Guanidinosuccinic acid
(Synonyms: 胍基琥珀酸) 目录号 : GC31413
A guanidino compound with epileptogenic activity
Cas No.:6133-30-8
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >97.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
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Animal experiment: |
Mice[2]Randomly bred Swiss mice (male and female, body weight 13-25 g for the first series of experiments) are housed under standard environmentally controlled conditions. For another series of experiments, young Swiss mice 7, 14 and 21 days old are used. Injections of Guanidinosuccinic acid suspensions are delivered in volumes of 0.1 mL per 10 g body weight, i.p. and in doses between 250 and 1000 mg/kg (5 mice per dose, in duplicate). After injection, the mice are put in individual cylindrical transparent cages and observed for 1 h (for 2 h in the case of the young mice). Both CD50 and LD50 are calculated by probit analysis or moving average interpolation[2]. |
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References: [1]. Milstien S, et al. Role of intestinal microflora in the metabolism of guanidinosuccinic acid. J Bacteriol. 1973 May;114(2):641-4. |
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N-Amidino-L-aspartic acid is a guanidino compound found in mammalian sera and the CNS.1 It induces whole-cell currents in rat hippocampal slices, an effect that can be reversed by the NMDA receptor antagonists D-AP5 and ketamine. Intrahippocampal administration of N-amidino-L-aspartic acid induces status epilepticus and neuronal cell death in rats.2 Cerebrospinal fluid and serum levels of N-amidino-L-aspartic acid are increased in patients with renal failure.1,2
1.D'Hooge, R., Raes, A., Lebrun, P., et al.N-methyl-D-aspartate receptor activation by guanidinosuccinate but not by methylguanidine: Behavioural and electrophysiological evidenceNeuropharmacology35(4)433-440(1996) 2.Pan, J.C., Pei, Y.Q., An, L., et al.Epileptiform activity and hippocampal damage produced by intrahippocampal injection of guanidinosuccinic acid in ratNeurosci. Lett.209(2)121-124(1996)
| Cas No. | 6133-30-8 | SDF | |
| 别名 | 胍基琥珀酸 | ||
| Canonical SMILES | O=C(O)C[C@@H](C(O)=O)NC(N)=N | ||
| 分子式 | C5H9N3O4 | 分子量 | 175.14 |
| 溶解度 | DMSO : 75 mg/mL (428.23 mM);Water : 6 mg/mL (34.26 mM) | 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。
Guanidinosuccinic acid in uremia
The pathobiochemistry of uremia and hyperargininemia further demonstrates a metabolic relationship between urea and guanidinosuccinic acid
To better understand the biosynthesis of guanidinosuccinic acid, we determined urea, arginine, and guanidinosuccinic acid levels in nondialyzed uremic and hyperargininemic patients. These substances were also determined during several years of therapy in one hyperarginiemic patient. Interrelationships of guanidinosuccinic acid levels with their corresponding urea and arginine levels were assessed by linear correlation studies. In uremic patients, a significant positive linear correlation (r = .821, p less than .001) was found between serum urea and guanidinosuccinic acid levels A significant positive linear correlation was also found between serum urea levels and urinary guanidinosuccinic acid levels (r = .828, P less than .001), but not between serum arginine levels and urinary guanidinosuccinic acid levels in hyperargininemic patients. In the intrahyperargininemic patient study, a similar significant positive correlation was found between serum urea levels and the corresponding urinary guanidinosuccinic acid levels (r = .866, P less than .001); the correlation between serum arginine levels and the corresponding urinary guanidinosuccinic acid levels was smaller. The presented analytical findings in uremic and hyperargininemic patients clearly demonstrate a metabolic relationship between urea and guanidinosuccinic acid.
The biosynthesis of guanidinosuccinic acid by perfused rat liver
The metabolic pathway for the synthesis of guanidinosuccinic acid was studied in the rat. Labeled guanidinosuccinic acid was isolated from the urine of animals given L-[guanidino-14C]arginine intraperitoneally but did not appear in the urine after administration of D,L-[guanidino-14C]canavanine. Radioactive arginine and nonradioactive aspartic acid and arginine were infused in the isolated, perfused rat liver. After 20 min, small amounts of both labeled and unlabeled guanidinosuccinic acid and large amounts of urea were detected in radiochromatograms of the perfusate. These results support the theory that guanidinosuccinic acid is formed in the liver from transamidination of arginine to aspartic acid.
Role of intestinal microflora in the metabolism of guanidinosuccinic acid
Among a variety of bacteria isolated from the gastrointestinal tracts of rats and humans, only streptococci of group N are capable of degrading guanidinosuccinic acid added to their culture medium. The urinary excretion of guanidinosuccinic acid by germfree rats is greater than that of conventional rats. The excretion of this compound by gnotobiotic rats correlates with the capacity of their intestinal microflora to degrade guanidinosuccinic acid in culture. Thus, guanidinosuccinic acid excretion is low in rats infected exclusively with Streptococcus faecalis, and the excretion is not altered when germfree rats are infected with an organism unable to degrade guanidinosuccinic acid (Lactobacillus). These findings suggest that the intestinal microflora, particularly Streptococcus, play a role in the metabolism of guanidinosuccinic acid by the host.