilage

Detection of Glucose Oxidation Products in Chilled Fresh Meats Undergoing Spoilage

Photooxidation, reduction of the ferric ion-glucose complex

Ferric ions in an acid solution of glucose are reduced by irradiation with light of wavelengths less than 400 nm. The action spectrum for this reaction and the oxidation products of glucose have been determined.

A discussion of the paper “the effect of glucose and some glucose oxidation products on the hydration of tricalcium aluminate” by N. B. Milestone

A discussion of the paper “the effect of glucose and some glucose oxidation products on the hydration of tricalcium aluminate” by N. B. Milestone

A reply to J. Bensted's discussion of the paper “the effect of glucose and some glucose oxidation products on the hydration of tricalcium aluminate”

A reply to J. Bensted's discussion of the paper “the effect of glucose and some glucose oxidation products on the hydration of tricalcium aluminate”

The effect of glucose and some glucose oxidation products on the hydration of tricalcium aluminate

The effect of glucose and some glucose oxidation products on tricalcium aluminate hydration has been studied. The results are in agreement with the theory that stabilization of hexagonal C 4AH 13 determines the retardation. It is assumed that the glucose oxidation products are more effective retarders than glucose because they are more stable in alkaline conditions.

Effect of growth temperature on the accumulation of glucose-oxidation products in Pseudomonas fluorescens.

The effect of the growth temperature, on the accumulation of glucose-oxidation products, was examined in aerated cultures with carbon excess in two strains of Pseudomonas fluorescens. At low growth temperatures (0 and 5 degrees C), 2-ketogluconate (KG) a-cumulated in the medium as the major oxidation product of glucose (up to 70%) before further metabolism. As the growth temperature was increased, the amount of 2-KG found to accumulate in the medium from glucose oxidation decreased. At a growth temperature of 20 degrees C, up to 25% of the glucose originally added accumulated in the medium as 2-KG. At the optimum growth temperature of 30 degrees C or above, no 2-KG was detected at any time during growth with glucose. Similar results were obtained when gluconate was used as the sole carbon and energy source. The results demonstrated a differential effect of growth temperature on the accumulation of oxidation products from glucose and gluconate. At low growth temperatures the major route for the catabolism of glucose and gluconate was the direct oxidative non-phosphorylated pathway.

Poly- -hydroxybutyrate biosynthesis and the regulation of glucose metabolism in Azotobacter beijerinckii.

Azotobacter beijerinckii possesses the enzymes of both the Entner-Doudoroff and the oxidative pentose phosphate cycle pathways of glucose catabolism and both pathways are subject to feedback inhibition by products of glucose oxidation. The allosteric glucose 6-phosphate dehydrogenase utilizes both NADP(+) and NAD(+) as electron acceptors and is inhibited by ATP, ADP, NADH and NADPH. 6-Phosphogluconate dehydrogenase (NADP-specific) is unaffected by adenosine nucleotides but is strongly inhibited by NADH and NADPH. The formation of pyruvate and glyceraldehyde 3-phosphate from 6-phosphogluconate by the action of the Entner-Doudoroff enzymes is inhibited by ATP, citrate, isocitrate and cis-aconitate. Glyceraldehyde 3-phosphate dehydrogenase is unaffected by adenosine and nicotinamide nucleotides but the enzyme is non-specific with respect to NADP and NAD. Citrate synthase is strongly inhibited by NADH and the inhibition is reversed by the addition of AMP. Isocitrate dehydrogenase, a highly active NADP-specific enzyme, is inhibited by NADPH, NADH, ATP and by high concentrations of NADP(+). These findings are discussed in relation to the massive synthesis of poly-beta-hydroxybutyrate that occurs under certain nutritional conditions. We propose that synthesis of this reserve material, to the extent of 70% of the dry weight of the organism, serves as an electron and carbon ;sink' when conditions prevail that would otherwise inhibit nitrogen fixation and growth.

Anodic oxidation of carbohydrates and their derivatives in neutral saline solution.

Rao and Drake1 have recently reported work on the oxidation of dextrose on platinized platinum in neutral buffer solution (pH 7.4). They have shown that anodic charging curves on platinized platinum electrodes in 0.5 M dextrose solution go through an inflexion at about 0.1 V referred to standard hydrogen electrode (SHE) (where platinum starts to adsorb oxygen in neutral solution), after which oxidation is inhibited. No square root dependence was noted for the transition time to this point, indicating that the inhibitive process was not under diffusion control. In addition, the total number of coulombs required to reach the point of inflexion decreased if increasing concentrations of gluconic acid were added to the dextrose solution. They reported open circuit potential (OCP) of + 0.3 V (SHE) in deaerated gluconic acid solution (10−4 to 10−1 M), and they detected no evidence of gluconic acid oxidation in the potential range −0.6 to 0.0 V (SHE). Their general conclusions were that the only oxidation product of glucose in these conditions is gluconic acid, which adsorbs on the electrode in the potential range −0.2 to 0.0 V (SHE), effectively inhibiting glucose oxidation.

Aerobic metabolism of Streptococcus agalactiae.

Streptococcus agalactiae cultures possess an aerobic pathway for glucose oxidation that is strongly inhibited by cyanide. The products of glucose oxidation by aerobically grown cells of S. agalactiae 50 are lactic and acetic acids, acetylmethylcarbinol, and carbon dioxide. Glucose degradation products by aerobically grown cells, as percentage of glucose carbon, were 52 to 61% lactic acid, 20 to 23% acetic acid, 5.5 to 6.5% acetylmethylcarbinol, and 14 to 16% carbon dioxide. There was no evidence for a pentose cycle or a tricarboxylic acid cycle. Crude cell-free extracts of S. agalactiae 50 possessed a strong reduced nicotinamide adenine dinucleotide (NADH(2)) oxidase that is also cyanide-sensitive. Dialysis or ultrafiltration of the crude, cell-free extract resulted in loss of NADH(2) oxidase activity. Oxidase activity was restored to the inactive extract by addition of the ultrafiltrate or by addition of menadione or K(3)Fe(CN)(6). Noncytochrome iron-containing pigments were present in cell-free extracts of S. agalactiae. The possible participation of these pigments in the respiration of S. agalactiae is presently being studied.

Carbohydrates Oxidation by Pseudomonas albosesamae nov. sp.

An oxidation product of glucose, gluconate and 2-ketogluconate by Pseudomonas albosesamae was isolated and examined for its chemical structure. Shaking culture is available for the high yield production. Paper chromatographic analysis of fermented broth for the product gives one spot as “an reducing acid.” The acid was isolated as the unstable powder of calcium salt by methanol precipitation. On periodate oxidation, oxalic and glycolic acids were formed, but formaldehyde was hardly detected. On Ruff’s oxidation of the reduced product prepared by sodium borohydrate or catalytic reduction, D-arabinose and a small amount of L-xylose were detected. On catalytic reduction using Raney nickel, 2-ketogluconic acid was isolated as the main reductant. Bis-2, 4-dinitrophenylhydrazone of the product was obtained as analytically pure yellow needle crystals, m.p. dec. 156~157°C, 5+57.0, pyridine, 1 dm. From the above results, the product was certified to be 2,5-diketogluconic acid.

Oxidation of glucose to γ- and δ-gluconolactone by microbial enzymes

The product of glucose oxidation by three particulate and two soluble glucose-oxidizing enzymes was determined. The particulate enzymes yield glucono-γ-lactone, whereas the soluble ones produce glucono-δ-lactone.

Oxidation of glucose to γ- and δ-gluconolactone by microbial enzymes

Abstract The product of glucose oxidation by three particulate and two soluble glucose-oxidizing enzymes was determined. The particulate enzymes yield glucono-γ-lactone, whereas the soluble ones produce glucono-δ-lactone.

糸状菌の糖類脱水素酵素に関する研究

The anaerobic oxidation of glucose by methylene blue in an alkaline solution containing phosphate or bicarbonate was studied by THUNBERG methylene blue method. To determine the oxidation, products of glucose, the paper chromatography, the color reaction and the isolation of produced matter were studied. By paper chromatogram of oxidation products, seven acid spots appeared in a paper sprayed with bromphenol blue reagent. The seven acid spots were congruent with gluconic acid, 5-ketogluconic acid, 2-ketogluconic acid, glycolic acid, succinic acid, lactic acid, and glyceric anid. The oxidation products indicated the color reactions of gluconic acid, 5-ketogluco nic acid, 2-ketogluconic acid, glycolic acid, succinic acid, lactic acid and glyceric acid. Fromthe oxidation products we obtained gluconic acid as Ca-salt. In the oxidation products of glucose we recognized that there was gluconic acid, and moreover we assumed that there were 5-ketogluconic, acid, 2-ketogluconic acid, glycolic acid, succinic acid, lactic acid, and glycric acid.

Ketonaemia and Ketonuria in Childhood

The formation of ketone bodies and their excretion in the urine in albnormall amounts have for many years been problems of much interest to both physiologist and clinician. Much of our present knowledge of the subject has been gained from the study of carbohydrate metabolism in diabetes, where ketonuria in its classical formi is frequently observed. From this it has been established that an excess of ketone bodies occurs in the blood when the fats are incompletely ' combusted ' as a result of abnormal carbohydrate metabolism, and ample justification has been provided for the well-known sta.tement myiade by Rosenfeld(l) in 1895 ' that fat burns only in the fire of carbohydrate.' A good review of our present knowledge of ketone production and its prevention is to be found in Shaffer's recent lecture entitled ' Antiketogenesis, its Mechanism and Signifiecance. '(2) A fu-ll discussion of the stubject in all its aspects is not within the scope of the present communication, but we may quote Shaffer's statement that ' there is to-day no question that ketosis is due to carbohydrate starvation,' and make special reference also to his remninder that the inhibitory effect of carbohydrate on ketone formation depends, not on the mnere existence of sufficient glucose, as glucose, in the blood (cf. diabetes), but on the presence of a siufficient armount of an oxidation product of glucose which reacts with one of the acetone bodies or its precursors. That ketosis has long been known to occur duiring fasting supports the view that it is due to the faulty cornbustion of fats in the absence of carbohydrate; for the first of the body reserves available is fat, which is then burned in the absence of sufficient glucose for its complete oxidation.