Urea, complex cation with

Figure 17. Molecular structure of the cation of complex 79 with AHA and urea ligands (127).

Heterocyclic phosphonium salts, e.g., (105), have been prepared by the reactions of urea-bridged P,P-dipho8phines with methyl triflate. - - Two ehantiomeric iron carbonyl complexes of the butadienylphosphonium salt (106) have been obtained by the trapping of a complexed organic cation with triphenylphosphine. ... 

Figure 3. Procyanidin-protein complexes formed in the absence of radicals are readily reversed by treatment with protein denaturants such as detergent, base, or urea. Complexes exposed to ABTS radical cation reacted with the radical, converting it to the colorless ABTS molecule, and converting the procyanidin-protein complex to a form that could not be reversed by any treatment. Protein in the absence of procyanidin did not react with the radical cation. Values are the averages of three determinations standard deviations are iindicated.

Bi2(CsH407)] 2K ) which has a complex stmcture. This salt is unstable in the stomach acid and precipitates out to form complex cationic species which form complexes with proteins in the stomach wall protecting ulcers from gastric add and pepsin, and these complexes are also toxic to H. pylori. The basis of the toxidty of bismuth salts to the bacteria may be due to formation of complexes with the tuease (which produces ammonia from urea) that the bacteria produce in large amounts in order to maintain the pH of their environment at around 6 so that they can survive tmder the addic conditions in the stomach/ Bismuth salts are usually used in combination with an H2-receptor antagonist and a tetracydine (see Ch. 22) which is also used to kill the bacteria. 

An interesting structural feature arises in the coordination of Li+ by urea in the complex Lil-2urea 62 each urea bridges two cations. This may be compared with LiCl-dioxane63 in which a related bridging occurs, and contrasted with NaCl-urea-H O64 in which the octahedral metal environment is due to two Cl- anions, two water oxygen atoms and two urea oxygen atoms. 

The first human experiments which suggested a toxic effect of ammonia in disease were done by Van Caulaert. The revival and extension of this work by the group led by Davidson (G2) in the Boston City Hospital has stimulated widespread interest in ammonia as a factor in the production of mental symptoms in liver disease. The ability of various factors, such as urea feedings, high-protein diet, cation resins in the ammonia cycle, and amino acids, to induce symptoms of coma in patients with liver disease (G2, M3, M4, P7, S8) made it quite clear that ammonia was associated with the symptom complex called hepatic coma. The severe toxicity of ammonia in animals and the ability of intravenous or oral ammonium salts to provoke episodes of impending liver coma tended to substantiate the clinical impressions. Rapid confirmation of these observations was furnished by the experiments of other groups (Bll, C2, E2, FI). 

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