Glucose biochemical oxidation

Hunt, J., Bottoms, M. and Mitchinson, M.J. (1993). Oxidative alterations in the experimental glycation model of diabetes mellitus are due to protein-glucose adduct oxidation. Biochem. J. 291, 529-535. 

Vitamin C, classified as either a pharmaceutical [5] or a food additive [6], has annual sales of 325 million dollars, the largest of all pharmaceuticals produced [7]. Pharmaceuticals, in general, lead in profitability for all industries [6]. Although vitamin C can be extracted from natural sources, it is primarily synthesized. In fact, it was the first vitamin to be produced in commercial quantities [6]. Jaffe [8] outlines the synthesis. Starting with D-glucose, vitamin C is produced in five chemical steps, one of which is a biochemical oxidation using the bacterium Acetobacter suboxydans. D-glucose is obtained from cornstarch in a process, which will be described later. 

Lizasoain, I., Moro, M.A., Knowles, R.G., Darley-Usmar, V., Moncada, S. (1996). Nitric oxide and peroxynitrite exert distinct effects on mitochondrial respiration which are differentially blocked by glutathione or glucose. Biochem. J. 314 877-80. 

One important application is in the field of carbohydrate transformations, the catalytic oxidation of D-glucose to D-gluconic acid represents an economically competitive route with respect to biochemical oxidation [4], This new process is the result of extensive studies on the selective Cl-hydroxyl group oxidation in the presence of O2 using a Pt or Pd catalyst modified with cocatalysts [5]. 

The complete biochemical oxidation of glucose to ATP is only 34% efficient in capturing the total amount of energy released. The remaining 66% is released as what form of energy ... 

Aerobic respiration A sequential series of biochemical processes ( glycolysis, Krebs cycle, and oxidative phosphorylation) where glucose is oxidized to CO2, HjO and energy in the forth of ATP. 

The first possibility is dubious, because there is no known biochemical oxidation reaction by which this would be accomplished. The other two possible pathways, acetone dicarboxylic acid or butyric acid, would both yield carboxyl-labeled acetoacetate, and thus 3,4-labeled glucose. The isolation of acetoacetate labeled only in the carboxyl group supports either possibility. An objection against the acetone dicarboxylic acid pathway is that acetoacetate, being a direct metabolic product of glutarate (see equation 6), should exhibit a higher specific activity than its resulting product, acetate. In the experiments of the above authors the specific... 

Biochemical Routes. Enzymatic oxidation of benzene or phenol leading to dilute solution of dihydroxybenzenes is known (62). Glucose can be converted into quinic acid [77-95-2] by fermentation. The quinic acid is subsequently oxidized to hydroquinone and -benzoquinone with manganese dioxide (63). 

Elucidation of the glycolysis process (by G. Embden and by O. Meyerhof) followed by the glucose oxidation process (H. A. Krebs. 1937) established the intimate involvement of P compounds in miiny biochemical reactions. 

Lactate, a product of glucose catabolism in oxygen-starved muscles, can be converted into pyruvate by oxidation. What coenzyme do you think is needed Write the equation in the normal biochemical format using a curved arrow. 

Hunt, J.V., Dean, R.T. and Wolff, S. (1988). Hydroxyl radical production and autoxidative glycosylation. Glucose oxidation as the cause of protein damage in the experimental glycation model of diabetes mellitus and ageing. Biochem. J. 256, 205-212. 

Grootveld, M.C., Henderson, E.B., Farrell, A., Blake, D.R. and Parkes, H.G. (1991). Oxidative damage to hyaluronate and glucose in synovial fluid during exercise of the inflamed rheumatoid joint. Detection of abnormal low-molecular mass metabolites by proton nmr spectroscopy. Biochem. J. 273, 459-467. 

Williams [176] has studied the rate of oxidation of C-labelled glucose in seawater by persulfate. After the oxidation, carbon dioxide was blown off and residual activity was measured. For glucose concentrations of 2000, 200, and 20 xg/l, residual radioactivities (as percentage of total original radioactivity) were 0.04, 0.05, and 0.025, respectively, showing that biochemical compounds are extensively oxidised by persulfate. With the exception of change of temperature, modifications of conditions had little or no effect. Oxidation for 2.5 h at 100 °C was the most efficient. 

In the 1930s, Peters and co-workers showed that thiamine deficiency in pigeons resulted in the accumulation of lactate in the brainstem [ 15]. Furthermore, they showed that the addition of small quantities of crystalline thiamine to the isolated brainstem tissue from thiamine-deficient birds in vitro resulted in normalization of lactate levels. These findings led to the formulation of the concept of the biochemical lesion in thiamine deficiency. Subsequent studies showed that the enzyme defect responsible for the biochemical lesion was a-KGDH rather than pyruvate dehydrogenase (PHDC), as had previously been presumed. a-KGDH and PHDC are major thiamine diphosphate (TDP)-dependent enzymes involved in brain glucose oxidation (Fig. 34-4). 

On the other hand, in rats, a single dose of 6,156 mg/kg hexachloroethane in mineral oil had no effects on a different set of biochemical indicators of liver function (microsomal protein, oxidative demethylase, NADP-NT reductase, glucose-6-phosphatase, or lipid conjugated diene concentration) when measured 2 hours after compound administration (Reynolds 1972). Each of these parameters is an indicator of microsomal function. The authors postulated that the observed lack of effects could have been the result of slow uptake of hexachloroethane by the liver in a 2-hour period. Gastrointestinal absorption of hexachloroethane in mineral oil is probably minimal because, unlike olive oil, mineral oil cannot be digested. Dissolved lipophilic materials could be excreted in the feces soon after administration because mineral oil can act as a laxative. Thus, the author s hypothesis that minimal hexachloroethane would reach the liver in 2 hours is reasonable. 

D8. Dickens, F., and Glock, G. E., Direct oxidation of glucose-6-phosphate, 6-phosphogluconate and pentose-5-phosphate by enzymes of animal origin. Biochem. ]. 50, 81-95 (1951). 

UDP-GA is formed from UDPglucose (see Box 12.4) by enzymic oxidation of the primary alcohol group. We have already noted in Section 12.6 that UDPglucose is also the biochemical precursor of glucose-containing polysaccharides, e.g. starch and glycogen (see Section 12.7). 

Welsh, N., and Sandler, S. (1992). Interleukin-lb induces nitric oxide prodution and inhibits the activity of aconitase without decreasing glucose oxidation rates in isolated mouse pancreatic islets. Biochem. Biophys. Res. Commun. 182, 333-340. 

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