Acetic acid metabolism

Bender, L., and K. H. Neumann. Investigation on the indole-3-acetic acid metabolism of carrot tissue cultures (Daucus carota). Z Pflanzenphysiol 1978 88 209. 

Spencer, H., Vankinscott, V., Lewin, I., and Lasslo, D., Removal of calcium in man by ethylene diamine tetra-acetic acid Metabolic study. /. Clin. Invest. 31, 1023-1027 (1952). 

Cutinelli, C., G. Ehrensvdrd, L. Reio, E. Saluste, and R. Stjernholm Acetic acid metabolism in Rhodospirillum rubrum under anaerobic conditions. Arkiv Kemi 3, 315-322 (1951). 

Studies of 2.4.5-T [(2,4,5-trichlorophenoxy)acetic acid] metabolism in soybean callus tissue also showed that formation of amino acid conjugates was a major metabolic fate of the herbicide... 

The microbiostatic action of benzoic acid is based on different inhibition mechanisms, mainly many enzymes in the microbial cell are inhibited (Bosund, 1962 Menon et al., 1990). E.g. in yeast, enzymes that control the acetic acid metabolism and oxidative phosphorylation are inhibited. Benzoic acid appears to intervene at various points in the citric acid cycle, especially that of a-ketoglutaric acid and succinic acid dehydrogenase. Besides its enzyme-inactivating effects, benzoic acid also acts on the cell wall. The types of action of benzoic acid are sometimes very similar to those of sorbic acid, although many more data exist for the latter. 

The active form is undissociated acid (pJC = 4.19 at 25 °C), which is about 100 times more effective than its anion. The antimicrobial effect is probably due to inhibition of amino acid utility by microorganisms, inhibition of transport of substrates and inhibition of enzymes involved in the acetic acid metabolism, oxidative phosphorylation and the citric acid cycle. 

Taroncher-Oldenburg G, Nishia K, Stephanopoulos G (2000) Identification and analysis of polyhydroxyalkanoate-specific P-ketothiola e and acetoacetyl coenzyme A reductase genes in cyanobacterium Synechocystis p. strain PCC6803. Appl Environ Microbiol 66 4440-4448 Thauer RK (1989) Biochemistry of acetic acid metabolism in anaerobic chemotropic bacteria. Ann Rev Microbiol 43 43-67 Toda K, Park YS, Asakura T, Cheng CY, Ohtake H (1989) High rate acetic acid production in a shallow flow bioreactor. Appl Microbiol Biotechnol 30 559-563 Tsai SP, Moon S-H (1998) An integrated bioconversion process for the production of L-lactic acid from starchy potato feed stocks. Appl Biochem Biotechnol 70-72 417-428... 

Baddiley, j., G. Ehrensvard, E. Klein, I. Reio, and E. Saluste Acetic acid metabolism in Torulopsis utilis II. Metabolic connection between acetic acid and tyrosine and a method of degradation of the phenolic ring structure in tyrosine. J. Biol. Chem. 183, 777 (1950). 

A closet member of this little group, revelation of whose i(>al nature requires metabolic transformation of an acetylenic linkage to an acetic acid moiety, is fl uretofen (14). The .ynthesis begins by Friedel-Crafts acylation of 2-fluorobi-phenyl (11) with acetic acid to give ketone 1. Heating with... 

Viprostol (81) also incorporates a hydroxy group moved to C-16 and protects this from facile metabolic oxidation by vinylation. It is a potent hypotensive and vasodilatory agent both orally and transdermally. The methyl ester moiety is rapidly hydrolyzed in skin and in the liver so it is essentially a prodrug. It is synthesized from protected E-iodo olefin 78 (compare with 75) by conversion to the mixed organocuprate and this added in a 1,4-sense to olefin 79 to produce protected intermediate 80. The synthesis of viprostol concludes by deblocking with acetic acid and then reesterification with diazomethane to give 81 [19]. 

Compounds called carboxylic acids, which contain the -C02H grouping, occur abundantly in all living organisms and are involved in almost all metabolic pathways. Acetic acid, pyruvic acid, and citric acid are examples. 

C2H5OH, ethanol is formed by bacteria in the gastrointestinal tract in low amounts. Most of the ethanol of bacterial source is metabolized during the first liver passage yielding acetaldehyde and subsequently acetic acid. 

Ethanol is oxidized by alcohol dehydrogenase (in the presence of nicotinamide adenine dinucleotide [NAD]) or the microsomal ethanol oxidizing system (MEOS) (in the presence of reduced nicotinamide adenine dinucleotide phosphate [NADPH]). Acetaldehyde, the first product in ethanol oxidation, is metabolized to acetic acid by aldehyde dehydrogenase in the presence of NAD. Acetic acid is broken down through the citric acid cycle to carbon dioxide (CO2) and water (H2O). Impairment of the metabolism of acetaldehyde to acetic acid is the major mechanism of action of disulfiram for the treatment of alcoholism. 

Figure 6.1 Synthesis and metabolism of acetylcholine. Choline is acetylated by reacting with acetyl-CoA in the presence of choline acetyltransferase to form acetylcholine (1). The acetylcholine binds to the anionic site of cholinesterase and reacts with the hydroxy group of serine on the esteratic site of the enzyme (2). The cholinesterase thus becomes acetylated and choline splits off to be taken back into the nerve terminal for further ACh synthesis (3). The acetylated enzyme is then rapidly hydrolised back to its active state with the formation of acetic acid (4)...

Histamine is synthesised by decarboxylation of histidine, its amino-acid precursor, by the specific enzyme histidine decarboxylase, which like glutaminic acid decarboxylase requires pyridoxal phosphate as co-factor. Histidine is a poor substrate for the L-amino-acid decarboxylase responsible for DA and NA synthesis. The synthesis of histamine in the brain can be increased by the administration of histidine, so its decarboxylase is presumably not saturated normally, but it can be inhibited by a fluoromethylhistidine. No high-affinity neuronal uptake has been demonstrated for histamine although after initial metabolism by histamine A-methyl transferase to 3-methylhistamine, it is deaminated by intraneuronal MAOb to 3-methylimidazole acetic acid (Fig. 13.4). A Ca +-dependent KCl-induced release of histamine has been demonstrated by microdialysis in the rat hypothalamus (Russell et al. 1990) but its overflow in some areas, such as the striatum, is neither increased by KCl nor reduced by tetradotoxin and probably comes from mast cells. 

The metabolism of NMOR in the rat is outlined in Figure 4. o-Hydroxylation yields the unstable intermediates and the latter hydrolyzes to (2-hydroxyethoxy)acetaldehyde [7] which has been identified as a liver microsomal metabolite by isolation of the corresponding 2,4-dinitrophenylhydrazone (59). (2-Hydroxy-ethoxy)acetaldehyde, which exists predominantly as the cyclic hemiacetal was not detected in the urine of rats gavaged with 125 mg/kg NMOR. However, (2-hydroxyethoxy)acetic acid was a major urinary metabolite (16% of the dose). These transformations are analogous to those observed with NPYR and NNN. 

The results presented above indicate that the previously unknown head-to-tail polymerization is the major reaction product of the iminium methide species. To investigate the generality of this reaction, we next studied a neutral ene-imine species shown in Scheme 7.9.48 As illustrated in this scheme, the generation of this reactive species requires quinone reduction followed by elimination of acetic acid. The ene-imine is structurally related to the methyleneindolenine reactive species that is a metabolic oxidation product of 3-methylindole (Scheme 7.9).57 59... 

Now, this tentative description of the development of a correlation, later to become information from bases to the synthesis of proteins, by no means solves the problem of the origin of this code nor does it bring into focus the fact that the very proteins which were produced are responsible for the synthesis of the basic metabolic units, formaldehyde and acetic acid and then the amino acids and bases and finally the polymers by catalysts which are the polymers themselves. We do state, however, that the set of reactions quite probably give the most kinetically stable products. Now, the amounts of the different amino acids, lipids, saccharides... 

The end product of the intermediary metabolism of fatty acids with an uneven number of carbons differs sharply from those formed after the breakdown of the even-chain fatty acids. Whereas glycogen is produced from the fatty acids having an uneven number of carbon atoms, those fatty acids with an even number of carbon atoms have no glycogenic activity, but, with the possible exception of acetic acid, they are all ketogenic and possess no ketolytic activity. 

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