Urea, formation

The alkylurea 576 and oxamide 577 are formed by oxidative carbonylation of amines under CO pressure using Pd/C as a catalyst[518]. The urea formation proceeds under atmospheric pressure using PdCh and CuCl2[519]. The mono-and double carbonylations of / -aminoethanol (578 and 579) afford the cyclic carbamate (oxazolidinones) 580 and oxamide (morpholinediones) 581 [520,521]. 

Phosgenation. Reaction of phosgene with arylamines to form ureas, and with reactive aryl species to form substituted hen zophen ones, are special cases of acylation. They are dealt with separately siace a more specialized plant is required than for other acylations. Urea formation takes place readily with water-soluble arylamines by simply passiag phosgeae through a slightly alkaline solutioa. An important example is carbonyl-J-acid from J-acid. 

Urea-formaldehyde resins are usually prepared by a two-stage reaction. The first stage involves the reaction of urea and formaldehyde under neutral or mildly alkaline conditions, leading to the production of mono and dimethylol ureas (Figure 24.1). The ratio of mono to dimethylol compounds will depend on the urea-to-formaldehyde ratio and it is important that there should be enough formaldehyde to allow some dimethylol urea formation. 

This means that, as a result of the urea formation, higher functional crosslink molecules are formed, which may influence the physical properties of the paint during curing. 

Ammonia (NH3) is just one of the toxins implicated in HE. It is a metabolic by-product of protein catabolism and is also generated by bacteria in the GI tract. In a normally functioning liver, hepatocytes take up ammonia and degrade it to form urea, which is then renally excreted. In patients with cirrhosis, the conversion of ammonia to urea is retarded and ammonia accumulates, resulting in encephalopathy. This decrease in urea formation is manifest on laboratory assessment as decreased blood urea nitrogen (BUN), but BUN levels do not correlate with degree of HE. Patients with HE commonly have elevated serum ammonia concentrations, but the levels do not correlate well with the degree of central nervous system impairment.20... 

Scheme 6.177 a-Methylenation of ketones [335], lactam formation from lactones [336], urea formation [337], and Knoevenagel condensation [338, 478]. 

For this library, we chose to use three types of isocyanates (neutral, electron rich, and electron deficient) to demonstrate the broad utility of the urea-formation reactions. Employing the above strategy and using the split-and-pool approach, we synthesized a 27-membered urea library with purities ranging from 95 to 99%. All the compounds prepared were characterized by 1FI NMR and mass spectroscopy. Acetonitrile can also be used as a substitute for DCM, but lower yields and product purities are generally observed. Attempts to use other protic solvents, such as isopropyl and ethyl alcohol, were unsuccessful. The best results were achieved when a chlorinated solvent (DCM) was used. The structure identity of all products was confirmed by 1FI NMR and MS spectroscopy. Expected molecular ions (M + Na+) were observed for all the products, and in all cases as the base peak. The compounds and yields are listed in Appendix 3.1. 

Lemkowitz et al. (4) used a similar model to that proposed by Van Krevelen et al. They correlated the equilibria in the C02+NH3+Urea+H20 system. The pseudoequilibrium constant for urea formation, as well as... 

This combination of reactions is known as transdeamination and is the mechanism for deamination of a number of amino acids (Table 8.9). The role of this process in catabolism is shown in Figure 8.10. The ammonia that is prodnced is converted, almost exclnsively, to urea for excretion. Becanse of the biochemical and clinical significance of ammonia, a whole chapter is devoted to it and to urea formation. 

The concentrations of amino acids in plasma of normal subjects and in cirrhotic patients were 2.6 and 3.5 mmol/L, respectively. To raise the plasma concentration, amino acids were infused. Note a much lower rate of urea formation in patients with a damaged Uver. Cirrhosis is characterised by deposition of collagen in the Uver and arises from a variety of causes a virus infection, deposition of fat in the Uver, undemutrition or chronic and excessive consumption of alcohol. 

Oxidative deamination, with the formation of NADH+H only applies to glutamate in animal metabolism. The reaction mainly takes place in the liver and releases NH3 for urea formation (see p. 178). 

The fumarate produced in step [4] is converted via malate to oxaloacetate [6, 7], from which aspartate is formed again by transamination [9]. The glutamate required for reaction [9] is derived from the glutamate dehydrogenase reaction [8], which fixes the second NH4 " in an organic bond. Reactions [6] and [7] also occur in the tricarboxylic acid cycle. However, in urea formation they take place in the cytoplasm, where the appropriate isoenzymes are available. 

The rate of urea formation is mainly controlled by reaction [1]. N-acetyl glutamate, as an allosteric effector, activates carbamoyl-phosphate synthase. In turn, the concentration of acetyl glutamate depends on arginine and ATP levels, as well as other factors. 

Several lines of investigation assert to the inability of canal ine to function as an effective ornithine antagonist. Ornithine interaction with canaline has been evaluated with the ornithine carbamoyl transferase (EC 2.1.3.3) of human liver. Neither canal ine nor ornithine inhibited this enzyme when the other member of this set served as the carbamoyl group recipient (29). The ornithine antagonist, 2,4-diaminobutyric acid drastically reduced urea production in the rat this reflected curtailment of the ornithine carbamoyl transferase-mediated conversion of ornithine to citrulline. Yet, canaline had no such effect on urea formation in this mammal (30). 

Attempts to prepare 2,3,5,6-tetraaminopyrazine (91) by Hoffman degradation of the diamide (88) were unsuccessful. This is apparently due to both intermolecular and intramolecular urea formation from the intermediate isocyanate giving a mixture of products, which upon attempted hydrolysis to 91 undergo a significant amount of attack on the pyrazine ring (70UP1). 

UUmann reaction anline, 536, 537, 541 phenol, 538 thiophenol, 527 Urea formation acylation, 547 amine interchange, 66 carbonyl diimidiazole, 510 chlorosulfonylisocyanate, 439 isocyanate, 65, 66, 293, 377 phosgene, 50, 526 Urethane... 

Urea Formation of urea in the liver is quantitatively the most hnpoe tant disposal route for ammonia. Urea travels in the blood from he liver to the kidneys, where it passes into the glomerular filtrate. 

A. An increase in gluconeogenesis from ammo acids results in a decrease in urea formation. 

Maintenance of adrenal cortex Promotes secretion of steroids, oxidative phosphorylation in adrenal cortex Mobilizes and increases oxidation of free fatty acid in adipose tissue Increases gluconeogenesis in liver increases cyclic adenosine monophosphate (AMP) in adrenal cortex Decreases urea formation in liver... 

Urea Formation Is a Complex and Costly Mode of Ammonia Detoxification... 

Ammonia is also the major nitrogenous end product in some of the simpler aquatic and marine animal forms, such as protozoa, nematodes, and even bony fishes, aquatic amphibia, and amphibian larvae. Such animals are called am-monotelic. But in many animals, NH3 is toxic, and its removal by simple diffusion is difficult. Thus, in terrestrial snails and amphibia, as well as in other animals living in environments in which water is limited, urea is the principal end product (fig. 22.6). Urea formation also helps to maintain osmotic balance with seawater in cartilagenous fishes. In such animals, most of the urea secreted by the kidney glomerulus is reabsorbed by the tubules. Indeed, the amount of nitrogen excreted by the kidneys of fishes is small com-... 

Urea formation in the liver starts with the multistep conversion of ornithine to arginine (fig. 22.7). This is followed by the breakdown of arginine into ornithine and urea. The cyclic nature of this pathway was first appreciated by Hans Krebs and Henseleit in 1932. In subsequent years the impor-... 

The urea cycle is a mechanism for removing unwanted nitrogen. Sources of nitrogens involved in urea formation are shown in red. Five enzymes are used in the urea cycle. Three of these function in the cytosol, and two, as shown, function in the mitochondrial matrix. 

The Krebs bicycle involves interaction between components of the aspartate to urea formation. The amino group originates from a... 

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