Argininic acid (BioDeep_00000027858)
human metabolite Endogenous blood metabolite Toxin
代谢物信息卡片
化学式: C6H13N3O3 (175.0957)
中文名称: (S)-5-胍基-2-羟基戊酸
谱图信息:
最多检出来源 Homo sapiens(feces) 36.02%
分子结构信息
SMILES: C(CC(C(=O)O)O)CN=C(N)N
InChI: InChI=1S/C6H13N3O3/c7-6(8)9-3-1-2-4(10)5(11)12/h4,10H,1-3H2,(H,11,12)(H4,7,8,9)/t4-/m0/s1
描述信息
Tissue accumulation of argininic acid (AA) occurs in hyperargininemia. Hyperargininemia, an inborn error of the urea cycle, is caused by a severe deficiency of liver arginase, resulting in elevated tissue levels of arginine (Arg) and other guanidino compounds (GC). Affected patients present a neurological syndrome consisting of a variable degree of mental retardation, epilepsy and progressive spasticity whose pathophysiology is far from understood. Guanidino compounds accumulate in other pathological conditions such as uremia and epilepsy and some evidence supports the hypothesis that these compounds contribute to the neurological dysfunction characteristic of these diseases. The increase of these compounds occurs by blockage of the arginase reaction, activating secondary biochemical pathways. Thus, Arg is converted to α-keto-δ-guanidinovaleric acid by transamination, and this compound forms AA by hydrogenation. (PMID 12615083). AA has been identified as a uremic toxin according to the European Uremic Toxin Working Group (PMID: 22626821).
Tissue accumulation of argininic acid (AA) occurs in hyperargininemia. Hyperargininemia, an inborn error of the urea cycle, is caused by a severe deficiency of liver arginase, resulting in elevated tissue levels of arginine (Arg) and other guanidino compounds (GC). Affected patients present a neurological syndrome consisting of a variable degree of mental retardation, epilepsy and progressive spasticity whose pathophysiology is far from understood. Guanidino compounds accumulate in other pathological conditions such as uremia and epilepsy and some evidence supports the hypothesis that these compounds contribute to the neurological dysfunction characteristic of these diseases. The increase of these compounds occurs by blockage of the arginase reaction, activating secondary biochemical pathways. Thus, Arg is converted to α-keto-δ-guanidinovaleric acid by transamination, and this compound forms AA by hydrogenation. (PMID 12615083) [HMDB]
同义名列表
数据库引用编号
7 个数据库交叉引用编号
- ChEBI: CHEBI:90000
- PubChem: 160437
- HMDB: HMDB0003148
- foodb: FDB023114
- chemspider: 140984
- CAS: 157-07-3
- RefMet: Argininic acid
分类词条
相关代谢途径
Reactome(0)
BioCyc(0)
PlantCyc(0)
代谢反应
0 个相关的代谢反应过程信息。
Reactome(0)
BioCyc(0)
WikiPathways(0)
Plant Reactome(0)
INOH(0)
PlantCyc(0)
COVID-19 Disease Map(0)
PathBank(0)
PharmGKB(0)
1 个相关的物种来源信息
在这里通过桑基图来展示出与当前的这个代谢物在我们的BioDeep知识库中具有相关联信息的其他代谢物。在这里进行关联的信息来源主要有：
- PubMed: 来源于PubMed文献库中的文献信息，我们通过自然语言数据挖掘得到的在同一篇文献中被同时提及的相关代谢物列表，这个列表按照代谢物同时出现的文献数量降序排序，取前10个代谢物作为相关研究中关联性很高的代谢物集合展示在桑基图中。
- NCBI Taxonomy: 通过文献数据挖掘，得到的代谢物物种来源信息关联。这个关联信息同样按照出现的次数降序排序，取前10个代谢物作为高关联度的代谢物集合展示在桑吉图上。
- Chemical Taxonomy: 在物质分类上处于同一个分类集合中的其他代谢物
- Chemical Reaction: 在化学反应过程中，存在为当前代谢物相关联的生化反应过程中的反应底物或者反应产物的关联代谢物信息。
点击图上的相关代谢物的名称，可以跳转到相关代谢物的信息页面。
| 亚细胞结构定位 | 关联基因列表 |
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文献列表
- Brian J Koos, Jeffrey A Gornbein. Early pregnancy metabolites predict gestational diabetes mellitus: implications for fetal programming.
American journal of obstetrics and gynecology.
2021 02; 224(2):215.e1-215.e7. doi:
10.1016/j.ajog.2020.07.050. [PMID: 32739399] - Elizabeth K Neumann, Lukasz G Migas, Jamie L Allen, Richard M Caprioli, Raf Van de Plas, Jeffrey M Spraggins. Spatial Metabolomics of the Human Kidney using MALDI Trapped Ion Mobility Imaging Mass Spectrometry.
Analytical chemistry.
2020 10; 92(19):13084-13091. doi:
10.1021/acs.analchem.0c02051. [PMID: 32668145] - Daniela Delwing-de Lima, Simone Sasso, Leticia Dalmedico, Débora Delwing-Dal Magro, Eduardo Manoel Pereira, Angela T S Wyse. Argininic acid alters markers of cellular oxidative damage in vitro: Protective role of antioxidants.
Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie.
2017 Oct; 69(8):605-611. doi:
10.1016/j.etp.2017.05.007. [PMID: 28554820] - Youri E C Taes, Bart Marescau, An De Vriese, Peter P De Deyn, Eva Schepers, Raymond Vanholder, Joris R Delanghe. Guanidino compounds after creatine supplementation in renal failure patients and their relation to inflammatory status.
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.
2008 Apr; 23(4):1330-5. doi:
10.1093/ndt/gfm793. [PMID: 18048424] - O Levillain, B Marescau, I Possemiers, M Al Banchaabouchi, P P De Deyn. Influence of 72\% injury in one kidney on several organs involved in guanidino compound metabolism: a time course study.
Pflugers Archiv : European journal of physiology.
2001 Jul; 442(4):558-69. doi:
10.1007/s004240100581. [PMID: 11510889] - O Levillain, B Marescau, P P de Deyn. Guanidino compound metabolism in rats subjected to 20\% to 90\% nephrectomy.
Kidney international.
1995 Feb; 47(2):464-72. doi:
10.1038/ki.1995.59. [PMID: 7536856] - P P De Deyn, P Robitaille, M Vanasse, I A Qureshi, B Marescau. Serum guanidino compound levels in uremic pediatric patients treated with hemodialysis or continuous cycle peritoneal dialysis. Correlations between nerve conduction velocities and altered guanidino compound concentrations.
Nephron.
1995; 69(4):411-7. doi:
10.1159/000188511. [PMID: 7777105]
