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The structure of the molecule of urea is O=C(−NH 2) 2.The urea molecule is planar when in a solid crystal because of sp 2 hybridization of the N orbitals. [8] [9] It is non-planar with C 2 symmetry when in the gas phase [10] or in aqueous solution, [9] with C–N–H and H–N–H bond angles that are intermediate between the trigonal planar angle of 120° and the tetrahedral angle of 109.5°.
The urea cycle and the citric acid cycle are independent cycles but are linked. One of the nitrogen atoms in the urea cycle is obtained from the transamination of oxaloacetate to aspartate. [12] The fumarate that is produced in step three is also an intermediate in the citric acid cycle and is returned to that cycle. [12]
The amino acids that are produced by protein catabolism can then be further catabolized in amino acid catabolism. Among the several degradative processes for amino acids are Deamination (removal of an amino group), transamination (transfer of amino group), decarboxylation (removal of carboxyl group), and dehydrogenation (removal of hydrogen).
The inhibition of urease is a significant goal in agriculture because the rapid breakdown of urea-based fertilizers is wasteful and environmentally damaging. [29] Phenyl phosphorodiamidate and N -( n -butyl)thiophosphoric triamide are two such inhibitors.
The excretion of urea is called ureotelism. Land animals, mainly amphibians and mammals, convert ammonia into urea, a process which occurs in the liver and kidney. These animals are called ureotelic. [3] Urea is a less toxic compound than ammonia; two nitrogen atoms are eliminated through it and less water is needed for its excretion.
Uric acid is a product of the metabolic breakdown of purine nucleotides, and it is a normal component of urine. [1] High blood concentrations of uric acid can lead to gout and are associated with other medical conditions, including diabetes and the formation of ammonium acid urate kidney stones.
Ammonia is toxic to the human system, and enzymes convert it to urea or uric acid by addition of carbon dioxide molecules (which is not considered a deamination process) in the urea cycle, which also takes place in the liver. Urea and uric acid can safely diffuse into the blood and then be excreted in urine.
Mutations in the human ASL gene causes argininosuccinic aciduria, a rare autosomal recessive disorder, and results in deficiencies of the urea cycle. Argininosuccinate lyase is an intermediate enzyme in the urea synthesis pathway and its function is imperative to the continuation of the cycle.