Fluoracetic acid

Xenon Tetrefluoride. XeF4 mw 207.30 colorl square or planar crysts mp 114°, 117° (separate values). V sol in anhydr liq HF sol in tetra-fluoracetic acid not sol in perfluoroheptane. Quant prepn is by an electrical discharge technique where a Fj/Xe mixt in the molar ratio of 2 1 is reacted at an operating pressure of from 2 to 15mm at -78° in a suitable vessel (Ref 4, p 282). The fluoride is very readily hydrolyzed, to the highly shock sensitive Xe oxides by traces of moisture (Ref 3)... 

In the mammal, complex polysaccharides which are susceptible to such treatment, are hydrolyzed by successive exposure to the amylase of the saliva, the acid of the stomach, and the disaccharidases (e.g., maltase, invertase, amylase, etc.) by exposure to juices of the small intestine. The last mechanism is very important. Absorption of the resulting monosaccharides occurs primarily in the upper part of the small intestine, from which the sugars are earned to the liver by the portal system. The absorption across die intestinal mucosa occurs by a combination of active transport and diffusion. For glucose, the aclive transport mechanism appears to involve phosphorylation The details are not yet fully understood. Agents which inhibit respiration (e.g., azide, fluoracetic acid, etc.) and phosphorylation (e.g., phlorizin), and those which uncouple oxidation from phosphorylation (e.g., dinitrophenol) interfere with the absorption of glucose. See also Phosphorylation (Oxidative). Once the various monosaccharides pass dirough the mucosa, interconversion of the other... 

The macroimlecuies formed in the copolymerization contain 9-alkylanthracene (IV) and 9-methylene-9,10-dihydroanthracene units(V). Under the usual conditions of the copolymerization of methyl methacrylate and III, the ratio of structures IV to V in the polymer varies from 1 15 to 1 50. If the copolymer is treated with tri-fluoracetic acid in a polar medium, units V undergo rearrangement, and LM units (Table 1 LMj) of 9,10-dialkylanthracene structure (VI) appear in the main chain. 

In acetic acid solution 30% hydrogen peroxide converts 2-imidazolyl methyl sulfides into sulfones" " and sometimes sulfoxides. In tri-fluoracetic acid the sulfoxides are formed preferentially periodate, too, can give the sulfoxides. Oxidation of 4-mercaptoimidazoles under mild conditions gives bis(4-imidazolyl) disulfides which can be cleaved by hydrogen sulfide. With 15% alkaline hydrogen peroxide at 90°C the sulfonic acid is the major product. Imidazole-5-sulfonyl chlorides give sulfonamides... 

The key to unraveling the toxicity of fluoracetate came from observations of Buffa and Peters (1949) that in animals treated with FAc, considerable quantities of citrate accumulated in some tissues. Oxygen uptake was also diminished. The citric acid cycle was thus implicated as the site of inhibition. Fluorcitrate was then isolated from the affected tissues. It was found to be a powerful competitive inhibitor of aconitase, thus blocking citrate oxidation. The suggestion was therefore made that fluoracetate was toxic not in itself, but because it was metabolized in cells via fluoracetyl CoA to give a toxic derivative, an example of lethal synthesis —the capacity of organisms to metabolize nontoxic compounds and convert them to potentially lethal products. 

SODIO, FLUORACETATO di (ITAUAN) SODIUM FLUOACETATE SODIUM FLUOACETIC ACID SODIUM FLUORACETATE de (FRENCH) SODIUM MONOFLUOROACETATE TL 869 YASOKNOCK... 

Peters, R.A. Wakelin, R.W., Rivett, D.E.A. Thomas, L.C. (1953) Fluoracetate poisoning comparison of synthetic fluorocitric acid with enzymically synthesized fluoro-tricarboxylic acid. Nature, 171, 1111-1112. 

The answer is a. (Murray, pp 182-189. Scriver, pp 1521-1552. Sack, pp 121-138. Wilson, pp 287-317.) Fluoracetate can be converted to fluorocitrate, which is an inhibitor of aconitase. Arsenic is not a direct inhibitor, but arsenite is an inhibitor of lipoic acid-containing enzymes such as a-ketoglutarate dehydrogenase. Malonate, not malic acid, is an inhibitor of... 

Synthesis of succinyl-CoA in mammalian cells such as the red cell and liver cell can be accomplished either from a-KG or from succinate. The formation of succinyl-CoA occurs in the mitochondria as part of the citric acid cycle reactions. The requirement for a citric acid cycle to form ALA or protoporphyrin or heme has been shown by tracer studies with acetate and succinate [39], and by inhibition studies with malonate, Ira j -aconitate, fluoracetate, and arsenite [49]. The requirement for an electron transfer system from the citric acid cycle to O2 has been shown by inhibition studies with anaerobiosis and CO. The requirement for oxidative phosphorylation has been shown by dinitrophenol inhibition of ALA synthesis dinitrophenol may also inhibit ALA-synthetase [3,49]. 

Dans les prises d essai avec pyruvate et NHi, dans lesquelles on avait bloqu5 la formation de c6to utarate k I aide de fluoracetate, la supplementation avec I acide cetoglutarique suscite une extra-... 

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