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The urea cycle converts highly toxic ammonia to urea for excretion. [1] This cycle was the first metabolic cycle to be discovered by Hans Krebs and Kurt Henseleit in 1932, [2] [3] [4] five years before the discovery of the TCA cycle. The urea cycle was described in more detail later on by Ratner and Cohen.
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.
Most studies, [1] [9] indicate that nitrogen losses can be reduced in these situations when a urease inhibitor is applied to the fertilizer. Urease inhibitors prevent the urease enzyme from breaking down the urea. This increases the probability that urea will be absorbed into the soil after a rain event rather than volatilized into the atmosphere.
The liver converts ammonia to urea through a series of reactions known as the urea cycle. Liver dysfunction, such as that seen in cirrhosis, may lead to elevated amounts of ammonia in the blood (hyperammonemia). Likewise, defects in the enzymes responsible for the urea cycle, such as ornithine transcarbamylase, lead to hyperammonemia.
Urea plant using ammonium carbamate briquettes, Fixed Nitrogen Research Laboratory, ca. 1930 Carl Bosch, 1927. The Bosch–Meiser process is an industrial process, which was patented in 1922 [1] and named after its discoverers, the German chemists Carl Bosch and Wilhelm Meiser [2] for the large-scale manufacturing of urea, a valuable nitrogenous chemical.
Ammonium carbamate is an intermediate in the industrial production of urea. A typical industrial plant that makes urea can produce up to 4000 tons a day. [15] in this reactor and can then be dehydrated to urea according to the following equation: [14] [NH 2 CO 2][NH 4] → (NH 2) 2 CO + H 2 O
The metabolic pathways that synthesize urea involve reactions that start in the mitochondria and then move into the cytosol. The process is known as the urea cycle, which comprises several enzymes acting in sequence. It is greatly exacerbated by common zinc deficiency, which raises ammonia levels further. [1]
Argininosuccinate lyase is an intermediate enzyme in the urea synthesis pathway and its function is imperative to the continuation of the cycle. A non-functioning enzyme results in patients' accumulation of ammonia, argininosuccinate, and citrulline in the blood, and argininosuccinate is excreted in the urine. [ 9 ]