Uric Acid (sodium salt)
(Synonyms: 尿酸钠,Monosodium urate) 目录号 : GC45126
An end product of purine metabolism
Cas No.:1198-77-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Uric acid is a ubiquitous end product of purine metabolism in humans that is mainly excreted in urine, whereas in other mammals it is further metabolized to allantoin by uricase. The final two steps in its production are catalyzed by xanthine oxidase, which generates superoxide. Uric acid acts as a potent peroxynitrite scavenger and antioxidant. However, high levels of serum uric acid (>120 µg/ml), termed hyperuricemia, are associated with gout, kidney stones, metabolic syndrome, hypertension, renal disease, and cardiovascular disease. Uric acid in the form of monosodium urate crystals has been proposed to trigger interleukin-1β-mediated inflammation by activating the NOD-like receptor protein 3 inflammasome.
| Cas No. | 1198-77-2 | SDF | |
| 别名 | 尿酸钠,Monosodium urate | ||
| Canonical SMILES | O=C(N1)NC2=C1C([O-])=NC(N2)=O.[Na+] | ||
| 分子式 | C5H3N4O3•Na | 分子量 | 190.1 |
| 溶解度 | 1 M NaOH: 25 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 | 5.2604 mL | 26.3019 mL | 52.6039 mL |
| 5 mM | 1.0521 mL | 5.2604 mL | 10.5208 mL |
| 10 mM | 0.526 mL | 2.6302 mL | 5.2604 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。
Thiazide and loop diuretics
J Clin Hypertens (Greenwich) 2011 Sep;13(9):639-43.PMID:21896142DOI:10.1111/j.1751-7176.2011.00512.x.
KEY POINTS AND PRACTICAL RECOMMENDATIONS: • Although chlorthalidone and hydrochlorothiazide are structurally similar, they are very different pharmacokinetically, with chlorthalidone having both an extremely long half-life (approximately 40 to 60 hours) and a large volume of distribution, with gradual elimination from the plasma compartment by tubular secretion. • Furosemide usage, the most widely used diuretic in the loop diuretic class, can be complicated by extremely erratic absorption, with a bioavailability range of 12% to 112%. • Chlorthalidone, at a dose of 25 mg, is comparatively more potent than 50 mg of hydrochlorothiazide, particularly as related to overnight blood pressure reduction. • In ALLHAT, there was no difference among chlorthalidone, amlodipine, lisinopril, and doxazosin for the primary outcome or mortality. • Secondary outcomes were similar except for a 38% higher rate of heart failure with amlodipine; a 10% higher rate of combined cardiovascular disease, a 15% higher rate of stroke, and a 19% higher rate of heart failure with lisinopril; and a 20% higher rate of cardiovascular disease, a 20% higher rate of stroke (40% higher rate in blacks), and an 80% higher rate of heart failure with doxazosin, compared with chlorthalidone. • The ACCOMPLISH study may affect future practice guidelines as a result of its findings favoring the amlodipine/benazepril combination; however, the generalizability to patient populations with a lesser cardiovascular risk profile remains in question and the dose of hydrochlorothiazide was only 12.5 mg to 25 mg daily, which was a dose lower than that used in placebo-controlled trials using hydrochlorothiazide. • Certain low-renin patient groups (eg, blacks, the elderly, and diabetics) as well as those who manifest the metabolic syndrome are commonly more responsive to thiazide-type diuretic therapy. • Diuretics can be successfully combined with β-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, centrally acting agents, and even calcium channel blockers. • Although thiazide-type diuretics are among the best-tolerated antihypertensive agents in terms of symptomatic adverse effects, diuretic-related adverse side effects include those with established mechanisms (eg, such as electrolyte changes and/or metabolic abnormalities) and other side effects, which are less well understood mechanistically (eg, impotence), although the latter is not universally accepted as a diuretic-related side effect. • Thiazide-induced hypokalemia is associated with increased blood glucose, and treatment of thiazide-induced hypokalemia may reverse glucose intolerance and possibly prevent diabetes. • Thiazide-induced hyperuricemia occurs as a result of volume contraction and competition with Uric Acid for renal tubular secretion, but does not necessarily contraindicate using a thiazide, especially if a uric acid-lowering drug such as allopurinol is being used. • Adverse interactions include the blunting of thiazide effects by nonsteroidal anti-inflammatory drugs and the potential to increase fatigue, lethargy, and increase in glucose when combined with β-blockers. • Thiazide-type diuretics are useful first-line agents in the treatment of hypertension because they have been proven to reduce cardiovascular mortality and morbidity in systolic and diastolic forms of hypertension and do so at low cost. • Loop diuretics should not be used as first-line therapy in hypertension since there are no outcome data with them. They should be reserved for conditions of clinically significant fluid overload (eg, heart failure and significant fluid retention with vasodilator drugs, such as minoxidil) or with advanced renal failure and can be combined with thiazide-type diuretics.
Umami-induced obesity and metabolic syndrome is mediated by nucleotide degradation and Uric Acid generation
Nat Metab 2021 Sep;3(9):1189-1201.PMID:34552272DOI:10.1038/s42255-021-00454-z.
Umami refers to the savoury taste that is mediated by monosodium glutamate (MSG) and enhanced by inosine monophosphate and other nucleotides. Umami foods have been suggested to increase the risk for obesity and metabolic syndrome but the mechanism is not understood. Here we show that MSG induces obesity, hypothalamic inflammation and central leptin resistance in male mice through the induction of AMP deaminase 2 and purine degradation. Mice lacking AMP deaminase 2 in both hepatocytes and neurons are protected from MSG-induced metabolic syndrome. This protection can be overcome by supplementation with inosine monophosphate, most probably owing to its degradation to Uric Acid as the effect can be blocked with allopurinol. Thus, umami foods induce obesity and metabolic syndrome by engaging the same purine nucleotide degradation pathway that is also activated by fructose and salt consumption. We suggest that the three tastes-sweet, salt and umami-developed to encourage food intake to facilitate energy storage and survival but drive obesity and diabetes in the setting of excess intake through similar mechanisms.
The Role of Uric Acid in Hypertension of Adolescents, Prehypertension and Salt Sensitivity of Blood Pressure
Med Sci Monit 2017 Feb 13;23:790-795.PMID:28190873DOI:10.12659/msm.899563.
Uric Acid is the end product of purine metabolism. Metabolic disorders of Uric Acid are associated with many disease states. Substantial evidence suggests the possible role of Uric Acid as a mediator of high blood pressure. Elevated Uric Acid is closely associated with new onset essential hypertension in adolescents and prehypertension; and urate-lowering agents can significantly improve these early stages of hypertension. Uric Acid also influences salt sensitivity of blood pressure through two phases. Local renin-angiotensin-aldosterone system activation initiates renal damage, arteriolopathy, and endothelium dysfunction, which is followed by the dysregulation of sodium homeostasis, thereby leading to increased salt sensitivity. In this review we summarize the available evidence to contribute to a better understanding of the casual relationship between Uric Acid and early or intermediate stages of hypertension. We hope our review can contribute to the prevention of hypertension or provide new insights into a treatment that would slow the progression of hypertension.
Salt-Toggled Capture Selection of Uric Acid Binding Aptamers
Chembiochem 2023 Jan 17;24(2):e202200564.PMID:36394510DOI:10.1002/cbic.202200564.
Uric Acid is the end-product of purine metabolism in humans and an important biomarker for many diseases. To achieve the detection of Uric Acid without using enzymes, we previously selected a DNA aptamer for Uric Acid with a Kd of 1 μM but the aptamer required multiple Na+ ions for binding. Saturated binding was achieved with around 700 mM Na+ and the binding at the physiological condition was much weaker. In this work, a new selection was performed by alternating Mg2+ -containing buffers with Na+ and Li+ . After 13 rounds of selection, a new aptamer sequence named UA-Mg-1 was obtained. Isothermal titration calorimetry confirmed aptamer binding in both selection buffers, and the Kd was around 8 μM. The binding of UA-Mg-1 to UA required only Mg2+ . This is an indicator of successful switching of metal dependency via the salt-toggled selection method. The UA-Mg-1 aptamer was engineered into a fluorescent biosensor based on the strand-displacement assay with a limit of detection of 0.5 μM Uric Acid in the selection buffer. Finally, comparison with the previously reported Na+ -dependent aptamer and a xanthine/Uric Acid riboswitch was also made.
Control of renal Uric Acid excretion and gout
Curr Opin Rheumatol 2008 Mar;20(2):192-7.PMID:18349750DOI:10.1097/BOR.0b013e3282f33f87.
Purpose of review: Impaired renal Uric Acid excretion is the major mechanism of hyperuricemia in patients with primary gout. This review highlights recent advances in the knowledge of normal mechanisms of renal Uric Acid handling and derangement of these mechanisms in Uric Acid underexcretion. Recent findings: The discovery of URAT1 has facilitated identification of other molecules potentially involved in Uric Acid transport in the renal tubules. Some of these molecules show gender differential expression in animal experiments. Sodium-dependent monocarboxylate cotransporters have been shown to transport lactate and butyrate, and may have roles in hyperuricemia associated with diabetic ketoacidosis and alcohol ingestion. Certain polymorphisms in SLC22A12 may be associated with the development of hyperuricemia or gout, although confirmation is needed. Mechanisms of hyperuricemia associated with Uric Acid underexcretion in patients with familial juvenile hyperuricemic nephropathy also remain to be clarified. Distal tubular salt wasting and compensatory upregulation of the resorption of sodium and Uric Acid in the proximal tubule may explain the hyperuricemia associated with this disorder. Summary: Much progress has been made in understanding the mechanisms of renal Uric Acid handling. Elucidation of the mechanisms of hyperuricemia in patients with familial juvenile hyperuricemic nephropathy will shed light on the function of uromodulin, functional impairment of which eventually results in diminished Uric Acid excretion.