D-Galactose (D-(+)-Galactose)
(Synonyms: D-半乳糖; D-(+)-Galactose) 目录号 : GC30795
A natural aldohexose
Cas No.:59-23-4
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
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Animal experiment: |
Rats: D-galactose is dissolved in water for administration at the dose of 100 mg/kg of body weight, and given by oral gavage, once a day, over a period of 1, 2, 4, 6 or 8 weeks. Animals are randomized into two groups: control animals (receiving water by oral gavage) or d-gal animals (receiving D-galactose by oral gavage). The behavioral tests and biochemical analysis are undertaken on the1st, 2nd, 4th, 6th and 8th weeks after the last administration of d-gal[3]. Mice: Male adult C57BL/6 mice are randomly divided into three groups (control, D-galactose, and D-galactose plus α-LA). D-galactose (100 mg/kg) is injected subcutaneously (s.c.) daily into mice for 7 weeks. α-LA (100 mg/kg body weight) is injected peritoneally (i.p.) daily concomitantly for 7 weeks. All control animals are given saline[2]. |
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References: [1]. Csiszovszki Z, et al. Structure and function of the D-galactose network in enterobacteria. MBio. 2011 Jun 28;2(4):e00053-11. |
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D-Galactose is a natural aldohexose and C-4 epimer of glucose. D-galactose is converted enzymatically into D-glucose for metabolism or polysaccharides for storage. Chronic, systemic exposure to D-galactose accelerates senescence in invertebrates and mammals and has been used as a model for aging.1 In bacteria, D-galactose is imported by a methyl-galactoside transport system to drive chemotaxis.2
D-半乳糖是一种天然的醛糖，也是葡萄糖的C-4异构体。D-半乳糖可以通过酶促反应转化为D-葡萄糖进行代谢或用于多糖的储存。长期、全身性的接触D-半乳糖会加速无脊椎动物和哺乳动物的衰老，因此被用作衰老的模型。[1]在细菌中，D-半乳糖通过甲基半乳糖运输系统进入细胞，驱动趋化。2
1.Cui, X., Zuo, P., Zhang, Q., et al.Chronic systemic D-galactose exposure induces memory loss, neurodegeneration, and oxidative damage in mice: Protective effects of R-α-lipoic acidJ. Neurosci. Res.84(3)647-654(2006) 2.Borrok, M.J., Kiessling, L.L., and Forest, K.T.Conformational changes of glucose/galactose-binding protein illuminated by open, unliganded, and ultra-high-resolution ligand-bound structuresProtein Sci.16(6)1032-1041(2007)
| Cas No. | 59-23-4 | SDF | |
| 别名 | D-半乳糖; D-(+)-Galactose | ||
| Canonical SMILES | O=C[C@@H]([C@H]([C@H]([C@@H](CO)O)O)O)O | ||
| 分子式 | C6H12O6 | 分子量 | 180.16 |
| 溶解度 | Water : ≥ 100 mg/mL (555.06 mM) | 储存条件 | Store at RT |
| 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 | 5.5506 mL | 27.7531 mL | 55.5062 mL |
| 5 mM | 1.1101 mL | 5.5506 mL | 11.1012 mL |
| 10 mM | 0.5551 mL | 2.7753 mL | 5.5506 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。
D-Galactose-induced accelerated aging model: an overview
To facilitate the process of aging healthily and prevent age-related health problems, efforts to properly understand aging mechanisms and develop effective and affordable anti-aging interventions are deemed necessary. Systemic administration of D-galactose has been established to artificially induce senescence in vitro and in vivo as well as for anti-aging therapeutic interventions studies. The aim of this article is to comprehensively discuss the use of D-galactose to generate a model of accelerated aging and its possible underlying mechanisms involved in different tissues/organs.
D-galactose-induced liver aging model: Its underlying mechanisms and potential therapeutic interventions
Aging is associated with a variety of morphological and functional changes in the liver. Oxidative stress and inflammation are now widely accepted as the main mechanisms involved in the aging process that may subsequently cause severe injury to mitochondrial DNA which leads to apoptosis. As aging may increase the risks for various liver diseases and plays as an adverse prognostic factor increasing the mortality rate, knowledge regarding the mechanisms of age-related liver susceptibility and the possible therapeutic interventions is imperative. Due to cost and time constraints, a mimetic aging model is generally preferred to naturally aged animals to study the underlying mechanisms of aging liver. The use of D-galactose in aging research is dated back to 1962 and has since been used widely. This review aims to comprehensively summarize the effects of D-galactose-induced aging on the liver and the underlying mechanisms involved. Its potential therapeutic interventions are also discussed. It is hoped that this invaluable information may facilitate researchers in choosing the appropriate aging model and provide a valuable platform for testing potential therapeutic strategies for the prevention and treatment of age-related liver diseases.
An overview of D-galactose utilization through microbial fermentation and enzyme-catalyzed conversion
D-Galactose is an abundant carbohydrate monomer in nature and widely exists in macroalgae, plants, and dairy wastes. D-Galactose is useful as a raw material for biomass fuel production or low-calorie sweetener production, attracting increased attention. This article summarizes the studies on biotechnological processes for galactose utilization. Two main research directions of microbial fermentation and enzyme-catalyzed conversion from galactose-rich biomass are extensively reviewed. The review provides the recent discoveries for biofuel production from macroalgae, including the innovative methods in the pretreatment process and technological development in the fermentation process. As modern people pay more attention to health, enzyme technologies for low-calorie sweetener production are more urgently needed. D-Tagatose is a promising low-calorie alternative to sugar. We discuss the recent studies on characterization and genetic modification of L-arabinose isomerase to improve the bioconversion of D-galactose to D-tagatose. In addition, the trends and critical challenges in both research directions are outlined at the end. KEY POINTS: ? The value and significance of galactose utilization are highlighted. ? Biofuel production from galactose-rich biomass is accomplished by fermentation. ? L-arabinose isomerase is a tool for bioconversion of D-galactose to D-tagatose.
Quercetin Attenuates Pancreatic and Renal D-Galactose-Induced Aging-Related Oxidative Alterations in Rats
Aging is an oxidative stress-associated process that progresses with age. Our aim is to delay or attenuate these oxidative alterations and to keep individuals healthy as they age using natural compounds supplementation. Therefore, we conducted the present study to investigate the protective potentials of quercetin against D-galactose (D-gal)-associated oxidative alterations that were induced experimentally in male Wistar rats. Forty-five rats were randomly allocated into five groups of nine rats each. The groups were a control group that was reared on a basal diet and injected subcutaneously with 120 mg D-gal dissolved in physiological saline solution (0.9% NaCl) per kg body weight daily and quercetin-treated groups that received the same basal diet and subcutaneous daily D-gal injections were supplemented orally with 25, 50, and 100 mg of quercetin per kg body weight for 42 days. Pancreatic and renal samples were subjected to histopathological, immunohistochemical, and relative mRNA expression assessments. Aging (p53, p21, IL-6, and IL-8), apoptotic (Bax, CASP-3, and caspase-3 protein), proliferative (Ki67 protein), antiapoptotic (Bcl2 and Bcl2 protein), inflammatory (NF-百B, IL-1汕, and TNF-汐), antioxidant (SOD1), and functional markers (GCLC and GCLM genes and insulin, glucagon, and podocin proteins) were determined to evaluate the oxidative alterations induced by D-gal and the protective role of quercetin. D-gal caused oxidative alterations of the pancreas and kidneys observed via upregulations of aging, apoptotic, and inflammatory markers and downregulated the antiapoptotic, proliferative, antioxidant, and functional markers. Quercetin potentially attenuated these aging-related oxidative alterations in a dose-dependent manner. Finally, we can conclude that quercetin supplementation is considered as a promising natural protective compound that could be used to delay the aging process and to maintain human health.
D-(+)-Galactose-induced aging: A novel experimental model of erectile dysfunction
Erectile dysfunction (ED) is defined as the inability to achieve and/or maintain penile erection sufficient for satisfactory sexual relations, and aging is one of the main risk factors involved. The D-(+)-Galactose aging model is a consolidated methodology for studies of cardiovascular aging; however, its potential for use with ED remain unexplored. The present study proposed to characterize a new experimental model for ED, using the D-(+)-Galactose aging model. For the experiments, the animals were randomly divided into three groups receiving: vehicle (CTL), D-galactose 150 mg/kg (DGAL), and D-(+)-galactose 150 mg/Kg + sildenafil 1.5 mg/Kg (DGAL+SD1.5) being administered daily for a period of eight weeks. All of the experimental protocols were previously approved by the Ethics Committee on the Use of Animals at the Federal University of Para赤ba n～ 9706070319. During the treatment, we analyzed physical, molecular, and physiological aspects related to the aging process and implicated in the development of ED. Our findings demonstrate for the first time that D-(+)-Galactose-induced aging represents a suitable experimental model for ED assessment. This was evidenced by an observed hyper-contractility in corpora cavernosa, significant endothelial dysfunction, increased ROS levels, an increase in cavernous tissue senescence, and the loss of essential penile erectile components.