N-Acetyl-L-aspartic acid
(Synonyms: N-乙酰-L-天门冬氨酸) 目录号 : GC33612
An acetylated form of L-aspartic acid
Cas No.:997-55-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
N-Acetyl-L-aspartic acid is an acetylated form of L-aspartic acid.1 It is formed from L-aspartate and acetyl-CoA by L-aspartate N-acetyltransferase (Asp-NAT) in neuronal mitochondria.2 N-Acetyl-L-aspartic acid is hydrolyzed to L-aspartate and acetate by aspartoacylase (ASPA), which is expressed by oligodendrocytes. N-Acetyl-L-aspartic acid levels are increased in the brain of patients with Canavan disease, an autosomal recessive disorder caused by loss-of-function ASPA mutations and characterized by cognitive and motor impairments.3,2,1
1.Baslow, M.H.A review of phylogenetic and metabolic relationships between the acylamino acids, N-acetyl-?-aspartic acid and N-acetyl-?-histidine, in the vertebrate nervous systemJ. Neurochem.68(4)1335-1344(1997) 2.Madhavarao, C.N., Arun, P., Moffett, J.R., et al.Defective N-acetylaspartate catabolism reduces brain acetate levels and myelin lipid synthesis in Canavan's diseaseProc. Natl. Acad. Sci. USA102(14)5221-5226(2004) 3.Bannerman, P., Guo, F., Chechneva, O., et al.Brain Nat8l knockdown suppresses spongiform leukodystrophy in an aspartoacylase-deficient Canavan disease mouse modelMol. Ther.26(3)793-800(2018)
| Cas No. | 997-55-7 | SDF | |
| 别名 | N-乙酰-L-天门冬氨酸 | ||
| Canonical SMILES | O=C(O)C[C@@H](C(O)=O)NC(C)=O | ||
| 分子式 | C6H9NO5 | 分子量 | 175.14 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 5.7097 mL | 28.5486 mL | 57.0972 mL |
| 5 mM | 1.1419 mL | 5.7097 mL | 11.4194 mL |
| 10 mM | 0.571 mL | 2.8549 mL | 5.7097 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
N-Acetyl-L-aspartic acid: a literature review of a compound prominent in 1H-NMR spectroscopic studies of brain
Neurosci Biobehav Rev 1989 Spring;13(1):23-31.PMID:2671831DOI:10.1016/s0149-7634(89)80048-x.
N-acetyl aspartic acid (NAA), discovered in 1956 by Tallan, is the major peak seen in water-suppressed NMR proton (hydrogen) spectroscopy. NAA makes up about one thousandth of the wet weight of human brain and appears to be limited solely to neurons. This compound has been shown to be relatively stable for a period of twenty-four hours post-mortem and the concentration of NAA is not changed by insulin-induced hypoglycemia. MAO inhibitors lower its concentration while reserpine and other drugs increase it. NAA has been implicated in many processes of the nervous system: it may be involved in the regulation of neuronal protein synthesis, myelin production, or the metabolism of several neurotransmitters such as aspartate or N-acetyl-aspartyl-glutamate. It is involved in the neurologic disorder Canavan disease and has grown to be a vital component of in vivo 1H-NMR spectroscopic studies.
Metabolomic changes in animal models of depression: a systematic analysis
Mol Psychiatry 2021 Dec;26(12):7328-7336.PMID:34471249DOI:10.1038/s41380-021-01269-w.
Extensive research has been carried out on the metabolomic changes in animal models of depression; however, there is no general agreement about which metabolites exhibit constant changes. Therefore, the aim of this study was to identify consistently altered metabolites in large-scale metabolomics studies of depression models. We performed vote counting analyses to identify consistently upregulated or downregulated metabolites in the brain, blood, and urine of animal models of depression based on 3743 differential metabolites from 241 animal metabolomics studies. We found that serotonin, dopamine, gamma-aminobutyric acid, norepinephrine, N-Acetyl-L-aspartic acid, anandamide, and tryptophan were downregulated in the brain, while kynurenine, myo-inositol, hydroxykynurenine, and the kynurenine to tryptophan ratio were upregulated. Regarding blood metabolites, tryptophan, leucine, tyrosine, valine, trimethylamine N-oxide, proline, oleamide, pyruvic acid, and serotonin were downregulated, while N-acetyl glycoprotein, corticosterone, and glutamine were upregulated. Moreover, citric acid, oxoglutaric acid, proline, tryptophan, creatine, betaine, L-dopa, palmitic acid, and pimelic acid were downregulated, and hippuric acid was upregulated in urine. We also identified consistently altered metabolites in the hippocampus, prefrontal cortex, serum, and plasma. These findings suggested that metabolomic changes in depression models are characterized by decreased neurotransmitter and increased kynurenine metabolite levels in the brain, decreased amino acid and increased corticosterone levels in blood, and imbalanced energy metabolism and microbial metabolites in urine. This study contributes to existing knowledge of metabolomic changes in depression and revealed that the reproducibility of candidate metabolites was inadequate in previous studies.
A review of phylogenetic and metabolic relationships between the acylamino acids, N-Acetyl-L-aspartic acid and N-acetyl-L-histidine, in the vertebrate nervous system
J Neurochem 1997 Apr;68(4):1335-44.PMID:9084403DOI:10.1046/j.1471-4159.1997.68041335.x.
N-Acetyl-L-histidine (NAH) and N-Acetyl-L-aspartic acid (NAA) are major constituents of vertebrate brain and eye with distinct phylogenetic distributions. They are characterized by high tissue concentrations, high tissue/extracellular fluid gradients, and a continuous regulated efflux into the extracellular fluid. As a result of parallel investigations over the past three decades, evidence has accumulated that suggests that the metabolism of NAA in the CNS of both homeothermic and poikilothermic vertebrates and the metabolism of NAH in the CNS of poikilothermic vertebrates are related. Tissue distribution and concentrations are similar, as well as timing of appearance during embryological development and their synthetic and degradative biochemistry. Both amino acids appear to be involved in a rapid tissue-to-fluid-space cycling phenomenon across a membrane. Evidence accumulating for each amino acid suggests a dynamic and important role in the CNS and the eye of vertebrates. A genetic disease in humans, Canavan's disease, is associated with NAA aciduria and aspartoacylase deficiency with concomitant accumulation of NAA and a spongy degeneration of the brain. In this article, evidence linking NAA and NAH metabolism is reviewed, and the hypothesis that NAA and NAH complement each other and are metabolic analogues involved with membrane transport is developed. Their enzyme systems also appear to exhibit plasticity in relation to osmoregulatory forces on an evolutionary time scale, with an apparent interface at the fish-tetrapod boundary.
Quantification of N-Acetyl-L-aspartic acid in urine by isotope dilution gas chromatography-mass spectrometry
J Inherit Metab Dis 1992;15(1):97-104.PMID:1583881DOI:10.1007/BF01800351.
A method for quantification of N-Acetyl-L-aspartic acid by isotope dilution gas chromatography-mass spectrometry using 15N-[2H3]acetyl-L-aspartic acid is described. The method is sufficiently sensitive to be used with solvent extraction techniques commonly employed for urinary organic acid analysis. The mean concentration of N-Acetyl-L-aspartic acid in 80 normal and abnormal control urine specimens was 19.7 +/- 10.8 mg/g creatinine (12.7 +/- 7.8 mmol/mol creatinine). Seven patients, ages 9 months to 7 years, with Canavan-van Bogaert syndrome had urinary N-Acetyl-L-aspartic acid levels from 606 to 4760 mg/g creatinine. The method can also be used with cerebrospinal fluid, in which the concentration of N-Acetyl-L-aspartic acid is about one-tenth of that in urine.
Mutagenicity studies with N-Acetyl-L-aspartic acid
Food Chem Toxicol 2009 Aug;47(8):1936-40.PMID:19445994DOI:10.1016/j.fct.2009.05.005.
Analytical studies have reported that N-Acetyl-L-aspartic acid (NAA) is present at low concentrations in many foods. The current studies were conducted to assess the mutagenicity of NAA using standard OECD guideline in vitro bacterial and in vivo mammalian mutagenicity studies. For comparison and control data, mutagenicity studies were also conducted with its constituent amino acid L-aspartate (ASP) because NAA is metabolized to ASP. The combination of an in vitro method for assessing point mutations in bacteria and an in vivo method to assess clastogenicity in an animal model provided adequate evidence for mutagenicity hazard assessment of NAA. No evidence of mutagenicity was observed in either test system with either NAA or ASP. The results from the current studies demonstrate that the presence of NAA in foods is not likely to represent a risk for mutagenicity.