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| 体外研究 (In Vitro) |
半乳糖在细菌的生存和致病性中起着重要作用。在大肠杆菌中，半乳糖主要由 Leloir 途径使用。三个 d-半乳糖末端基团中的每一个都具有不同的功能； α-d-半乳糖作为碳源，而β-d-半乳糖则刺激生物合成糖基化过程中UDP-半乳糖的合成[1]。
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| 体内研究 (In Vivo) |
在动物模型中，D-半乳糖可用于创建白内障追踪和小鼠亚急性休眠模型。长期接触 D-半乳糖会增加氧化损伤，增强 caspase 介导的细胞展示，并抑制小鼠的神经发生和神经迁移，所有这些都会导致神经变性。此外，D-半乳糖诱导的致敏是研究药物过程以及神经退行性和神经保护治疗的有用模型[2]。最终建议的 D-半乳糖途径会导致氧化损伤和认知障碍。在 d-gal 塔后 4 周和 6 周的旷场测试中发现了认知缺陷，而在 d-gal 塔后 6 周的迷宫测试中发现了空间记忆缺陷 [3]。
- C57BL/6小鼠经腹腔注射D-半乳糖（D-Galactose）（100 mg/kg/天）处理8周后，出现显著记忆丧失。Morris水迷宫测试显示逃避潜伏期延长（从25±3秒增至58±5秒）、目标象限停留时间缩短（从35±4%降至18±3%）；Y迷宫测试显示自发交替率降低（从72±5%降至45±4%）。组织学检查（苏木精-伊红染色）发现海马和皮质神经元数量减少约30%；氧化损伤指标改变：脑内丙二醛（MDA）水平升高45%，超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）活性分别降低30%和25%[2] - Wistar大鼠经口服D-半乳糖（D-Galactose）（300 mg/kg/天）处理8周后，出现认知障碍。Morris水迷宫测试显示逃避潜伏期延长60%；新物体识别测试显示识别指数从68±5%降至42±4%。海马和皮质氧化损伤明显：MDA水平分别升高38%和32%，GSH-Px活性降低28%[3] - C57BL/6J小鼠经腹腔注射D-半乳糖（D-Galactose）（120 mg/kg/天）处理6周后，出现行为学衰老表型。旷场测试显示自发活动减少（总移动距离降低40%）；被动回避测试显示避暗潜伏期缩短（从300±20秒降至120±15秒），提示学习记忆受损[4] - 年轻雄性Sprague-Dawley大鼠经腹腔注射D-半乳糖（D-Galactose）（500 mg/kg/天）处理10天后，出现类似自然衰老的症状。体重增长减缓15%，肝、肾器官系数分别降低10%和8%；血清氧化指标显示MDA升高35%，SOD降低25%[5] - C57BL/6J小鼠经腹腔注射D-半乳糖（D-Galactose）（200 mg/kg/天）处理10周后，被诱导形成白内障。80%小鼠晶状体混浊度达3级（对照组为0%）；晶状体氧化损伤确认：MDA水平升高50%，SOD活性降低40%[6] - Sprague-Dawley大鼠经腹腔注射D-半乳糖（D-Galactose）（500 mg/kg/天）处理4周后，建立稳定白内障模型。90%大鼠晶状体混浊度达4级，组织学检查显示晶状体纤维细胞变性、空泡化[7] |
| 动物实验 |
- C57BL/6 mouse model for memory loss and neurodegeneration: Male C57BL/6 mice (8-week-old) were randomly divided into control and D-Galactose groups. D-Galactose was dissolved in normal saline and administered via intraperitoneal injection at 100 mg/kg/day for 8 weeks; the control group received equal volume of normal saline. After treatment, memory function was evaluated by Morris Water Maze and Y-maze tests, and brain tissues were collected to detect oxidative markers (MDA, SOD, GSH-Px) and histological changes via hematoxylin-eosin staining [2]
- Wistar rat model for cognitive impairment: Male Wistar rats (6-week-old) were divided into control and D-Galactose groups. D-Galactose was dissolved in distilled water and given by oral gavage at 300 mg/kg/day for 8 weeks; the control group received distilled water. Cognitive function was assessed by Morris Water Maze and novel object recognition test, and hippocampal/cortical tissues were analyzed for oxidative markers [3] - C57BL/6J mouse model for behavioral aging: Male C57BL/6J mice (7-week-old) were assigned to control and D-Galactose groups. D-Galactose in normal saline was injected intraperitoneally at 120 mg/kg/day for 6 weeks. Locomotor activity was tested by open field test, and learning/memory was evaluated by passive avoidance test [4] - Young Sprague-Dawley rat model for aging simulation: Male Sprague-Dawley rats (4-week-old) were treated with D-Galactose (dissolved in normal saline) via intraperitoneal injection at 500 mg/kg/day for 10 days. Body weight was recorded weekly, and serum was collected to measure MDA and SOD levels; liver and kidney were weighed to calculate organ coefficients [5] - C57BL/6J mouse model for cataract: Female C57BL/6J mice (6-week-old) were divided into control and D-Galactose groups. D-Galactose in normal saline was injected intraperitoneally at 200 mg/kg/day for 10 weeks. Lens opacity was graded weekly using a slit lamp, and lenses were harvested to detect MDA and SOD levels [6] - Sprague-Dawley rat model for cataract: Female Sprague-Dawley rats (5-week-old) were treated with D-Galactose (dissolved in normal saline) via intraperitoneal injection at 500 mg/kg/day for 4 weeks. Lens opacity was graded by slit lamp, and lens tissues were fixed for histological examination (hematoxylin-eosin staining) to observe fiber cell changes [7] |
| 毒性/毒理 (Toxicokinetics/TK) |
D-galactose can induce neurotoxicity in mice: intraperitoneal injection of 100 mg/kg/day for 8 weeks resulted in loss of hippocampal and cortical neurons, increased MDA levels in the brain (oxidative damage), and decreased activity of antioxidant enzymes (SOD, GSH-Px), leading to memory loss and neurodegeneration [2]
- D-galactose can induce cognitive toxicity in rats: oral administration of 300 mg/kg/day for 8 weeks resulted in impaired learning and memory (decreased new object recognition index, prolonged maze escape latency), and increased oxidative damage in the hippocampus and cortex (increased MDA, decreased GSH-Px) [3] - D-galactose can induce aging-related toxicity in young rats: intraperitoneal injection of 500 mg/kg/day for 10 days resulted in slowed weight gain, decreased liver and brain tissue function, increased kidney organ coefficient, and increased serum oxidative stress (increased MDA, decreased SOD) [5] - D-galactose can cause ocular toxicity in mice and rats: intraperitoneal injection of 200 mg/kg/day for 8 weeks resulted in decreased MDA levels in the hippocampus and cortex (decreased MDA, decreased SOD) [5] mg/kg/day (mice, 10 weeks) or 500 mg/kg/day (rats, 4 weeks) can induce lens opacity (cataract), lens fibroblast degeneration, and increased lens MDA levels and decreased SOD activity [6][7] |
| 参考文献 |
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| 其他信息 |
Aldehyde-D-galactose is a D-galactose and also an aldehyde galactose. It is the enantiomer of aldehyde-L-galactose. (2R,3S,4S,5R)-2,3,4,5,6-pentahydroxyhexanal has been reported in tea (Camellia sinensis), Ascochyta medicaginicola, and other organisms with relevant data. Galactose is a metabolite found in or produced by Saccharomyces cerevisiae. It is a naturally occurring aldose, present in its D-form in lactose, cerebrosides, gangliosides, and mucins. Galactosyl-1-phosphate uridine transferase deficiency (galactosyl-1-phosphate uridine transferase deficiency) leads to abnormal galactose metabolism, known as galactosemia, resulting in elevated blood galactose levels. See also: D-galactose (note moved to).
- The mechanism by which D-galactose induces damage involves the overproduction of reactive oxygen species (ROS), leading to oxidative stress (increased MDA and decreased antioxidant enzymes). This oxidative stress can further lead to tissue damage, such as neuronal loss (memory impairment), lens fibrosis (cataracts), and organ dysfunction (changes in liver and kidney weight).[2][3][5][6][7] - D-galactose is widely used to establish animal models of aging, cognitive impairment, and cataracts to evaluate the protective effects of drugs (e.g., antioxidants, neuroprotectives, anti-cataract drugs). These models are characterized by phenotypic stability, low cost, and good reproducibility.[2][4][6][7] - In Enterobacteriaceae, D-galactose participates in metabolic networks, including transport (via GalP permease) and catabolism (via the Leloir pathway), but this is unrelated to its toxicity or pharmacological effects in mammals.[1] |
| 分子式 |
C6H12O6
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|---|---|
| 分子量 |
180.1559
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| 精确质量 |
180.063
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| CAS号 |
59-23-4
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| 相关CAS号 |
D-Galactose-13C;70849-30-8;D-Galactose-13C6;74134-89-7;D-Mannose;3458-28-4;D-Galactose-13C-2;478518-56-8;D-Galactose-d2-1;1176791-08-4;D-Galactose-13C,d;370565-96-1;D-Galactose-13C-3;478518-58-0;D-Galactose-13C-4;478518-60-4;D-Galactose-13C-5;478518-62-6;D-Galactose-d;64267-73-8;D-Galactose-d-1;64429-86-3;D-Galactose-d-2;478518-70-6;D-Galactose-d-3;478518-71-7;D-Galactose-d2;35669-34-2
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| PubChem CID |
3037556
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| 外观&性状 |
White to off-white solid powder
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| 密度 |
1.6±0.1 g/cm3
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| 沸点 |
527.1±50.0 °C at 760 mmHg
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| 熔点 |
168-170 °C(lit.)
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| 闪点 |
286.7±26.6 °C
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| 蒸汽压 |
0.0±3.1 mmHg at 25°C
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| 折射率 |
1.573
|
| LogP |
-3.17
|
| tPSA |
110.38
|
| 氢键供体(HBD)数目 |
5
|
| 氢键受体(HBA)数目 |
6
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| 可旋转键数目(RBC) |
5
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| 重原子数目 |
12
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| 分子复杂度/Complexity |
138
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| 定义原子立体中心数目 |
4
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| SMILES |
C([C@H]([C@@H]([C@@H]([C@H](C=O)O)O)O)O)O
|
| InChi Key |
GZCGUPFRVQAUEE-KCDKBNATSA-N
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| InChi Code |
InChI=1S/C6H12O6/c7-1-3(9)5(11)6(12)4(10)2-8/h1,3-6,8-12H,2H2/t3-,4+,5+,6-/m0/s1
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| 化学名 |
(2R,3S,4S,5R)-2,3,4,5,6-pentahydroxyhexanal
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| HS Tariff Code |
2934.99.9001
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| 存储方式 |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| 运输条件 |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| 溶解度 (体外实验) |
H2O : ~62.5 mg/mL (~346.91 mM)
DMSO : ~50 mg/mL (~277.53 mM) |
|---|---|
| 溶解度 (体内实验) |
配方 1 中的溶解度: ≥ 2.5 mg/mL (13.88 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 25.0 mg/mL澄清DMSO储备液加入到400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。 *生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。 配方 2 中的溶解度: ≥ 2.5 mg/mL (13.88 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。 例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。 *20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。 View More
配方 3 中的溶解度: ≥ 2.5 mg/mL (13.88 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。 配方 4 中的溶解度: 100 mg/mL (555.06 mM) in PBS (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液; 超声助溶. 1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液)); 2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方): 10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline); 假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL； 3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例; 4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶; 5、为保证最佳实验结果，工作液请现配现用！ 6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们; 7、 以上所有助溶剂都可在 Invivochem.cn网站购买。 |
| 制备储备液 | 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 |
1、根据实验需要选择合适的溶剂配制储备液 (母液)：对于大多数产品，InvivoChem推荐用DMSO配置母液 (比如：5、10、20mM或者10、20、50 mg/mL浓度），个别水溶性高的产品可直接溶于水。产品在DMSO 、水或其他溶剂中的具体溶解度详见上”溶解度 (体外)”部分;
2、如果您找不到您想要的溶解度信息，或者很难将产品溶解在溶液中，请联系我们;
3、建议使用下列计算器进行相关计算（摩尔浓度计算器、稀释计算器、分子量计算器、重组计算器等）;
4、母液配好之后，将其分装到常规用量，并储存在-20°C或-80°C，尽量减少反复冻融循环。
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)。如该浓度超过该批次药物DMSO溶解度，请首先与我们联系。
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 ddH2O，混匀澄清。
(1) 请确保溶液澄清之后，再加入下一种溶剂 (助溶剂) 。可利用涡旋、超声或水浴加热等方法助溶；
(2) 一定要按顺序加入溶剂 (助溶剂) 。
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