Z-D-serine
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Z-D-serine

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Category
CBZ-Amino Acids
Catalog number
BAT-003306
CAS number
6081-61-4
Molecular Formula
C11H13NO5
Molecular Weight
239.20
Z-D-serine
IUPAC Name
(2R)-3-hydroxy-2-(phenylmethoxycarbonylamino)propanoic acid
Synonyms
Z-D-Ser-OH; Z-D-β-hydroxyalanine; (R)-Z-2-amino-3-hydroxypropionic acid
Appearance
White powder
Purity
≥ 98.5% (HPLC)
Density
1.354 g/cm3
Melting Point
116-119°C
Boiling Point
487.5°C
Storage
Store at 2-8°C
InChI
InChI=1S/C11H13NO5/c13-6-9(10(14)15)12-11(16)17-7-8-4-2-1-3-5-8/h1-5,9,13H,6-7H2,(H,12,16)(H,14,15)/t9-/m1/s1
InChI Key
GNIDSOFZAKMQAO-SECBINFHSA-N
Canonical SMILES
C1=CC=C(C=C1)COC(=O)NC(CO)C(=O)O
1. Separation and detection of D-/L-serine by conventional HPLC
Hiroki Shikanai, Kazuko Ikimura, Momoko Miura, Tsugumi Shindo, Akane Watarai, Takeshi Izumi MethodsX. 2022 Jun 17;9:101752. doi: 10.1016/j.mex.2022.101752. eCollection 2022.
D-serine has a role as an endogenous allosteric agonist of N-methyl-D-aspartate (NMDA) receptor in the mammalian brain. In this study, we present a detailed description of our method that measures D-/L-serine by using conventional high performance liquid chromatography (HPLC). · We reacted D-serine and L-serine with ortho-phthalaldehyde (OPA) and N-acetyl-L-cysteine (NAC) to form diastereomeric isoindole derivatives, then we separated and detected them by conventional reversed phase HPLC with electrochemical detector (ECD). · We present typical measurement data of rat brain homogenate as an example of a convenient, appropriate method for measuring brain concentrations of D-serine. · Since many peaks appear in biological samples, we confirmed that the peaks were derived from serine by treating the sample with D-amino oxidase and catalase to decompose D-serine. As a results, one peak disappeared, suggesting that it is derived from D-serine.
2. The effect of L-theanine and S-ketamine on d-serine cellular uptake
Péter P Lakatos, István Vincze, Noel Nyariki, Fruzsina Bagaméry, Tamás Tábi, Éva Szökő Biochim Biophys Acta Proteins Proteom. 2020 Oct;1868(10):140473. doi: 10.1016/j.bbapap.2020.140473. Epub 2020 Jun 20.
Decreased extracellular level of d-Serine (D-Ser), a co-agonist of the N-methyl-d-aspartate (NMDA) receptors was connected to receptor hypofunction in the brain and the related deficit of cognitive functions. Extracellular D-Ser concentration is modulated by ASCT neutral amino acid transporters. L-Theanine (L-Tea), a neutral amino acid component of green tea was reported to improve cognitive functions. We thus intended to investigate the possible inhibitory effect of L-Tea on the D-Ser uptake of SH-SY5Y neuroblastoma cells, which was previously found as a good model of D-Ser transport into astrocytes. Cells were incubated with D-Ser and various concentrations of L-Tea or the reference compound S-ketamine (S-Ket). The effect on the uptake was assessed by measuring the intracellular D-Ser concentration using a capillary electrophoresis - laser induced fluorescence detection method. L-Tea competitively inhibited D-Ser uptake into SH-SY5Y cells with an IC50 value of 9.68 mM. Having previously described as an inhibitor of ASCT-2 transporter, S-Ket was intended to be used as a positive control. However, no acute inhibition of D-Ser transport by S-Ket was observed. Its long-term effect on the transport was also examined. No significant difference in D-Ser uptake in control and S-Ket-treated cells was found after 72 h treatment, although the intracellular D-Ser content of the 50 μM S-Ket pre-treated cells was significantly higher. L-Tea was found to be a weak competitive inhibitor of the ASCT transporters, while S-Ket did not directly affect D-Ser uptake or modify the uptake kinetics after a long-term incubation period.
3. Impairment of Glycolysis-Derived l-Serine Production in Astrocytes Contributes to Cognitive Deficits in Alzheimer's Disease
Juliette Le Douce, et al. Cell Metab. 2020 Mar 3;31(3):503-517.e8. doi: 10.1016/j.cmet.2020.02.004.
Alteration of brain aerobic glycolysis is often observed early in the course of Alzheimer's disease (AD). Whether and how such metabolic dysregulation contributes to both synaptic plasticity and behavioral deficits in AD is not known. Here, we show that the astrocytic l-serine biosynthesis pathway, which branches from glycolysis, is impaired in young AD mice and in AD patients. l-serine is the precursor of d-serine, a co-agonist of synaptic NMDA receptors (NMDARs) required for synaptic plasticity. Accordingly, AD mice display a lower occupancy of the NMDAR co-agonist site as well as synaptic and behavioral deficits. Similar deficits are observed following inactivation of the l-serine synthetic pathway in hippocampal astrocytes, supporting the key role of astrocytic l-serine. Supplementation with l-serine in the diet prevents both synaptic and behavioral deficits in AD mice. Our findings reveal that astrocytic glycolysis controls cognitive functions and suggest oral l-serine as a ready-to-use therapy for AD.
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