Uric acid
(Synonyms: 尿酸) 目录号 : GC33827
Uric Acid (2,6,8-Trioxypurine, 2,6,8-Trihydroxypurine, 2,6,8-Trioxopurine), a normal component of urine, is a product of the metabolic breakdown of purine nucleotides.
Cas No.:69-93-2
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
|
Cell experiment: |
Human colon carcinoma cells (Caco-2) are used and grown in Eagle’s minimum essential medium supplemented with 10% FBS, 1% non-essential amino acid mixture, and 1% Pen-Strep at 37°C in a humidified atmosphere with 5% CO2. Caco-2 cells are incubated with indomethacin in the presence or absence of Uric acid for 24 or 48 hours[1]. |
|
Animal experiment: |
To evaluate the effect of oral administration of Uric acid on NSAID-induced enteropathy, mice are given Uric acid (2.5, 10, 25, 100, or 250 mg/kg body weight) suspended in 0.5% carboxymethyl cellulose orally at 30 minutes before, and 12 hours after indomethacin or vehicle treatment. To evaluate the effect of intraperitoneal administration of inosinic acid plus potassium oxonate on NSAID-induced enteropathy, mice are given inosinic acid (500 mg/kg body weight) plus potassium oxonate (250 mg/kg body weight) 24 intraperitoneally at 30 minutes before, and 12 hours after indomethacin or vehicle treatment[1]. |
|
References: [1]. Yasutake Y, et al. Uric acid ameliorates indomethacin-induced enteropathy in mice through its antioxidant activity. J Gastroenterol Hepatol. 2017 Nov;32(11):1839-1845. |
|
Uric Acid (2,6,8-Trioxypurine, 2,6,8-Trihydroxypurine, 2,6,8-Trioxopurine), a normal component of urine, is a product of the metabolic breakdown of purine nucleotides.
Uric acid activates NFκB in a variety of cell culture models including proximal tubular cells. Uric acid suppresses 1-α hydroxylase mRNA and protein expression in dose dependent and time dependent manner[1].
Uric acid is synthesized mainly in the liver, intestines and the vascular endothelium as the end product of an exogenous pool of purines, and endogenously from damaged, dying and dead cells, whereby nucleic acids, adenine and guanine, are degraded into uric acid. Uric acid is a strong reactive oxygen species (ROS) and peroxynitrite scavenger and antioxidant. Uric acid may exert fundamental roles in tissue healing via initiating the inflammatory process that is necessary for tissue repair, scavenging oxygen free radicals, and mobilizing progenitor endothelial cells[2].
[1] Chen W, et al. Metabolism. 2014, 63(1):150-60. [2] Rashika El Ridi, et al. J Adv Res. 2017, 8(5): 487-493.
| Cas No. | 69-93-2 | SDF | |
| 别名 | 尿酸 | ||
| Canonical SMILES | O=C(N1)NC2=C(NC(N2)=O)C1=O | ||
| 分子式 | C5H4N4O3 | 分子量 | 168.11 |
| 溶解度 | DMSO : < 1 mg/mL (insoluble or slightly soluble);Water : < 0.1 mg/mL (insoluble) | 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。 |
||
| 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 5.9485 mL | 29.7424 mL | 59.4849 mL |
| 5 mM | 1.1897 mL | 5.9485 mL | 11.897 mL |
| 10 mM | 0.5948 mL | 2.9742 mL | 5.9485 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。
Uric acid and the kidney
Pediatr Nephrol 2014 Jun;29(6):999-1008.PMID:23824181DOI:10.1007/s00467-013-2549-x.
Uric acid, the end product of purine metabolism, is excreted predominantly by the proximal tubules. Abnormal serum levels of Uric acid are due to alterations in production or excretion. Fractional excretion of Uric acid is helpful in determining the underlying etiology of hypouricemia or hyperuricemia in children. Abnormalities in the molecular mechanisms that control renal Uric acid tubular transport are implicated in various disorders associated with abnormal Uric acid levels. Gout is rare in children; yet its presence necessitates evaluation for enzymatic defects in purine metabolism. Well-known effects of Uric acid on the kidney include nephrolithiasis and acute kidney injury (AKI) in the setting of tumor lysis. However, recent data suggest that Uric acid may be an important factor in the pathogenesis of AKI in general, as well as of chronic kidney disease (CKD) and hypertension. Hence, Uric acid may not only be a marker but also a potential therapeutic target in kidney disease. Nonetheless, because of confounders, more studies are needed to clarify the association between Uric acid and multifactorial disorders of the kidney.
Recent Progress on Uric acid Detection: A Review
Crit Rev Anal Chem 2020;50(4):359-375.PMID:31296022DOI:10.1080/10408347.2019.1637711.
Uric acid (UA), scavenger of oxygen radical, is a very important antioxidant that help maintains the stability of blood pressure and antioxidant stress. However, an abnormal UA concentration may be connected with many diseases: a higher UA concentration, comings from improper lifestyle such as purine excessive intake and excessive drinking, may reveal hyperuricemia, gout and some cardiovascular diseases; meanwhile, some genetic diseases can result in a low level UA relatively for a long time. Therefore, to develop a rapid and accurate detection method of UA is urgent and important. Recently many detection methods have been developed to measure the level of UA in human serum and urine sample even saliva and nails and tears. This review outlines the importance of UA detection and the history of the development of UA detection methods. UA detection include spectral (ultraviolet absorption, fluorescence), electrochemical (voltammetry, electrochemiluminescence, surface plasmon resonance), chromatography (liquid and gas phase), capillary electrophoresis and isotope dilution mass spectrometry, etc. Most of the above detection methods contain both enzymatic and nonenzymatic strategies. The materials used in mentioned methods above tend to be diversified, hence an overview of materials used in UA detection are also reported.
Uric acid as a Marker of Kidney Disease: Review of the Current Literature
Dis Markers 2015;2015:382918.PMID:26106252DOI:10.1155/2015/382918.
Uric acid has been implicated in the pathophysiology of renal disease; however renal clearance makes a causal relationship difficult to prove. We examine the current literature to support a potential role of Uric acid in the development of kidney disease and to determine the potential to use Uric acid as a marker for future renal decline. After review, we conclude that Uric acid is definitively linked to the development of chronic kidney disease and can be a poor prognostic factor for the development of acute renal failure, as well. However, further human research is needed before predictive models utilizing Uric acid can be developed and used in the clinical setting.
Molecular Imprinting Technology for Determination of Uric acid
Int J Mol Sci 2021 May 10;22(9):5032.PMID:34068596DOI:10.3390/ijms22095032.
The review focuses on the overview of electrochemical sensors based on molecularly imprinted polymers (MIPs) for the determination of Uric acid. The importance of robust and precise determination of Uric acid is highlighted, a short description of the principles of molecular imprinting technology is presented, and advantages over the others affinity-based analytical methods are discussed. The review is mainly concerned with the electro-analytical methods like cyclic voltammetry, electrochemical impedance spectroscopy, amperometry, etc. Moreover, there are some scattered notes to the other electrochemistry-related analytical methods, which are capable of providing additional information and to solve some challenges that are not achievable using standard electrochemical methods. The significance of these overviewed methods is highlighted. The overview of the research that is employing MIPs imprinted with Uric acid is mainly targeted to address these topics: (i) type of polymers, which are used to design Uric acid imprint structures; (ii) types of working electrodes and/or other parts of signal transducing systems applied for the registration of analytical signal; (iii) the description of the Uric acid extraction procedures applied for the design of final MIP-structure; (iv) advantages and disadvantages of electrochemical methods and other signal transducing methods used for the registration of the analytical signal; (vi) overview of types of interfering molecules, which were analyzed to evaluate the selectivity; (vi) comparison of analytical characteristics such as linear range, limits of detection and quantification, reusability, reproducibility, repeatability, and stability. Some insights in future development of Uric acid sensors are discussed in this review.
Uric acid and hypertension
Curr Hypertens Rep 2006 May;8(2):111-5.PMID:16672142DOI:10.1007/s11906-006-0005-z.
Epidemiologic studies published during the past 3 years support the possible role of Uric acid in the onset of essential hypertension. Data from several large, longitudinal cardiovascular disease studies indicate that elevated serum Uric acid is a predictor of incident hypertension and blood pressure progression. In a pediatric study, more than 90% of children with essential hypertension have serum Uric acid levels above 5.5 mg/dL. During the same period, laboratory studies have provided compelling mechanistic evidence to explain the clinical observations. Uric acid causes hypertension in a rat model through the activation of the renin-angiotensin system, downregulation of nitric oxide, and induction of endothelial dysfunction and vascular smooth muscle proliferation. Ongoing clinical trials will elucidate the role of Uric acid in human hypertension and will determine whether control of Uric acid may be a new way to prevent or treat essential hypertension.