Acetoacetic acid Acetone

Trivial name Acetaldehyde Acetamide Acetic acid Acetic anhydride Acetoacetic acid Acetone Acetonitrile Acetophenone Acetyl chloride Acetylene Acrolein Acrylamide Acrylic acid Acrylonitrile Adipic acid Amyl acetate Amyl alcohol tert-Amy alcohol Aniline Azelaic acid Benzoic acid Benzoyl peroxide Benzyl alcohol Bisphenol A... 

Polyhydroxybutyric acid is a storage compound for excess carbon in many microorganisms (E 2.2). It may be used in the production of plastics (F 4). Acetoacetic acid, acetone, and /S-hydroxybutyric acid are excreted in the urine of people with a pathologically high blood sugar level (diabetes mellitus) (E 1). Their appearance is of diagnostic value. Butyric acid, butanol, and acetone are products of microbial fermentations. 

A group of compounds which include acetoacetic acid, acetone and >3-hydroxybutyrate. They result from fatty acid oxidation... 

Acetoacetic acid, acetone, and beta-hydroxybutyric acid. 

Examples are j8-hydroxy-butyric acid, acetoacetic acid, acetone, homogentisic acid, Bence-Jones protein, pentoses, lactose, methaemoglobin, haematoporphyrin. 

Hydrolysis. Ethyl acetoacetate when treated w ith cold dilute sodium hydroxide solution gives the sodium salt of acetoacetic acid. This acid is unstable, and readily breaks down into acetone and carbon dioxide it is of considerable... 

Water hydroly2es pure diketene only slowly to give acetoacetic acid [541-50-4] which quickly decomposes to acetone and carbon dioxide, but increasing the pH or adding catalysts (amines, palladium compounds) increases the rate of hydrolysis. The solvolysis of diketene in ammonia results in aceto acetamide [5977-14-0] if used in stoichiometric amounts (99), and P-arninocrotonarnide [15846-25-0] if used in excess (100). 

A mixture of 4.98 g of acetoacetic acid N-benzyl-N-methylaminoethyl ester, 2.3 g of aminocrotonic acid methyl ester, and 3 g of m-nitrobenzaldehyde was stirred for 6 hours at 100°C in an oil bath. The reaction mixture was subjected to a silica gel column chromatography (diameter 4 cm and height 25 cm) and then eluted with a 20 1 mixture of chloroform and acetone. The effluent containing the subject product was concentrated and checked by thin layer chromatography. The powdery product thus obtained was dissolved in acetone and after adjusting the solution with an ethanol solution saturated with hydrogen chloride to pH 1 -2, the solution was concentrated to provide 2 g of 2,6-dimethyl-4-(3 -nitrophenyl)-1,4-dihydropyridlne-3,5-dicarboxylic acid 3-methylester-5- -(N-benzyl-N-methylamino)ethyl ester hydrochloride. The product thus obtained was then crystallized from an acetone mixture, melting point 136°Cto 140°C (decomposed). 

It is also possible to use the dilithium derivative of acetoacetic acid as the synthetic equivalent of acetone enolate.49 In this case, the hydrolysis step is unnecessary and decarboxylation can be done directly on the alkylation product. 

In ethyl acetoacetate the methylene group is united to —CO.CH3 and —COOR. Free acetoacetic acid is even much less stable than malonic acid and, on merely warming in solution, decomposes in fundamentally similar fashion, into acetbne and carbon dioxide. Since all synthetic derivatives of ethyl acetoacetate behave in the same way, so that the acetoacetic acids, obtained by hydrolysis of their esters with aqueous mineral acids, decompose spontaneously with loss of carbon dioxide when heated, numerous derivatives of acetone are made available by this synthesis, by what is called Icetonic hydrolysis, e.g. 

Plant. In plants, mevinphos is hydrolyzed to phosphoric acid dimethyl ester, phosphoric acid, and other less toxic compounds (Hartley and Kidd, 1987). In one day, the compound is almost completely degraded in plants (Cremlyn, 1991). Casida et al. (1956) proposed two degradative pathways of mevinphos in bean plants and cabbage. In the first degradative pathway, cleavage of the vinyl phosphate bond affords methylacetoacetate and acetoacetic acid, which may be precursors to the formation of the end products dimethyl phosphoric acid, methanol, acetone, and carbon dioxide. In the other degradative pathway, direct hydrolysis of the carboxylic ester would yield vinyl phosphates as intermediates. The half-life of mevinphos in bean plants was 0.5 d (Casida et ah, 1956). In alfalfa, the half-life was 17 h (Huddelston and Gyrisco, 1961). 

Acetamido-4-amino-6-chloro-s-triazine, see Atrazine Acetanilide, see Aniline, Chlorobenzene, Vinclozolin Acetic acid, see Acenaphthene, Acetaldehyde, Acetic anhydride. Acetone, Acetonitrile, Acrolein, Acrylonitrile, Aldicarb. Amyl acetate, sec-Amyl acetate, Bis(2-ethylhexyl) phthalate. Butyl acetate, sec-Butyl acetate, ferf-Butyl acetate, 2-Chlorophenol, Diazinon. 2,4-Dimethylphenol, 2,4-Dinitrophenol, 2,4-Dinitrotoluene, 1,4-Dioxane, 1,2-Diphenylhydrazine, Esfenvalerate. Ethyl acetate, Flucvthrinate. Formic acid, sec-Hexyl acetate. Isopropyl acetate, Isoamyl acetate. Isobutyl acetate, Methanol. Methyl acetate. 2-Methvl-2-butene. Methyl ferf-butvl ether. Methyl cellosolve acetate. 2-Methvlphenol. Methomvl. 4-Nitrophenol, Pentachlorophenol, Phenol. Propyl acetate. 1,1,1-Trichloroethane, Vinyl acetate. Vinyl chloride Acetoacetic acid, see Mevinphos Acetone, see Acrolein. Acrylonitrile. Atrazine. Butane. 

Acetone cyanohydrin nitrate, a reagent prepared from the nitration of acetone cyanohydrin with acetic anhydride-nitric acid, has been used for the alkaline nitration of alkyl-substituted malonate esters. In these reactions sodium hydride is used to form the carbanions of the malonate esters, which on reaction with acetone cyanohydrin nitrate form the corresponding nitromalonates. The use of a 100 % excess of sodium hydride in these reactions causes the nitromalonates to decompose by decarboxylation to the corresponding a-nitroesters. Alkyl-substituted acetoacetic acid esters behave in a similar way and have been used to synthesize a-nitroesters. Yields of a-nitroesters from both methods average 50-55 %. 

Examples of this approach to the synthesis of ketones and carboxylic acids are presented in Scheme 1.6. In these procedures, an ester group is removed by hydrolysis and decarboxylation after the alkylation step. The malonate and acetoacetate carbanions are the synthetic equivalents of the simpler carbanions lacking the ester substituents. In the preparation of 2-heptanone (entries 1, Schemes 1.5 and 1.6), for example, ethyl acetoacetate functions as the synthetic equivalent of acetone. It is also possible to use the dilithium derivative of acetoacetic acid as the synthetic equivalent of acetone enolate.29 In this case, the hydrolysis step is unnecessary, and decarboxylation can be done directly on the alkylation product. 

Hamilton marked the carbonyl group of acetoacetic acid with ieO, and then carried out the enzymic decarboxylation (Hamilton and Westheimer, 1959). The product of the decarboxylation, acetone, contained none of the label. This result is demanded by the ketimine mechanism, whereas the mechanism of uncatalyzed decarboxylation would have required that the label appear intact in the product. Of course, in order to make these statements we had to carry out an elaborate set of control experiments, since 180 is washed out of both acetone and acetoacetic acid by buffers and even more... 

Acetoacetic Acid, Ethyl Ester Acetoacetic Ester Acetone... 

Primary amine catalysis (usually involving a lysine residue) has been recognised to play an important role in various enzyme-catalysed reactions. Examples are the conversion of acetoacetate to acetone catalysed by acetoacetate decarboxylase, the condensation of two molecules of S-aminolevulinic acid catalysed by -aminolevulinic deshydratase during the biosynthesis of porphyrins, and the reversible aldol condensation of dihydroxy-acetone phosphate with glyceraldehyde which in the presence of aldolase yields fructose-1-phosphate (64) (For reviews see, for example, Snell and Di Mari,... 

Precursors. Precursors for this reaction are compounds exhibiting keto-enol tau-tomerism. These compounds are usually secondary metabolites derived from the glycolysis cycle of yeast metabolism during fermentation. Pyruvic acid is one of the main precursor compounds involved in this type of reaction. During yeast fermentation it is decarboxylated to acetaldehyde and then reduced to ethanol. Acetone, ace-toin (3-hydroxybutan-2-one), oxalacetic acid, acetoacetic acid and diacetyl, among others, are also secondary metabolites likely to participate in this kind of condensation reaction with anthocyanins. 

Acetyl-CoA is regenerated in this process. The overall product yields in moles per mole of glucose converted are approximately 0.5 acetate, 0.75 butyrate, 2 CO2, and 2 H2 2.5 mol ATP are formed. The nonacidic compounds, acetone, 1-butanol, and 2-propanol, are formed by transformation of some of the acetoacetyl-CoA into acetoacetic acid, which is the precursor of acetone and 2-propanol. Some of the butyryl-CoA is the precursor of 1-butanol via intermediate butyraldehyde. Ethanol is formed by reduction of small amounts of acetyl-CoA. The end result of the production of the neutral products by these additional pathways is that the yields of the other products are reduced. The neutral products are in a lower oxidation state than the acidic products and require additional reducing power as NADH to be formed. Some of the product Hj serves to sustain and provide NADH because higher partial pressures of H2 during the fermentation promote higher yields of the neutral products, whereas removal of the product H2 as it is formed has the opposite effect. 

Like other sulfhydryl-containing compounds, captopril can cause false-positive ketonuria when assessed with the Legal reaction (sodium nitroprusside reacting with acetoacetic acid and possibly with acetone). It has therefore been suggested that in patients with diabetes taking such drugs ketonuria should be assessed with the Acetest (20). Alternatively, a blood ketone test with Acetest and/ or enzymatic detection of beta-hydroxybutyric acid can be performed for confirmation. 

During prolonged starvation or when carbohydrate metabolism is severely impaired, as in uncontrolled diabetes mel-iitus (see Chapter 25), the formation of acetyl-CoA exceeds the supply of oxaioacetate. The abundance of acetyl-CoA results from excessive mobilization of fatty acids from adipose tissue and excessive degradation of the fatty acids by p-oxidation in the liver. The resulting acetyl-CoA excess is diverted to an alternative pathway in the mitochondria and forms acetoacetic acid, P-hydroxybutyric acid, and acetone—three compounds known collectively as ketone bodies (Figure 26-9). The presence of ketone bodies is a frequent finding in severe, uncontrolled diabetes melUtus. 

What quantity of acetone can be produced from 125 mg of acetoacetic acid (CH3COCH2CO2H) ... 

The answer is d. (Murray, pp 190-198. Scriver, pp 1521-1552. Sack, pp 121-138. Wilson, pp 287-317.) Ketone bodies include acetoacetic acid and P-hydroxybutyrate, which are formed in the liver, and acetone, which is spontaneously formed from excess acetoacetate in the blood. Starvation results in glycogen depletion and deficiency of carbohydrates, causing increased use of lipids as energy sources. Increased oxidation of fatty acids produces acetyl coenzyme A (CoA) and acetoacetyl CoA, a precursor of ketone bodies. Although the liver synthesizes ketone bodies from excess... 

Ketone bodies Acetoacetate, P-hydroxybntyrate, and acetone. Acetoacetate and P-hydroxybntyrate are formed by liver enzymes that condense molecnles of acetyl-CoA, thns regenerating CoA for continual use in P-oxidation of fatty acids. Acetone is a spontaneous decomposition prodnct of acetoacetate. Ketone bodies are exported from the liver and can be nsed by some extrahepatic tissnes for energy generation. 

When the production of acetyl-CoA exceeds the body s capacity to oxidize it, acetoacetic acid, /5-hydroxybutyrate, and acetone accumulate. When generated in large amounts, these substances can exceed the blood s buffering capacity. As the blood pH falls, the ability of red blood cells to carry oxygen is affected. Subsequently, the brain can be starved for oxygen, and a fatal coma can result. Explain how severe dieting can produce this condition. 

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