5,6-Dihydrouridine
(Synonyms: 5,6-二氢尿苷) 目录号 : GC33502
A pyrimidine nucleoside and derivative of uridine
Cas No.:5627-05-4
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
5,6-Dihydrouridine is a pyrimidine nucleoside and derivative of uridine . It is present in, and provides conformational flexibility to, tRNA from bacteria, eukaryotes, and some archaea.1,2 5,6-Dihydrouridine inhibits E. coli cytidine deaminase in a cell-free assay (Ki = 3.4 ?M).3 Serum levels of 5,6-dihydrouridine are increased in patients with prostate cancer and positively correlated with lethality.4
1.Kasprzak, J.M., Czerwoniec, A., and Bujnicki, J.M.Molecular evolution of dihydrouridine synthasesBMC Bioinformatics13153(2012) 2.Dalluge, J.J., Hashizume, T., Sopchik, A.E., et al.Conformational flexibility in RNA: The role of dihydrouridineNucleic Acids Res.24(6)1073-1079(1996) 3.Cohen, R.M., and Woldender, R.Cytidine deaminase from Escherichia coli. Purification, properties and inhibition by the potential transition state analog 3,4,5,6-tetrahydrouridineJ. Biol. Chem.246(24)7561-7656(1971) 4.Huang, J., Mondul, A.M., Weinstein, S.J., et al.Prospective serum metabolomic profiling of lethal prostate cancerInt. J. Cancer145(12)3231-3243(2019)
| Cas No. | 5627-05-4 | SDF | |
| 别名 | 5,6-二氢尿苷 | ||
| Canonical SMILES | OC[C@@H]1[C@H]([C@H]([C@H](N2CNC(NC2=O)=O)O1)O)O | ||
| 分子式 | C8H13N3O6 | 分子量 | 247.21 |
| 溶解度 | DMSO : ≥ 125 mg/mL (505.64 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 | 4.0451 mL | 20.2257 mL | 40.4514 mL |
| 5 mM | 0.809 mL | 4.0451 mL | 8.0903 mL |
| 10 mM | 0.4045 mL | 2.0226 mL | 4.0451 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。
5,6-Dihydrouridine: a marker ribonucleoside for determining whole body degradation rates of transfer RNA in man and rats
Clin Chim Acta 1993 Sep 17;218(1):73-82.PMID:8299222DOI:10.1016/0009-8981(93)90223-q.
It has previously been demonstrated that N6-threoninocarbonyladenosine is virtually quantitatively excreted in urine. From the similarity of the average molar ratio of 5,6-Dihydrouridine to N6-threoninocarbonyladenosine in the urine of human adults (12.6), newborns (12.6) and rats (13.6) with the respective ratio in cytoplasmic tRNA (11.8) we conclude that 5,6-Dihydrouridine is also virtually quantitatively excreted in urine. Therefore, excreted 5,6-Dihydrouridine is suitable as a marker to assess the whole body degradation rate of tRNA. Relative degradation rates of tRNA determined via excreted 5,6-Dihydrouridine in urine are 4.7 times higher in rats (2.2 +/- 0.33 mumol/kg per day) than in human adults (0.48 +/- 0.05 mumol/kg per day) which is similar to the respective difference in the resting metabolic rate per weight unit.
Isolation and identification of urinary nucleosides. Applications of high-performance liquid chromatographic methods to the synthesis of 5'-deoxyxanthosine and the simultaneous determination of 5,6-Dihydrouridine and pseudouridine
J Chromatogr 1990 Aug 31;515:537-46.PMID:2283377DOI:10.1016/s0021-9673(01)89352-3.
Modified nucleosides from pooled normal human urine were extracted using a boronate affinity gel column and fractionated by reversed-phase high-performance liquid chromatography (RP-HPLC). The major constituents in each of the 30 RP-HPLC fractions were determined by gas chromatography-mass spectrometry of the trimethylsilyl derivatives of the fractions. The same RP-HPLC method was used in the synthesis of 5'-deoxyxanthosine from authentic 5'-deoxyadenosine. In addition, the simultaneous determination of urinary 5,6-Dihydrouridine (D) and pseudouridine (psi) was carried out by RP-HPLC using two ODS columns in series. The level of D in pooled normal urine was 4.87 nmol/mumols creatinine. The RP-HPLC method was applied to the measurement of D and psi levels in urines collected before and after surgery from four patients with gastrointestinal cancer. A large decline in both nucleoside levels in urines after surgery was observed in three of the four cancer patients.
The identification of 5,6-Dihydrouridine in normal human urine by combined gas chromatography/mass spectrometry
Anal Biochem 1989 Sep;181(2):302-8.PMID:2817393DOI:10.1016/0003-2697(89)90247-9.
The identification of 5,6-Dihydrouridine in normal human urine is reported. Partial purification and isolation of the compound by boronate gel affinity chromatography and reversed-phase high-performance liquid chromatography preceded its characterization as a trimethylsilyl derivative by combined gas chromatography/mass spectrometry. Structure proof is based upon a comparison of mass spectral and chromatographic features of the urinary component to that of an authentic reference sample. Additional data derived from high resolution mass measurements and deuterium isotope-labeling experiments provide confirmation of fragment ion structure. The poor detectability inherent in the HPLC/uv analysis of nucleosides is also discussed.
Metabolite Biomarkers of CKD Progression in Children
Clin J Am Soc Nephrol 2021 Aug;16(8):1178-1189.PMID:34362785DOI:10.2215/CJN.00220121.
Background and objectives: Metabolomics facilitates the discovery of biomarkers and potential therapeutic targets for CKD progression. Design, setting, participants, & measurements: We evaluated an untargeted metabolomics quantification of stored plasma samples from 645 Chronic Kidney Disease in Children (CKiD) participants. Metabolites were standardized and logarithmically transformed. Cox proportional hazards regression examined the association between 825 nondrug metabolites and progression to the composite outcome of KRT or 50% reduction of eGFR, adjusting for age, sex, race, body mass index, hypertension, glomerular versus nonglomerular diagnosis, proteinuria, and baseline eGFR. Stratified analyses were performed within subgroups of glomerular/nonglomerular diagnosis and baseline eGFR. Results: Baseline characteristics were 391 (61%) male; median age 12 years; median eGFR 54 ml/min per 1.73 m2; 448 (69%) nonglomerular diagnosis. Over a median follow-up of 4.8 years, 209 (32%) participants developed the composite outcome. Unique association signals were identified in subgroups of baseline eGFR. Among participants with baseline eGFR ≥60 ml/min per 1.73 m2, two-fold higher levels of seven metabolites were significantly associated with higher hazards of KRT/halving of eGFR events: three involved in purine and pyrimidine metabolism (N6-carbamoylthreonyladenosine, hazard ratio, 16; 95% confidence interval, 4 to 60; 5,6-Dihydrouridine, hazard ratio, 17; 95% confidence interval, 5 to 55; pseudouridine, hazard ratio, 39; 95% confidence interval, 8 to 200); two amino acids, C-glycosyltryptophan, hazard ratio, 24; 95% confidence interval 6 to 95 and lanthionine, hazard ratio, 3; 95% confidence interval, 2 to 5; the tricarboxylic acid cycle intermediate 2-methylcitrate/homocitrate, hazard ratio, 4; 95% confidence interval, 2 to 7; and gulonate, hazard ratio, 10; 95% confidence interval, 3 to 29. Among those with baseline eGFR <60 ml/min per 1.73 m2, a higher level of tetrahydrocortisol sulfate was associated with lower risk of progression (hazard ratio, 0.8; 95% confidence interval, 0.7 to 0.9). Conclusions: Untargeted plasma metabolomic profiling facilitated discovery of novel metabolite associations with CKD progression in children that were independent of established clinical predictors and highlight the role of select biologic pathways.
Insights into Mechanisms of Damage Recognition and Catalysis by APE1-like Enzymes
Int J Mol Sci 2022 Apr 14;23(8):4361.PMID:35457179DOI:10.3390/ijms23084361.
Apurinic/apyrimidinic (AP) endonucleases are the key DNA repair enzymes in the base excision repair (BER) pathway, and are responsible for hydrolyzing phosphodiester bonds on the 5' side of an AP site. The enzymes can recognize not only AP sites but also some types of damaged bases, such as 1,N6-ethenoadenosine, α-adenosine, and 5,6-Dihydrouridine. Here, to elucidate the mechanism underlying such a broad substrate specificity as that of AP endonucleases, we performed a computational study of four homologous APE1-like endonucleases: insect (Drosophila melanogaster) Rrp1, amphibian (Xenopus laevis) APE1 (xAPE1), fish (Danio rerio) APE1 (zAPE1), and human APE1 (hAPE1). The contact between the amino acid residues of the active site of each homologous APE1-like enzyme and the set of damaged DNA substrates was analyzed. A comparison of molecular dynamic simulation data with the known catalytic efficiency of these enzymes allowed us to gain a deep insight into the differences in the efficiency of the cleavage of various damaged nucleotides. The obtained data support that the amino acid residues within the "damage recognition" loop containing residues Asn222-Ala230 significantly affect the catalytic-complex formation. Moreover, every damaged nucleotide has its unique position and a specific set of interactions with the amino acid residues of the active site.