Pentosidine
(Synonyms: 戊糖素) 目录号 : GC40914An advanced glycation end product
Cas No.:124505-87-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Advanced glycation end products (AGEs) are compounds formed by non-enzymatic chemical reactions following the bonding of sugars to proteins or lipids during diabetes, uremia, aging, rheumatic arthritis, and other conditions. A receptor for the AGEs (RAGE) binds certain members of this class to initiate cell signaling.[1][2] Pentosidine is a well-characterized natural AGE that is often used as a biomarker for the production of all AGEs. While pentosidine can be measured in urine, the majority of this AGE is catabolized before excretion.[3]
Reference：
[1]. Neeper, M., Schmidt, A.M., Brett, J., et al. Cloning and expression of a cell surface receptor for advanced glycosylation end products of proteins. The Journal of Biological Chemisty 267(21), 14998-15004 (1992).
[2]. Brett, J., Schmidt, A.M., Yan, S.D., et al. Survey of the distribution of a newly characterized receptor for advanced glycation end products in tissues. American Journal of Pathology 143(6), 1699-1712 (1993).
[3]. Miyata, T., Ueda, Y., Horie, K., et al. Renal catabolism of advanced glycation end products: The fate of pentosidine. Kidney International 53, 416-422 (1998).
| Cas No. | 124505-87-9 | SDF | |
| 别名 | 戊糖素 | ||
| Canonical SMILES | [H]N(CCC[C@H](N)C(O)=O)C1=NC2=CC=CN(CCCC[C@H](N)C(O)=O)C2=N1 | ||
| 分子式 | C17H26N6O4 | 分子量 | 378.4 |
| 溶解度 | DMF: 21.4 mg/ml,DMSO: 22.4 mg/ml,Ethanol: 31.3 mg/ml,PBS (pH 7.2): 10 mg/ml | 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 | 2.6427 mL | 13.2135 mL | 26.4271 mL |
| 5 mM | 0.5285 mL | 2.6427 mL | 5.2854 mL |
| 10 mM | 0.2643 mL | 1.3214 mL | 2.6427 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。
Pentosidine: a molecular marker for the cumulative damage to proteins in diabetes, aging, and uremia
Diabetes Metab Rev 1991 Dec;7(4):239-51.PMID:1813279DOI:10.1002/dmr.5610070404.
Collagen undergoes progressive browning with age and diabetes characterized by yellowing, fluorescence, and cross-linking. The present research was undertaken in order to investigate the nature of the collagen-linked fluorescence. Human collagen was exhaustively cleaved into peptides by enzymatic digestion. Upon purification, a highly fluorescent chromophore was identified and purified from old human collagen. Structure elucidation revealed the presence of an imidazo [4,5-b] pyridinium-type structure acting as a cross-link between arginine, lysine, and a pentose. This advanced glycosylation end-product and protein cross-link results from the reaction of pentoses with proteins and was named Pentosidine. Further work indicated that long-term glycosylation of proteins with hexoses also leads to Pentosidine formation through sugar fragmentation. The proposed mechanism of Pentosidine formation involves the dehydration of the pentose-derived Amadori compound to form an intermediate which is attacked under base catalysis by the guanido group of arginine. The strict requirement for the Amadori rearrangement is uncertain. However, oxidation is definitely involved since Pentosidine is not formed in the absence of oxygen. Five-carbon sugars contributing to Pentosidine formation could be formed from larger sugars by oxidative fragmentation or from trioses, tetroses, and ketoses by condensation and/or reverse aldol reactions. Pentosidine increases exponentially in human skin at autopsy. Mean age-adjusted skin levels were significantly increased in subjects with uremia and especially in type 1 diabetics with uremia vs. controls. In skin biopsy, levels were significantly elevated in all diabetic (type 1) vs. control subjects. The highest degree of association was with the cumulative grade of diabetic complication (retinopathy, nephropathy, arterial stiffness, and joint stiffness). Pentosidine also forms in various proteins other than collagen, although to a much lesser extent. In blood, Pentosidine is mainly associated with plasma proteins and is highly elevated during uremia. In the lens, it is associated with both water-soluble and -insoluble protein fractions and is especially elevated during brunescent cataract formation. The origin of Pentosidine in vivo is uncertain. Evidence suggests that the pentoses are the most reactive sugars in Pentosidine formation in vitro; however, the origin and importance of free pentoses in vivo, especially during the diabetic state, are not certain. Possible origins include hemolysis and/or a defect in the primary pentose metabolism.(ABSTRACT TRUNCATED AT 400 WORDS)
[Pentosidine: a new biomarker in diabetes mellitus complications]
Med Clin (Barc) 2011 Mar 19;136(7):298-302.PMID:20226481DOI:10.1016/j.medcli.2009.12.001.
Diabetes mellitus causes an increase of morbidity and mortality. Advanced glycosilation end products (AGE) are formed by non-enzymatic glycation between proteins and reducing sugars as glucose. Oxidative reactions (glycoxidations) are essential for the formation of some AGE, for example Pentosidine. Increased concentrations of Pentosidine can be found in pathological conditions associated with hyperglycaemia and also related to increased oxidative stress. In individuals with diabetes mellitus, Pentosidine formation and accumulation is developed at an accelerated rate in cells without insulin control for glucose uptake. Pentosidine has a pivotal role in diabetic complications, probably as a consequence of the diverse properties of this compound, which alters the structure and function of molecules in biological systems. The following review discusses the alterations in the concentration of Pentosidine in the body, particularly in relation to changes occurring in diabetes and its complications such as vascular and bone disease, nephropathy, neuropathy and retinopathy. Novel therapeutic approaches which can prevent or ameliorate the toxic effects of AGE in the initiation and progression of diabetic complications are reviewed.
Review of Pentosidine and pyrraline in food and chemical models: formation, potential risks and determination
J Sci Food Agric 2018 Jul;98(9):3225-3233.PMID:29280151DOI:10.1002/jsfa.8853.
Pyrraline and Pentosidine are advanced Maillard reaction products derived from the reaction of glucose with the lysine amino group on proteins. They have been implicated in uremia, diabetes, and related complications, including inflammation, retinopathy, and nephropathy. This review focuses on the formation mechanism, human potential risks, and detections of Pentosidine and pyrraline and lays the foundation for further study of Pentosidine and pyrraline. © 2017 Society of Chemical Industry.
Pentosidine correlates with nanomechanical properties of human jaw bone
J Mech Behav Biomed Mater 2019 Oct;98:20-25.PMID:31176091DOI:10.1016/j.jmbbm.2019.06.002.
Initial intimate apposition between implant fixtures and host bone at the surgical site is a critical factor for osseointegration of dental implants. The advanced glycation end products accumulated in the jaw bone could lead to potential failure of a dental implant during the initial integration stage, because of the inferior bone mechanical property associated with the abnormal collagen cross-linking at the material level. Here, we demonstrate the lowered creep deformation resistance and reduced dimensional recovery of jaw bone in line with high levels of Pentosidine accumulation in the bone matrix which likely correlate with the Pentosidine level in blood plasma. Peripheral blood samples and cortical bone samples at the surgical site were obtained from patients scheduled for dental implants in the mandible. The Pentosidine levels in blood plasma were assessed. Subsequently, the relative Pentosidine levels and the mechanical properties of the jaw bone were quantified by Raman microspectroscopy and nanoindentation, respectively. The nanoindentation tests revealed less creep deformation resistance and reduced time-dependent dimensional recovery of bone samples with the increase in the relative Pentosidine level in the bone matrix. Higher tan δ values at the various frequencies during the dynamic indentation tests also suggested that viscoelasticity is associated with the relative intensity of Pentosidine in the jaw bone matrix. We found a positive correlation between the Pentosidine levels in blood plasma and the bone matrix, which in turn reduced the mechanical property of the jaw bone at the material level. Increased creep and reduced dimensional recovery of the jaw bone may diminish the mechanical interlocking of dental implants during the initial integration stage. Given the likely correlation between the plasma Pentosidine level and the mechanical properties of bone, measurement of the plasma Pentosidine level could serve as a new index to assess jaw bone matrix quality in advance of implant surgery.
The association between urinary Pentosidine levels and cognition in drug-naïve patients with Parkinson's disease
Neurol Sci 2022 Nov;43(11):6323-6328.PMID:35960387DOI:10.1007/s10072-022-06332-0.
Advanced glycation end products (AGEs) are suggested to play a potential role in the progression of Parkinson's disease (PD). The association between urinary levels of Pentosidine, one of the best-characterized AGEs, and clinical conditions such as motor severity and cognition were investigated in patients with PD. Data on the clinical characteristics and urinary levels of Pentosidine for 44 drug-naïve patients aged 60 years or older with PD were collected. The association between urinary Pentosidine levels and severity of motor symptoms and cognition was analyzed using the Montreal Cognitive Assessment Scale (MoCA). Urinary Pentosidine values increased with age (R2 = 0.286, p < 0.001) and were negatively correlated with the MoCA score (R2 = 0.255, p = 0.001). Urinary Pentosidine levels were significantly correlated with age (r = 0.535, p < 0.001), Hoehn-Yahr stage (r = 0.340, p < 0.05), and total MoCA score (r = - 0.505, p < 0.001). Multiple linear regression analysis showed that older age (β = 0.543; 95% confidence interval [CI] 0.300, 1.307; p = 0.003) was significantly associated with severity of motor symptoms, and that older age (β = - 0.456; 95% CI - 0.287, - 0.054; p = 0.005) and urinary Pentosidine levels (β = - 0.311; 95% CI - 0.428, - 0.004; p = 0.046) were significantly associated with a lower MoCA score. Urinary Pentosidine levels were significantly associated with lower cognition in drug-naïve PD patients. These findings have important clinical implications and suggest that Pentosidine may be a potential marker for cognitive impairment in early PD.