Choline-d9 (chloride)
(Synonyms: 氯化胆碱 d9 (氯化物)) 目录号 : GC49856
An internal standard for the quantification of choline
Cas No.:61037-86-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Choline-d9 is intended for use as an internal standard for the quantification of choline by GC- or LC-MS. Choline is an essential nutrient with roles in liver, neurological, hematological, and skeletal muscle homeostasis.1,2,3,4 It is a precursor in the biosynthesis of membrane phospholipids, such as phosphatidylcholine, which facilitate cell signaling and transport across the membrane, and a precursor to the neurotransmitter acetylcholine. Choline is required for hepatic lipid transport.1 Perinatal administration of choline (18.8 mg/kg) improves prenatal alcohol exposure-induced cognitive deficits in rats.2 Choline (13 mg/animal per day) improves motor coordination and behavioral deficits in a mouse model of Rett syndrome, as well as improves deficits in recognition memory induced by early-life iron deficiency in rats when administered in the drinking water at a concentration of 5 ppm.3 Deficiencies in choline intake are positively correlated with muscle wasting, and dietary administration of choline (1,000 mg/kg) increases leg and breast muscle protein content in broiler chickens.4
1.Sanders, L.M., and Zeisel, S.H.Choline: Dietary requirements and role in brain developmentNutr. Today42(4)181-186(2007) 2.Thomas, J.D., Garrison, M., and O’Neill, T.M.Perinatal choline supplementation attenuates behavioral alterations associated with neonatal alcohol exposure in ratsNeurotoxicol. Teratol.26(1)35-45(2004) 3.Derbyshire, E., and Obeid, R.Choline, neurological development and brain function: A systematic review focusing on the first 1000 daysNutrients12(6)1731(2020) 4.Moretti, A., Paoletta, M., Liguori, S., et al.Choline: An essential nutrient for skeletal muscleNutrients12(7)E2144(2020)
| Cas No. | 61037-86-3 | SDF | Download SDF |
| 别名 | 氯化胆碱 d9 (氯化物) | ||
| Canonical SMILES | [2H]C([2H])([2H])[N+](C([2H])([2H])[2H])(C([2H])([2H])[2H])CCO.[Cl-] | ||
| 分子式 | C5H5D9NO • Cl | 分子量 | 148.7 |
| 溶解度 | DMSO: slightly soluble,Ethanol: 2 mg/ml,PBS (pH 7.2): 2 mg/ml | 储存条件 | -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 | 6.7249 mL | 33.6247 mL | 67.2495 mL |
| 5 mM | 1.345 mL | 6.7249 mL | 13.4499 mL |
| 10 mM | 0.6725 mL | 3.3625 mL | 6.7249 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。
MTHFR C677T genotype influences the isotopic enrichment of one-carbon metabolites in folate-compromised men consuming d9-choline
Am J Clin Nutr 2011 Feb;93(2):348-55.PMID:21123458DOI:10.3945/ajcn.110.005975.
Background: Homozygosity for the variant 677T allele in the methylenetetrahydrofolate reductase (MTHFR) gene increases the requirement for folate and may alter the metabolic use of choline. The choline adequate intake is 550 mg/d for men, although the metabolic consequences of consuming extra choline are unclear. Objective: Deuterium-labeled choline (d9-choline) as tracer was used to determine the differential effects of the MTHFR C677T genotype and the effect of various choline intakes on the isotopic enrichment of choline derivatives in folate-compromised men. Design: Mexican American men with the MTHFR 677CC or 677TT genotype consumed a diet providing 300 mg choline/d plus supplemental choline chloride for total choline intakes of 550 (n = 11; 4 with 677CC and 7 with 677TT) or 1100 (n = 12; 4 with 677CC and 8 with 677TT) mg/d for 12 wk. During the last 3 wk, 15% of the total choline intake was provided as d9-choline. Results: Low but measurable enrichments of the choline metabolites were achieved, including that of d3-phosphatidylcholine (d3-PtdCho)--a metabolite produced in the de novo pathway via choline-derived methyl groups. Men with the MTHFR 677TT genotype had a higher urinary enrichment ratio of betaine to choline (P = 0.041), a higher urinary enrichment of sarcosine (P = 0.041), and a greater plasma enrichment ratio of d9-betaine to d9-PtdCho with the 1100 mg choline/d intake (P = 0.033). Conclusion: These data show for the first time in humans that choline itself is a source of methyl groups for de novo PtdCho biosynthesis and indicate that the MTHFR 677TT genotype favors the use of choline as a methyl donor.
Different choline supplement metabolism in adults using deuterium labelling
Eur J Nutr 2023 Feb 25.PMID:36840817DOI:10.1007/s00394-023-03121-z.
Background: Choline deficiency leads to pathologies particularly of the liver, brain and lung. Adequate supply is important for preterm infants and patients with cystic fibrosis. We analysed the assimilation of four different enterally administered deuterium-labelled (D9-) choline supplements in adults. Methods: Prospective randomised cross-over study (11/2020-1/2022) in six healthy men, receiving four single doses of 2.7 mg/kg D9-choline equivalent each in the form of D9-choline chloride, D9-phosphorylcholine, D9-alpha-glycerophosphocholine (D9-GPC) or D9-1-palmitoyl-2-oleoyl-glycero-3-phosphoryl-choline (D9-POPC), in randomised order 6 weeks apart. Plasma was obtained at baseline (t = - 0.1 h) and at 0.5 h to 7d after intake. Concentrations of D9-choline and its D9-labelled metabolites were analysed by tandem mass spectrometry. Results are shown as median and interquartile range. Results: Maximum D9-choline and D9-betaine concentrations were reached latest after D9-POPC administration versus other components. D9-POPC and D9-phosphorylcholine resulted in lower D9-trimethylamine (D9-TMAO) formation. The AUCs (0-7d) of plasma D9-PC concentration showed highest values after administration of D9-POPC. D9-POPC appeared in plasma after fatty acid remodelling, predominantly as D9-1-palmitoyl-2-linoleyl-PC (D9-PLPC), confirming cleavage to 1-palmitoyl-lyso-D9-PC and re-acylation with linoleic acid as the most prominent alimentary unsaturated fatty acid. Conclusion: There was a delayed increase in plasma D9-choline and D9-betaine after D9-POPC administration, with no differences in AUC over time. D9-POPC resulted in a higher AUC of D9-PC and virtually absent D9-TMAO levels. D9-POPC is remodelled according to enterocytic fatty acid availability. D9-POPC seems best suited as choline supplement to increase plasma PC concentrations, with PC as a carrier of choline and targeted fatty acid supply as required by organs. This study was registered at Deutsches Register Klinischer Studien (DRKS) (German Register for Clinical Studies), DRKS00020498, 22.01.2020. Study registration: This study was registered at Deutsches Register Klinischer Studien (DRKS) (German Register for Clinical Studies), DRKS00020498.
Choline supplementation for preterm infants: metabolism of four Deuterium-labeled choline compounds
Eur J Nutr 2023 Apr;62(3):1195-1205.PMID:36460779DOI:10.1007/s00394-022-03059-8.
Background: Supply of choline is not guaranteed in current preterm infant nutrition. Choline serves in parenchyma formation by membrane phosphatidylcholine (PC), plasma transport of poly-unsaturated fatty acids (PUFA) via PC, and methylation processes via betaine. PUFA-PC concentrations are high in brain, liver and lung, and deficiency may result in developmental disorders. We compared different deuterated (D9-) choline components for kinetics of D9-choline, D9-betaine and D9-PC. Methods: Prospective study (1/2021-12/2021) in 32 enterally fed preterm infants (28 0/7-32 0/7 weeks gestation). Patients were randomized to receive enterally a single dose of 2.7 mg/kg D9-choline-equivalent as D9-choline chloride, D9-phosphoryl-choline, D9-glycerophosphorylcholine (D9-GPC) or D9-1-palmitoyl-2-oleoyl-PC(D9-POPC), followed by blood sampling at 1 + 24 h or 12 + 60 h after administration. Plasma concentrations were analyzed by tandem mass spectrometry. Results are expressed as median (25th/75th percentile). Results: At 1 h, plasma D9-choline was 1.8 (0.9/2.2) µmol/L, 1.3 (0.9/1.5) µmol/L and 1.2 (0.7/1.4) µmol/L for D9-choline chloride, D9-GPC and D9-phosphoryl-choline, respectively. D9-POPC did not result in plasma D9-choline. Plasma D9-betaine was maximal at 12 h, with lowest concentrations after D9-POPC. Maximum plasma D9-PC values at 12 h were the highest after D9-POPC (14.4 (9.1/18.9) µmol/L), compared to the other components (D9-choline chloride: 8.1 [5.6/9.9] µmol/L; D9-GPC: 8.4 (6.2/10.3) µmol/L; D9-phosphoryl-choline: 9.8 (8.6/14.5) µmol/L). Predominance of D9-PC comprising linoleic, rather than oleic acid, indicated fatty-acyl remodeling of administered D9-POPC prior to systemic delivery. Conclusion: D9-Choline chloride, D9-GPC and D9-phosphoryl-choline equally increased plasma D9-choline and D9-betaine. D9-POPC shifted metabolism from D9-betaine to D9-PC. Combined supplementation of GPC and (PO) PC may be best suited to optimize choline supply in preterm infants. Due to fatty acid remodeling of (PO) PC during its assimilation, PUFA co-supplementation with (PO) PC may increase PUFA-delivery to critical organs. This study was registered (22.01.2020) at the Deutsches Register Klinischer Studien (DRKS) (German Register for Clinical Studies), DRKS00020502. Study registration: This study was registered at the Deutsches Register Klinischer Studien (DRKS) (German Register for Clinical Studies), DRKS00020502.
Mass Spectrometric Enzyme Histochemistry for Choline Acetyltransferase Reveals De Novo Acetylcholine Synthesis in Rodent Brain and Spinal Cord
ACS Chem Neurosci 2021 Jun 16;12(12):2079-2087.PMID:34078081DOI:10.1021/acschemneuro.0c00720.
Choline acetyltransferase (ChAT), responsible for the synthesis of acetylcholine, plays an important role in neurotransmission. However, no method to visualize the ChAT activity in tissues has been reported to date. In this study, mass spectrometry imaging (MSI) was used to visualize ChAT activity insitu, which is difficult with conventional enzyme histochemistry. By using choline chloride-trimethyl-d9 (Choline-d9) as a substrate and simultaneously supplying an inhibitor of cholinesterase to tissues, we succeeded in directly visualizing the ChAT activity in the rodent brain and spinal cord. The findings revealed heterogeneous ChAT activity in the striatum of the mouse brain and in the spinal lower motor neurons that connect the anterior horn to the ventral root. Furthermore, extending the developed method to spinal cord injury (SCI) model mice revealed the site-specific effect of primary and secondary injury on ChAT activity. This study shows that the MSI-based enzyme histochemistry of ChAT could be a useful tool for studying cholinergic neurons.
Effect of potassium propionate on free and bound acetylcholine in frog muscle
Brain Res 1989 Jan 16;477(1-2):109-17.PMID:2784707DOI:10.1016/0006-8993(89)91398-x.
Frog sartorius muscles were homogenized under various conditions which allowed, by means of mass spectrometry, the measurement of total ACh, and different ACh compartments in the tissue: 'bound', 'free-1' and 'free-2' ACh. Bound ACh presumably corresponded to the vesicular compartment, and the free-1 and free-2 fractions to the cytoplasmic compartments of ACh. Stimulation of ACh release by La3+ ions for 60 min caused a decrease of both bound and free-2 ACh, but at 20 min bound ACh was reduced much more than free-2 ACh. Stimulation of ACh release by isotonic potassium propionate (KPr) solution for only 5 min caused a decrease of bound ACh, in contrast to free-1 and free-2 ACh which were not significantly changed. When muscles after 5 min stimulation in KPr were allowed to recover in normal Ringer, free-1 ACh did not change, but free-2 and bound ACh increased; after 180 min in Ringer bound ACh had recovered to control values. When ACh synthesis was prevented by hemicholinium-3 during recovery of the muscles in Ringer, bound ACh increased at the expense of free-2 ACh. In deuterium labeling experiments, in which the Ringer contained Choline-d9, much more ACh-d9 was formed in stimulated than in unstimulated muscles. It appeared that almost all newly formed ACh was ACh-d9, since no significant synthesis of unlabeled ACh (ACh-d0) took place. Yet again, the amount of bound ACh-d0 significantly increased, apparently at the expense of preformed free-2 ACh-d0.(ABSTRACT TRUNCATED AT 250 WORDS)