urea cycle

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cycle

 [si´k'l]
a succession or recurring series of events.
cardiac cycle a complete cardiac movement, or heart beat, including systole, diastole, and the intervening pause.
Cardiac cycle. From Applegate, 2000.
cell cycle the cycle of biochemical and morphological events occurring in a reproducing cell population; it consists of the S phase, occurring toward the end of interphase, in which DNA is synthesized; the G2 phase, a relatively quiescent period; the M phase, consisting of the four phases of mitosis; and the G1 phase of interphase, which lasts until the S phase of the next cycle.
citric acid cycle tricarboxylic acid cycle.
estrous cycle the recurring periods of estrus in adult females of most mammalian species and the correlated changes in the reproductive tract from one period to another.
hair cycle the successive phases of the production and then loss of hair, consisting of anagen, catagen, and telogen.
menstrual cycle see menstrual cycle.
ovarian cycle the sequence of physiologic changes in the ovary involved in ovulation; see also ovulation and reproduction.
reproductive cycle the cycle of physiologic changes in the reproductive organs, from the time of fertilization of the ovum through gestation and childbirth; see also reproduction.
sex cycle (sexual cycle)
1. the physiologic changes that recur regularly in the reproductive organs of nonpregnant female mammals.
2. the period of sexual reproduction in an organism that also reproduces asexually.
tricarboxylic acid cycle the cyclic metabolic mechanism by which the complete oxidation of the acetyl portion of acetyl-coenzyme A is effected; the process is the chief source of mammalian energy, during which carbon chains of sugars, fatty acids, and amino acids are metabolized to yield carbon dioxide, water, and high-energy phosphate bonds. Called also citric acid cycle, Krebs cycle, and TCA cycle.
 Central pathways of metabolism: How the body produces energy from the energy-containing nutrients using the tricarboxylic acid cycle. From Davis and Sherer, 1994.
urea cycle a cyclic series of reactions that produce urea; it is a major route for removal of the ammonia produced in the metabolism of amino acids in the liver and kidney.

u·re·a cy·cle

the sequence of chemical reactions, occurring primarily in the liver, that results in the production of urea; the key reaction is the hydrolysis of l-arginine by arginase to l-ornithine and urea; l-ornithine is then converted to l-citrulline by a carbamoylation reaction, then to l-argininosuccinate by an amination reaction involving l-aspartic acid; finally, a lyase-dependent step generates arginine and fumarate.

urea cycle

n.
The sequence of chemical reactions occurring in the liver that results in the production of urea. The key reaction is the hydrolysis of arginine by arginase to ornithine and urea.

urea cycle

see ORNITHINE CYCLE.

Krebs,

Sir Hans Adolph, German biochemist in England and Nobel laureate, 1900-1981.
Krebs cycle - together with oxidative phosphorylation, the main source of energy in the mammalian body and the end toward which carbohydrate, fat, and protein metabolism are directed. Synonym(s): tricarboxylic acid cycle
Krebs-Henseleit cycle - the sequence of chemical reactions, occurring primarily in the liver, that results in the production of urea. Synonym(s): urea cycle
Krebs-Ringer solution - a modification of Ringer solution.
References in periodicals archive ?
Significant gender-related differences in metabolic profiles in male and female rats within exhaustive exercise occur, with increased rates of TCA cycling, glucose metabolism, amino acid catabolism and fatty acid metabolism in male rats, whereas, female rats might have an increased propensity to oxidize lipid and conserve carbohydrate and protein metabolism against physical stress.
* Exhaustive exercise increased the rates of the TCA cycling, glucose metabolism, amino acid catabolism and fatty acid metabolism in male rats, whereas, female rats demonstrated an increase propensity to lipid utilization and conserve carbohydrate and proteolytic metabolism.
In MDM, IFN-[alpha] stimulation was associated with a downregulation of multiple genes associated with branched-chain amino acid catabolism including branched-chain aminotransferase 2 (BCAT2), isovaleryl-CoA dehydrogenase (IVD), hydroxyacyl-CoA dehydrogenase (HADH), and methylmalonyl-CoA epimerase (MCEE).
Enrichment analysis, pathway mapping, and network construction identified alterations in central metabolic pathways in early IFN-[alpha] responses including glycolysis, oxidative phosphorylation, redox regulation, nucleotide metabolism, amino acid catabolism, and lipid metabolism.
Alterations in genes associated with tryptophan and branched-chain amino acid catabolism were pronounced in early IFN responses.
However, even if amino acid oxidation is able to maintain neuronal energy levels, the increased amounts of ammonia released during amino acid catabolism could lead to neuronal cell death because all of the enzymes of the urea cycle needed to detoxify ammonia are not present in neurons or glia.
There has not been much data generated on how the brain maintains balances of amino acids and total nitrogen levels during times of neuronal amino acid catabolism, but it is likely that BCAAs can be taken up through the blood-brain barrier (BBB) and glutamate can be released to maintain nitrogen balance [75].
Neurons contain very low levels of fatty acid beta-oxidation enzymes [87], so they instead rely upon ketone body catabolism, amino acid catabolism, or catabolism of lactate released from astrocytes [88] to maintain cellular ATP levels.
Figure 1 summarizes amino acid catabolism leading up to and including the urea cycle.
By starvation-induced autophagy experiment and specific antibodies against GmbZIP53, BCAT, and ATG8i, we demonstrate that the nutrient starvation activates a sucrose-induced transcription factor GmbZIP53A at transcription and protein levels, which possibly play a key role in the regulatory network of amino acid catabolism and autophagy of soybean.
Recently, low energy stresses such as reduced photosynthesis and/or sucrose starvation appeared to induce dramatic change of amino acid catabolism for asparagine biosynthesis by inducing the expression of asparagine synthase (AtASN1), aspartate aminotransferase (AtASP3), proline dehydrogenase 1 (AtProDH), and branched chain amino acid transaminase (AtBCAT2) [18-20].
Furthermore, it was shown that the bZIP1 and bZIP53 are master transcription factors regulating the expression of ASN1, ProDH, and BCAT2, which are involved in amino acid catabolism and nitrogen translocation [7].