3-Hydroxymandelic Acid
(Synonyms: 3-羟基扁桃酸) 目录号 : GC306383-HydroxymandelicAcid是Phenylephrine的代谢物,Phenylephrine是α受体(α-receptor)的激动剂。
Cas No.:17119-15-2
Sample solution is provided at 25 µL, 10mM.
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3-Hydroxymandelic Acid, a metabolite of Phenylephrine, Phenylephrine is a α-receptor agonist.
Phenylephrine, an alpha-receptor agonist is metabolized to m-hydroxyphenylglycol (MHPG) and m-hydroxymandelic acid (MHMA) in the human body[1]. It is probable that urinary MHMA originates from m-octopamine or m-synephrine (Phenylephrine) or both[1].
[1]. Gumbhir K, et al. Determination of m-hydroxymandelic acid, m-hydroxyphenylglycol and their conjugates in human plasma using liquid chromatography with electrochemical detection. J Pharm Biomed Anal. 1994 Jul;12(7):943-9. [2]. Crowley JR, et al. Normal excretion of m-hydroxymandelic acid in hypertensive patients. Clin Chim Acta. 1981 Jan 22;109(2):125-31.
Cas No. | 17119-15-2 | SDF | |
别名 | 3-羟基扁桃酸 | ||
Canonical SMILES | O=C(O)C(O)C1=CC=CC(O)=C1 | ||
分子式 | C8H8O4 | 分子量 | 168.15 |
溶解度 | DMSO : 100 mg/mL (594.71 mM; Need ultrasonic) | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg | |
1 mM | 5.9471 mL | 29.7354 mL | 59.4707 mL |
5 mM | 1.1894 mL | 5.9471 mL | 11.8941 mL |
10 mM | 0.5947 mL | 2.9735 mL | 5.9471 mL |
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2.
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Determination of m-hydroxymandelic acid, m-hydroxyphenylglycol and their conjugates in human plasma using liquid chromatography with electrochemical detection
An LC method for the analysis of m-hydroxymandelic acid (MHMA) and m-hydroxyphenylglycol (MHPG) and their conjugates in human plasma was developed and validated. The method for the quantitation involved extraction of acidified plasma (subject to hydrolysis with beta-glucuronidase for 120 min with 500 units of enzyme/0.25 ml of plasma at 37 degrees C for the conjugates) with an organic phase (methyl-tert-butyl ether). Analysis of MHMA, MHPG and the internal standard (3-hydroxy-4-methoxymandelic acid) was carried out on an ODS stationary phase: 100 x 4.6 mm, 5 mu followed by a 75 x 4.6 mm, 3 mu using 1% acetonitrile in 0.1 M acetic acid as the mobile phase. An electrochemical detector operated at +1.15 V vs Ag/AgCl was employed for the detection. The standard curves were linear in the range of 10.0-250.0 ng ml-1 for MHMA and 5.0-125.0 ng ml-1 for MHPG. The limit of quantitation was 10.0 ng ml-1 for MHMA and MHPG. Acceptable accuracy and precision were obtained during the intra-batch and inter-batch analysis for both the assays.
Normal excretion of m-hydroxymandelic acid in hypertensive patients
o-Hydroxymandelic acid (OHMA), m-hydroxymandelic acid (MHMA) and p-hydroxymandelic acid (PHMA) were measured in the urine of 42 normotensive and 54 hypertensive patients. Patients having high urinary MHMA levels were all found to be ingesting medications containing m-synephrine (phenylephrine). These patients also had high levels of urinary m-synephrine which was excreted as the glucuronide. When patients ingesting m-synephrine were excluded from the analysis, no significant differences were observed between the two groups for the urinary excretion of OHMA, MHMA and PHMA.
Hemp and buckwheat are valuable sources of dietary amino acids, beneficially modulating gastrointestinal hormones and promoting satiety in healthy volunteers
Purpose: This study evaluated the postprandial effects following consumption of buckwheat, fava bean, pea, hemp and lupin compared to meat (beef); focussing on biomarkers of satiety, gut hormones, aminoacids and plant metabolites bioavailability and metabolism.
Methods: Ten subjects (n = 3 men; n = 7 women; 42 ± 11.8 years of age; BMI 26 ± 5.8 kg/m2) participated in six 1-day independent acute interventions, each meal containing 30 g of protein from buckwheat, fava bean, pea, hemp, lupin and meat (beef). Blood samples were collected during 24-h and VAS questionnaires over 5-h.
Results: Volunteers consumed significantly higher amounts of most amino acids from the meat meal, and with few exceptions, postprandial composition of plasma amino acids was not significantly different after consuming the plant-based meals. Buckwheat meal was the most satious (300 min hunger scores, p < 0.05).Significant increase in GLP-1 plasma (AUC, iAUC p = 0.01) found after hemp compared with the other plant-based meals. Decreased plasma ghrelin concentrations (iAUC p < 0.05) found on plant (hemp) vs. meat meal. Several plasma metabolites after hemp meal consumption were associated with hormone trends (partial least squares-discriminant analysis (PLS-DA): 4-hydroxyphenylpyruvic acid, indole 3-pyruvic acid, 5-hydoxytryptophan, genistein and biochanin A with GLP-1, PYY and insulin; 3-hydroxymandelic acid and luteolidin with GLP-1 and ghrelin and 4-hydroxymandelic acid, benzoic acid and secoisolariciresinol with insulin and ghrelin. Plasma branched-chain amino acids (BCAAs), (iAUC, p < 0.001); and phenylalanine and tyrosine (iAUC, p < 0.05) were lower after buckwheat comparison with meat meal.
Conclusion: Plants are valuable sources of amino acids which are promoting satiety. The impact of hemp and buckwheat on GLP-1 and, respectively, BCAAs should be explored further as could be relevant for aid and prevention of chronic diseases such as type 2 diabetes. Study registered with clinicaltrial.gov on 12th July 2013, study ID number: NCT01898351.
The metabolism of L-m-tyrosine: the use of a putative precursor to investigate the increased production of m-hydroxymandelic acid in phenylketonuria
Several urinary meta-substituted phenols appear to be of endogenous origin. However, the production of these compounds is reduced in phenylketonuria with the exception of m-hydroxymandelic acid whose excretion is approximately doubled. This phenomenon has been investigated in two patients with phenylketonuria using the putative precursor L-m-tyrosine labelled with deuterium. Metabolism of this compound in these patients was comparable to that in healthy adults although much less was converted to m-hydroxymandelic acid and the excretion pattern of this metabolite was different. This apparent anomaly is attributed to smaller metabolic compartments in phenylketonuria and a lower threshold for the metabolism of m-tyramine via beta-hydroxylation. Incorporation into the natural pathway was shown by depletion of endogenous m-hydroxymandelic acid. The results are further support for the ideas that the amine precursors of m-hydroxymandelic acid, m-tyramine and m-octopamine, have a functional role and may be important in the pathogenesis of phenylketonuria.
The mammalian metabolism of R-(-)-m-synephrine
The metabolism of R-(-)-m-synephrine (administered orally and by inhalation in man and intraperitoneally in rats) was studied quantitatively by a gas chromatography-mass spectrometry-selected ion monitoring (g.c.-m.s.-s.i.m.) method using deuterated internal standards. When m-synephrine hydrochloride was administered orally to humans in normal dosage regimens four main metabolites were excreted in urine: (i) unconjugated m-hydroxymandelic acid (MHMA, 30%), (ii) m-hydroxyphenylglycol (MHPG) sulphate (6%), (iii) m-synephrine sulphate (47%) and (iv) m-synephrine glucuronide (12%). The comparable figures after inhalation of the drug were 24, 6, 56 and 5%. Intraperitoneal injection of m-synephrine into rats gave: unconjugated MHMA (5%), MHPG sulphate (35%), unconjugated m-synephrine (7%) and conjugates of m-synephrine (9%:4% as the glucuronide and 5% as the sulphate).