Vanilpyruvic acid (Vanylpyruvic acid)
(Synonyms: 4-羟基-3-甲氧基苯基丙酮酸,Vanylpyruvic acid) 目录号 : GC30994香草丙酮酸 (Vanylpyruvic acid) 是儿茶酚胺代谢物和香草乳酸的前体。
Cas No.:1081-71-6
Sample solution is provided at 25 µL, 10mM.
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Vanilpyruvic acid is a catecholamine metabolite and precursor to vanillactic acid.
The catecholamines, dopamine, norepinephrine, and epinephrine, constitute a class of chemical neurotransmitters and hormones that occupy key positions in the regulation of physiological processes and the development of neurological, psychiatric, endocrine, and cardiovascular diseases[1]. Catecholamines, namely dopamine (3,4-dihydrophenylethylamine), norepinephrine (noradrenaline) and epinephrine (adrenaline), act as neurotransmitters or hormones at central and peripheral levels. In addition to being the most abundant of the monoamine neurotransmitters, dopamine is also found in non-neuronal tissues such as the gastrointestinal tract and the kidney, where it participates in the regulation of sodium balance[2].
[1]. Eisenhofer G, et al. Catecholamine metabolism: a contemporary view with implications for physiology and medicine. Pharmacol Rev. 2004 Sep;56(3):331-49. [2]. Bicker J, et al. Liquid chromatographic methods for the quantification of catecholamines and their metabolites in several biological samples--a review. Anal Chim Acta. 2013 Mar 20;768:12-34.
Cas No. | 1081-71-6 | SDF | |
别名 | 4-羟基-3-甲氧基苯基丙酮酸,Vanylpyruvic acid | ||
Canonical SMILES | O=C(O)C(CC1=CC=C(O)C(OC)=C1)=O | ||
分子式 | C10H10O5 | 分子量 | 210.18 |
溶解度 | DMSO : ≥ 27 mg/mL (128.46 mM) | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg | |
1 mM | 4.7578 mL | 23.7891 mL | 47.5783 mL |
5 mM | 0.9516 mL | 4.7578 mL | 9.5157 mL |
10 mM | 0.4758 mL | 2.3789 mL | 4.7578 mL |
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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。
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URINARY VANILPYRUVIC ACID NEUROBLASTOMA
Determination of vanilpyruvic acid in urine by high-speed liquid chromatography
Metabolism of 3, 4-dihydroxyphenylalanine, its metabolites and analogues in vivo in the rat: urinary excretion pattern
The metabolism and interrelationships of orally and intraperitoneally administered L-dopa, related amino acids and their metabolites have been studied 2. Amino acids were decarboxylated. N-Methyldopa formed dopamine but not epinine. D-Dopa was absorbed from the intestine and metabolized by a series of reactions which resulted in greater decarboxylation than was observed after L-dopa. Transamination was a minor pathway. 3. m-Hydroxylated phenylpyruvic acids were poorly reduced, but vanilpyruvic acid was reduced fairly readily. Lactic acids were largely unchanged. Lactic and pyruvic acids formed phenylethylamines and their metabolites. Small amounts of phenylpyruvic acids may be decarboxylated to phenylacetic acids. 4. Glycine conjugates were formed from phenylacetic acids, a partially reversible change 3,4-Dihydroxyphenylacetic acid was metabolized to homovanillic and m-hydroxyphenylacetic acids, especially when given orally. Little 3-hydroxy-4-methoxyphenylacetic acid was oxidized to 3,4-dihydroxyphenylacetic acid but some increase in m-hydroxyphenylacetic acid excretion was observed. 5. 2-Phenylethanol analogues were largely converted to the corresponding acids. 3,4-Dihydroxyphenylethanol was partially m-O-methylated before oxidation. 6. beta-Phenylethylamine analogues were oxidized mainly to phenylacetic acids. but a variable amount of analogous phenylethanol was also formed, especially from m-tyramine. Dopamine was O-methylated, a process not readily reversible. It was also p-dehydroxylated following oral and intraperitoneal administration but not after oral neomycin; biliary excretion of amines may be involved in this sequence of events. N-Methylated amines were oxidized less readily than the parent amine. 7. Differences in route of administration resulted in quantitative changes in degradation pathways, an effect deriving, to some extent, from p-dehydroxylation and O-methylation in the gut.
Aromatic l-aminoacid decarboxylase deficiency: unusual neonatal presentation and additional findings in organic acid analysis
Aromatic l-aminoacid decarboxylase (AADC) deficiency is a neurotransmitter defect leading to a combined deficiency of catecholamines and serotonin. Patients are usually detected in infancy due to developmental delay, hypotonia, and extrapyramidal movements. Diagnosis is based on an abnormal neurotransmitter metabolite profile in CSF and reduced AADC activity in plasma. An elevation of vanillactic acid (VLA) has been described as the only abnormality detected in organic acid analysis (OA) of urine. We report a patient who presented in the neonatal period with lethargy, hypotonia, metabolic acidosis, and hypoglycemia. Blood ammonia, lactic acid, and acylcarnitines were normal, but OA of a urine sample showed a small increase of VLA, raising the suspicion of AADC deficiency. The patient was lost to follow-up until the age of 8 months, when he presented with dystonia, abnormal movements, oculogyric crises, and hypothermia. Repeat OA showed not only increased levels of VLA, but also increased vanilpyruvic acid (VPA), N-acetyl-vanilalanine (AVA) and N-acetyl-tyrosine (NAT). Neurotransmitter analysis in CSF showed increased vanilalanine (1200 nmol/L, ref<100) with decreased levels of 5-hydroxy-indoleacetic acid (5-HIAA, < 5 nmol/L; ref 152-462), homovanillic acid (HVA, 83 nmol/L; ref 302-845), and methoxy-hydroxy-phenyl-glycol (<5 nmol/L; ref 51-112). AADC activity in plasma was nearly undetectable. In the urine, low excretion of vanilmandelic acid (<0.3 micromol/mmol creat; ref 0.3-20) and 5-HIAA (0.9 micromol/mmol creat; ref 4-18), was found, but HVA was normal and dopamine even elevated. This contradictory phenomenon of hyperdopaminuria has been described earlier in AADC deficient patients. We postulate that VPA and AVA could originate from vanilalanine (through a transaminase and an acetylase respectively), while NAT could originate from tyrosine through an AA acetylase. This report expands the clinical presentation of AADC deficiency and adds new markers of the disease for OA analysis, improving detection of AADC deficient patients in general metabolic screening procedures.