Citric acid
(Synonyms: 柠檬酸) 目录号 : GC14203
柠檬酸是一种天然防腐剂和食品酸味增强剂。
Cas No.:77-92-9
Sample solution is provided at 25 µL, 10mM.
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Citric acid is a weak organic tricarboxylic acid found in citrus fruits. Citric acid is a natural preservative and food tartness enhancer.
Citric acid induces apoptosis through the mitochondrial pathway in the human keratinocyte cell line HaCaT. It inhibits proliferation of HaCaT cells in a dose-dependent manner, but also induces apoptosis and cell cycle-arrest at the G2/M phase (before 24 h) and S phase (after 24 h)[1].
Citric acid is found in all animal tissues as an intermediary substance in oxidative metabolism. The administration of citric acid (1–2 g/kg) attenuates LPS-induced elevations in brain MDA, nitrite, TNF-α, GPx, and PON1 activity. In the liver, nitrite is decreased by 1 g/kg citric acid. Citric acid (1-2 g/kg) decreases brain lipid peroxidation and inflammation, liver damage, and DNA fragmentation[2]. Citric acid supplementation increases intestinal calcium and phosphorus absorption and the retention/intake ratio only in rats fed the 1% Ca diet. Citric acidsupplementation together with a calcium-rich diet allows to obtain an increased retention of calcium and phosphorus in bone. The prolonged administration of calcium citrate supplements may therefore help to increase bone mineral concentration[3]. Oral administration of citric acid ameliorates ketosis and protects against the development of diabetic complications in an animal model of type 1 diabetes[4].
Reference:
[1]. Ying TH, et al. Citric acid induces cell-cycle arrest and apoptosis of human immortalized keratinocyte cell line (HaCaT) via caspase- and mitochondrial-dependent signaling pathways. Anticancer Res. 2013 Oct;33(10):4411-20.
[2]. Abdel-Salam OM, et al. Citric acid effects on brain and liver oxidative stress in lipopolysaccharide-treated mice. J Med Food. 2014 May;17(5):588-98.
[3]. Lacour B, et al. Stimulation by citric acid of calcium and phosphorus bioavailability in rats fed a calcium-rich diet. Miner Electrolyte Metab. 1997;23(2):79-87.
[4]. Nagai R, et al. Citric acid inhibits development of cataracts, proteinuria and ketosis in streptozotocin (type 1) diabetic rats. Biochem Biophys Res Commun. 2010 Feb 26;393(1):118-22.
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Cell experiment: |
HaCaT cells are treated with different concentrations of citric acid (2.5, 5, 7.5, 10, 12.5 mM) for 24 h; 0.5% of DMSO (vehicle) is used as a control. Cells are then centrifuged at 1000 ×g for 5 min, and cell pellets are dissolved with 0.5 mL of Phosphate buffered saline (PBS) containing 5 μg/mL PI and viable cells are determined by using a flow cytometer for determination of viable cells[1]. |
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Animal experiment: |
Rats: Rats are induced of diabetes and divided randomly into an untreated diabetic group and two treated diabetic groups, receiving citric acid (2 g/L) in the drinking water, or insulin therapy. Insulin-treated rats receive 3 IU of neutral protamine Hagedorn insulin three times per week. Fasting (12 hr) blood samples are obtained from the tail vein two days after insulin injection for measurement of blood glucose, HbA1c and ketone bodies[4]. [2]Mice: Citric acid is prepared in sterile physiological saline. Mice are randomly divided into five equal groups (six mice each). Mice are treated with either 0.2mL of: sterile physiological saline (group 1) or citric acid at doses of 1, 2, and 4 g/kg, orally (groups 2-4). Treatments are given just prior to endotoxin administration (LPS: 200 lg/kg, injected intraperitoneally, 0.1 mL). The fifth group received just the vehicle, no LPS (negative control). Mice are euthanized after 4 h of LPS or vehicle injection by decapitation under ether anesthesia, where the brain and liver of each mouse are then removed for analysis[2]. |
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References: [1]. Ying TH, et al. Citric acid induces cell-cycle arrest and apoptosis of human immortalized keratinocyte cell line (HaCaT) via caspase- and mitochondrial-dependent signaling pathways. Anticancer Res. 2013 Oct;33(10):4411-20. |
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| Cas No. | 77-92-9 | SDF | |
| 别名 | 柠檬酸 | ||
| 化学名 | 2-hydroxypropane-1,2,3-tricarboxylic acid | ||
| Canonical SMILES | OC(CC(O)=O)(C(O)=O)CC(O)=O | ||
| 分子式 | C6H8O7 | 分子量 | 192.12 |
| 溶解度 | ≥ 19.2mg/mL in Water | 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 | 5.2051 mL | 26.0254 mL | 52.0508 mL |
| 5 mM | 1.041 mL | 5.2051 mL | 10.4102 mL |
| 10 mM | 0.5205 mL | 2.6025 mL | 5.2051 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。
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet