Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Acetyl coenzyme formation from pyruvic acid

Indeed both -lactylthiamine pyrophosphate (XX) and a-hydroxyethyl-thiamine pyrophosphate (XXI) have been isolated and identified as products after incubation of pyruvate with a purified carboxylase preparation " . When [2- - C]pyruvate is used, the radioactivity is found in the thiazole part of the molecule after sulfite cleavage of XXL Acetaldehyde is formed from pyruvic acid by yeast carboxylase by enzymic cleavage of intermediate XXI, Uberating thiamine pyTophosphate . XXI has also been identified as intermediate in the formation of acetyl-coenzyme A from pyruvic acid by p3u uvic oxidase . The transketolase reaction has been shown to proceed via a gly-colaldehyde-enzyme intermediate here one may expect to find dihydroxy-ethylthiamine pyrophosphate as active glycol-aldehyde . Such experiments strongly support Breslow s concept of the reaction mechanism. [Pg.26]

Lewisite is the most important of the organo-arseni-cal CW agents. Exposure to lewisite is quite painful, and onset of symptoms occurs rapidly (seconds to minutes) (31) in contrast to sulfur mustard for which a latency period occurs of several hours between exposure and symptoms (32). Although it is not known to have been used as a CW agent, lewisite is still considered a potential threat due to the relative ease of production and its rapid onset of action. Moreover, substantial stockpiles of lewisite are present in the United States, Russia, and in China abandoned by the Japanese Imperial Army. This may constitute a potential hazard for public health (33). The toxicity of lewisite is inter alia caused by the high affinity for the vicinal di-thiol system present in dihydrolipoic acid, a component of the pyruvate dehydrogenase complex, as is the case for other arsenicals (34). This prevents the formation of acetyl coenzyme A from pyruvate. [Pg.441]

A diet high in D-fructose produces increased concentrations of pyruvate, malate, and acetyl coenzyme A (AcSCoA).294 295 D-Fructose enhances formation of AcSCoA from pyruvate by stimulating pyruvate oxidation.296 As D-fructose causes a fall in the hepatic ATP concentration, pyruvate dehydrogenase (EC 1.2.4.1) is activated, and it produces an increase in AcSCoA formation from pyruvate.297 Thus, dietary sucrose and D-fructose produce higher hepatic fatty acid synthesis than does dietary D-glucose, because of their stimulation of AcSCoA formation. [Pg.327]

In thiamine deficiency, therefore, the formation from pyruvate of acetyl-coenzyme A, which is normally followed by the oxidation of the 2-C acetyl fragment to CO2 and H2O via the citric acid cycle is blocked, and the pyruvate formed by glycolysis consequently accumulates. In addition in its role in the oxidative decarboxylation of pyruvate, thiamine pyrophosphate is also needed as a co-enzyme in the similar decarboxylation of the closely related a-oxoglutarate, one of the intermediaries in the citric acid cycle. [Pg.5]

Biotin (5) is the coenzyme of the carboxylases. Like pyridoxal phosphate, it has an amide-type bond via the carboxyl group with a lysine residue of the carboxylase. This bond is catalyzed by a specific enzyme. Using ATP, biotin reacts with hydrogen carbonate (HCOa ) to form N-carboxybiotin. From this activated form, carbon dioxide (CO2) is then transferred to other molecules, into which a carboxyl group is introduced in this way. Examples of biotindependent reactions of this type include the formation of oxaloacetic acid from pyruvate (see p. 154) and the synthesis of malonyl-CoA from acetyl-CoA (see p. 162). [Pg.108]

Biotin (vitamin B ) is widespread in foods and is also synthesized by intestinal bacteria. It is a coenzyme for the carboxylation of pyruvate, acetyl-coenzyme-A (CoA), propionyl CoA, and /1-methyl-crotonyl CoA and is involved in fatty acid formation and in energy release from carbohydrates. In humans deficiencies only occur in patients with an abnormal gut flora and manifests itself as exfoliative dermatitis and alopecia. [Pg.474]

Pyruvate is converted to acetyl CoA with the formation of NADH, and fatty acids (attached to CoA) are also converted to acetyl CoA with formation of NADH and FADH. Oxidation of acetyl CoA in the citric acid cycle generates NADH and FADH2. Stage 2 Electrons from these reduced coenzymes are transferred via electron-transport complexes (blue boxes) to O2 concomitant with transport of H ions from the matrix to the intermembrane space, generating the proton-motive force. Electrons from NADH flow directly from complex I to complex III, bypassing complex II. [Pg.308]

Glycolysis takes place in the cell cytoplasm, whereas the decarboxylation of pyruvate and the subsequent oxidation of acetyl-coenzyme A via the tricarboxylic acid cycle take place in the mitochondrial matrix. Under anaerobic conditions, oxygen is not available for the oxidation of reduced NAD by oxidative phosphorylation, in order to allow the release of a small amount of energy by continuing the breakdown of glucose to pyruvate, reduced NAD must be converted to the oxidised form, if not, step 7 of Fig. 9.4 will not take place and energy production will be blocked. Oxidation of reduced NAD may be achieved under such conditions by the formation of lactate from pyruvate in the presence of lactate dehydrogenase ... [Pg.201]

Fatty acids are synthesized in a multienzyme complex from a crucially important primary metabolite, acetyl-coenzyme A (7.5). The principal source of acetyl-CoA (7.5) is pyruvic acid (7.5) and the conversion of (7.5) into (7.5) involves the coenzymes, thiamine pyrophosphate (7.5) and lipoic acid (7.5) (Scheme 1.1). The key to the action of thiamine is the ready formation of the zwitterion 1.4) at the beginning and end of the reaction cycle. The lipoic acid (7.5) is enzyme linked via the side chain of a lysine residue (7.7). The disulphide functionality is thus at the end of a long (14 A) arm. It has been suggested that this arm allows the lipoate to swing from one... [Pg.2]

Studies of the enzymic mechanism of the citric acid synthesis by Stern and Ochoa have directly shown that citric acid, and not aconitic acid, is the primary product. It had earlier been thought that the mechanism of citric acid synthesis might be similar to that of the reaction leading in vitro to the formation of citric acid from oxalacetic and pyruvic acid in the presence of hydrogen peroxide, where oxalocitramalic acid is an intermediate. Martins, however, found this substance to be metabolically inert in animal tissue. Stern and Ochoa found that aqueous extracts of acetone-dried pigeon liver formed citrate when acetate, oxalacetate, ATP, coenzyme A, and Mg or Mn ions were present. Thus the condensation reaction is preceded by the decarboxylation of pyruvic acid and the formation of an active form of acetate. This active acetate, as discussed below, is acetyl coenzyme A. [Pg.124]

Liedvogel B, B uerle R. Fatty acid synthesis in chloroplasts from mustard Sinapis alba L.) cotyledons Formation of acetyl coenzyme A by intraplastid glycolytic enzymes and a pyruvate dehydrogenase complex. Planta 1986 169 481-489. [Pg.60]

FNOR activity can be determined by measuring the formation of NADPH from NADP using reduced P. furiosus ferredoxin as the electron donor. Reduced ferredoxin is generated by P. furiosus pyruvate ferredoxin oxidoreductase (POR), which oxidatively decarboxylates pyruvate to acetyl-CoA. The reaction is carried out anaerobically under argon in a serum-stoppered cuvette (3 ml), since the reduced ferredoxin is rapidly oxidized in air. The 2 ml reaction mixture contains 100 mM EPPS [N-(2-hydroxyethyl)piperazine-iV -(3-propanesulfonic acid)] buffer, pH 8.0, 10 mM pyruvate, 0.2 mM coenzyme A, 80 p,g POR purified from P. furiosusf 12.5 jLg ferredoxin purified from P. furiosus, 0.3 mM NADP, and 10 (xg FNOR. The assay temperature is 80°. The reaction can be initiated by adding FNOR, ferredoxin, NADP, or POR as the final component. The production of NADPH is measured at 365 nm and the molar absorbance of 3400 M cm is used to calculate the concentration of NADPH. One unit of enzyme activity is equal to 1 p,mol NADPH produced per min. [Pg.43]

In addition to acetoinic substances, the pyruvate molecules coming from citrate have other destinations. First of all, if the coenzyme NADH, produced by other pathways, is available, it leads to the formation of lactate. Next comes the decarboxylation of pyruvate and then a reduction produces ethanol. Finally, the pyruvate derived from citrate participates in the synthesis of fatty acids and lipids via acetyl CoA. The radioactivity of labeled citrate supplied to the bacteria is incorporated into the cellular material. In this pathway, part of the acetyl CoA can also generate acetate molecules (Figure 5.6). [Pg.150]


See other pages where Acetyl coenzyme formation from pyruvic acid is mentioned: [Pg.469]    [Pg.174]    [Pg.63]    [Pg.149]    [Pg.281]    [Pg.489]    [Pg.1376]    [Pg.190]    [Pg.27]    [Pg.306]    [Pg.778]    [Pg.218]    [Pg.1026]    [Pg.511]    [Pg.341]    [Pg.272]    [Pg.324]    [Pg.580]    [Pg.244]   
See also in sourсe #XX -- [ Pg.1016 ]




SEARCH



Acetyl coenzyme

Acetyl coenzyme acids

Acetyl-pyruvic acid

Acetylation coenzyme

Coenzyme formation

Coenzyme pyruvate

Coenzymes acetyl coenzyme

From pyruvate

Pyruvate formation

Pyruvate formation from

Pyruvate/pyruvic acid

Pyruvic acid

© 2024 chempedia.info