SDMA (Symmetric dimethylarginine)
(Synonyms: 对称N,N-二甲基精氨酸,Symmetric dimethylarginine; NG,NG'-Dimethyl-L-arginine) 目录号 : GC33824
SMDA (symmetric dimethylarginine) is a methylated form of arginine found within all nucleated cells that is released into circulation after proteolysis, then excreted through the kidneys, and correlates well with GFR (glomerular filtration rate) in people, dogs, and cats.
Cas No.:30344-00-4
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
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Cell experiment: |
SDMA stock solution is prepared in 0.9% NaCl and diluted in the cell culture medium or in heparinized whole blood resulting in a maximal uremic concentration of 6.1 μM SDMA. Whole blood is incubated with saline (control) or different doses of ADMA (0.6, 3.6, and 36 μM) or SDMA (1.5, 3.1, and 6.1 μM) for 2 hours in a humidified atmosphere of 5% CO2 in air at 37°C. Cells are finally stained for intracellular TNF-α or IL-6. Samples are analyzed with a flow cytometer[2]. |
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Animal experiment: |
Mice: Eight-week-old male C57Bl/6 mice receives vehicle-controlled infusion of SDMA (250 µmol/kg/days) for 28 days using osmotic minipumps (n=24/group). Glomerular filtration rate, cardiac function and blood pressure are monitored. Blood samples for SDMA determination are obtained at baseline, 2 and 4 weeks. Mice are euthanized at 4 weeks to obtain tissue for renal histology[4]. |
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References: [1]. Bode-B ger SM,et al. Symmetrical dimethylarginine: a new combined parameter for renal function and extent ofcoronary artery disease. |
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SMDA (symmetric dimethylarginine) is a methylated form of arginine found within all nucleated cells that is released into circulation after proteolysis, then excreted through the kidneys, and correlates well with GFR (glomerular filtration rate) in people, dogs, and cats.
| Cas No. | 30344-00-4 | SDF | |
| 别名 | 对称N,N-二甲基精氨酸,Symmetric dimethylarginine; NG,NG'-Dimethyl-L-arginine | ||
| Canonical SMILES | N[C@@H](CCCN/C(NC)=N/C)C(O)=O | ||
| 分子式 | C8H18N4O2 | 分子量 | 202.25 |
| 溶解度 | DMSO : 50 mg/mL (247.22 mM; ultrasonic and adjust pH to 3 with 1M HCl) | 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 | 4.9444 mL | 24.7219 mL | 49.4438 mL |
| 5 mM | 0.9889 mL | 4.9444 mL | 9.8888 mL |
| 10 mM | 0.4944 mL | 2.4722 mL | 4.9444 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。
Symmetric dimethylarginine: Improving the Diagnosis and Staging of Chronic Kidney Disease in Small Animals
Vet Clin North Am Small Anim Pract 2016 Nov;46(6):941-60.PMID:27499007DOI:10.1016/j.cvsm.2016.06.010.
Chronic kidney disease (CKD) is a common condition in cats and dogs, traditionally diagnosed after substantial loss of kidney function when serum creatinine concentrations increase. Symmetric dimethylarginine (SDMA) is a sensitive circulating kidney biomarker whose concentrations increase earlier than creatinine as glomerular filtration rate decreases. Unlike creatinine SDMA is unaffected by lean body mass. The IDEXX SDMA test introduces a clinically relevant and reliable tool for the diagnosis and management of kidney disease. SDMA has been provisionally incorporated into the International Renal Interest Society guidelines for CKD to aid staging and targeted treatment of early and advanced disease.
Toxic Dimethylarginines: Asymmetric Dimethylarginine (ADMA) and Symmetric dimethylarginine (SDMA)
Toxins (Basel) 2017 Mar 6;9(3):92.PMID:28272322DOI:10.3390/toxins9030092.
Asymmetric and Symmetric dimethylarginine (ADMA and SDMA, respectively) are toxic, non-proteinogenic amino acids formed by post-translational modification and are uremic toxins that inhibit nitric oxide (NO) production and play multifunctional roles in many human diseases. Both ADMA and SDMA have emerged as strong predictors of cardiovascular events and death in a range of illnesses. Major progress has been made in research on ADMA-lowering therapies in animal studies; however, further studies are required to fill the translational gap between animal models and clinical trials in order to treat human diseases related to elevated ADMA/SDMA levels. Here, we review the reported impacts of ADMA and SDMA on human health and disease, focusing on the synthesis and metabolism of ADMA and SDMA; the pathophysiological roles of these dimethylarginines; clinical conditions and animal models associated with elevated ADMA and SDMA levels; and potential therapies against ADMA and SDMA. There is currently no specific pharmacological therapy for lowering the levels and counteracting the deleterious effects of ADMA and SDMA. A better understanding of the mechanisms underlying the impact of ADMA and SDMA on a wide range of human diseases is essential to the development of specific therapies against diseases related to ADMA and SDMA.
Evaluation of Symmetric dimethylarginine (SDMA) in Dogs with Acute Pancreatitis
Vet Sci 2020 Jun 1;7(2):72.PMID:32492828DOI:10.3390/vetsci7020072.
Symmetric dimethylarginine (SDMA) is considered an important biomarker of kidney dysfunction. The aims of the study were to evaluate SDMA in dogs with acute pancreatitis (AP) and its relationship with the presence of kidney injury and mortality. A cohort study including fifty-four dogs with AP diagnosed using compatible clinical and laboratory parameters, abnormal SNAP cPL and compatible abdominal ultrasound within 48 h from admission, was conducted. Dogs with history of renal and/or urinary diseases were excluded, along with dogs exposed to nephrotoxic drugs. Serum urea and creatinine and urinary output (UO) were recorded. Acute kidney injury (AKI) was diagnosed and graded using International Renal Interest Society (IRIS) guidelines. SDMA was measured using high performance liquid chromatography. Fifty-four dogs were included and divided in non-AKI (n = 37) and AKI dogs (n = 17). Twenty-three dogs (14 non-AKI) had SDMA > 15 μg/dL. Median SDMA was higher in AKI dogs than non-AKI dogs (25.7 vs. 13.93 μg/dL; p = 0.03). Dogs with normal creatinine (AP and AKI 1 dogs) had SDMA above reference range in 38% and 33% of cases, respectively. In AKI dogs, SDMA and creatinine were positively correlated (p = 0.006 r = 0.7). SDMA was not significantly different between survivors and non-survivors. Although further studies are warranted, SDMA may be a useful tool in canine AP, as a high SDMA may be related to subclinical kidney impairment.
Asymmetric dimethylarginine (ADMA), Symmetric dimethylarginine (SDMA) and homoarginine (hArg): the ADMA, SDMA and hArg paradoxes
Cardiovasc Diabetol 2018 Jan 4;17(1):1.PMID:29301528DOI:10.1186/s12933-017-0656-x.
NG-Methylation of L-arginine (Arg) residues in certain proteins by protein arginine methyltransferases and subsequent proteolysis yields NG-monomethyl-L-arginine (MMA), NG,NG-dimethyl-L-arginine (asymmetric dimethylarginine, ADMA) and NG,N'G-dimethyl-L-arginine (Symmetric dimethylarginine, SDMA). Biological MMA, ADMA and SDMA occur as free acids in the nM-range and as residues of proteins of largely unknown quantity. Arginine:glycine amidinotransferase (AGAT) catalyzes the synthesis of L-homoarginine (hArg) from free Arg and L-lysine. Biological hArg is considered to occur exclusively as free acid in the lower µM-range. Nitric oxide synthase (NOS) catalyzes the conversion of Arg (high affinity) and hArg (low affinity) to nitric oxide (NO) which is a pleiotropic signaling molecule. MMA, ADMA and SDMA are inhibitors (MMA > ADMA ≫ SDMA) of NOS activity. Slightly elevated ADMA and SDMA concentrations and slightly reduced hArg concentrations in the circulation are associated with many diseases including diabetes mellitus. Yet, this is paradox: (1) free ADMA and SDMA are weak inhibitors of endothelial NOS (eNOS) which is primarily responsible for NO-related effects in the cardiovascular system, with free hArg being a poor substrate for eNOS; (2) free ADMA, SDMA and hArg are not associated with oxidative stress which is considered to induce NO-related endothelial dysfunction. This ADMA/SDMA/hArg paradox may be solved by the assumption that not the free acids but their precursor proteins exert biological effects in the vasculature, with hArg antagonizing the effects of NG-methylated proteins.
Novel Biomarkers in the Diagnosis of Chronic Kidney Disease and the Prediction of Its Outcome
Int J Mol Sci 2017 Aug 4;18(8):1702.PMID:28777303DOI:10.3390/ijms18081702.
In its early stages, symptoms of chronic kidney disease (CKD) are usually not apparent. Significant reduction of the kidney function is the first obvious sign of disease. If diagnosed early (stages 1 to 3), the progression of CKD can be altered and complications reduced. In stages 4 and 5 extensive kidney damage is observed, which usually results in end-stage renal failure. Currently, the diagnosis of CKD is made usually on the levels of blood urea and serum creatinine (sCr), however, sCr has been shown to be lacking high predictive value. Due to the development of genomics, epigenetics, transcriptomics, proteomics, and metabolomics, the introduction of novel techniques will allow for the identification of novel biomarkers in renal diseases. This review presents some new possible biomarkers in the diagnosis of CKD and in the prediction of outcome, including asymmetric dimethylarginine (ADMA), Symmetric dimethylarginine (SDMA), uromodulin, kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), miRNA, ncRNA, and lincRNA biomarkers and proteomic and metabolomic biomarkers. Complicated pathomechanisms of CKD development and progression require not a single marker but their combination in order to mirror all types of alterations occurring in the course of this disease. It seems that in the not so distant future, conventional markers may be exchanged for new ones, however, confirmation of their efficacy, sensitivity and specificity as well as the reduction of analysis costs are required.