Peroxynitrite
(Synonyms: 四(1-甲基-4-吡啶基)卟啉锰; Sodium Peroxynitrite) 目录号 : GC44602体内NO与超氧化物反应生成过氧亚硝酸盐。
Cas No.:14042-01-4
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >90.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Peroxynitrite is formed in vivo by the reaction of NO with superoxide.[1],[2],[3] It is a powerful oxidizing agent that can initiate lipid peroxidation, oxidize sulfhydryls, and nitrate the aromatic residues of proteins.
For long term storage, we suggest that peroxynitrite be stored as supplied at -80°C. It will be stable for at least three months.
Peroxynitrite is supplied as a solution in 0.3 M NaOH. Peroxynitrite is highly unstable and slowly decomposes even at -80°C but not to any significant extent within one month. The half-life of peroxynitrite in alkaline solutions at room temperature is about 5 hours. Peroxynitrite decomposes instantaneously under acidic conditions and the half-life at pH 7.4 is only few seconds [3]. Further dilutions of the stock solution can be performed using cold 0.3 M NaOH. We recommend that the actual concentration of peroxynitrite be measured following the procedure given below before using it in any experiments:
Thaw the peroxynitrite solution carefully and keep it on ice. Dilute an aliquot of the stock solution 40-fold with cold 0.3 M NaOH (e.g. add 25 μl of the stock to 975 μl of 0.3 M NaOH) and measure the absorbance at 302 nm with 0.3 M NaOH as blank. Concentration of the stock solution can be calculated using the extinction coefficient for peroxynitrite(1670 M-1cm-1).
体内NO与超氧化物反应生成过氧亚硝酸盐。[1] ，[2]，[3]它是一种强大的氧化剂，可以引发脂质过氧化，氧化巯基，并硝酸蛋白质的芳香残基。
对于长期储存，我们建议过氧亚硝酸盐应在-80°C下储存。它将稳定至少三个月。
过氧亚硝酸盐以0.3 M NaOH溶液的形式提供。过氧亚硝酸盐高度不稳定，即使在-80°C下也会缓慢分解，但在一个月内不会分解到任何显著程度。过氧亚硝酸盐在碱性溶液中室温下的半衰期约为5小时。过亚硝酸根在酸性条件下瞬间分解，在pH 7.4下的半衰期只有几秒钟[3]。储备溶液的进一步稀释可以使用冷的0.3M NaOH进行。我们建议在任何实验中使用过氧亚硝酸盐之前，按照以下程序测量过氧亚硝酸酯的实际浓度：
小心地解冻过氧亚硝酸盐溶液，并将其放在冰上。用冷的0.3 M NaOH将储备溶液的等分试样稀释40倍（例如，将25μl储备溶液添加到975μl 0.3 M NaOH中），并用0.3 M NaOH作为空白在302 nm处测量吸光度。可以使用过氧亚硝酸盐的消光系数（1670 M-1cm-1）来计算储备溶液的浓度。
Reference:
[1]. Pryor, W.A., and Squadrito, G.L. The chemistry of peroxynitrite: A product from the reaction of nitric oxide with superoxide. American Journal of Physiology 268, L699-L722 (1995).
[2]. Beckman, J.S., and Koppenol, W.H. Nitric oxide, superoxide, and peroxynitrite: The good, the bad, and the ugly. Am. J. Physiol. 271(5 Pt 1), C1424-C1437 (1996).
[3]. Koppenol, W.H., Moreno, J.J., Pryor, W.A., et al. Peroxynitrite, a cloaked oxidant formed by nitric oxide and superoxide. Chemical Research in Toxicology 5, 834-842 (1992).
| Cas No. | 14042-01-4 | SDF | |
| 别名 | 四(1-甲基-4-吡啶基)卟啉锰; Sodium Peroxynitrite | ||
| 化学名 | peroxynitrous acid, sodium salt | ||
| Canonical SMILES | O=NO[O-].[Na+] | ||
| 分子式 | ONO2 • Na | 分子量 | 85 |
| 溶解度 | A solution in 0.3 M sodium hydroxide | 储存条件 | Storage -80°C, protect from light |
| 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 | 11.7647 mL | 58.8235 mL | 117.6471 mL |
| 5 mM | 2.3529 mL | 11.7647 mL | 23.5294 mL |
| 10 mM | 1.1765 mL | 5.8824 mL | 11.7647 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。
Oxygen radicals, nitric oxide, and Peroxynitrite: Redox pathways in molecular medicine
Proc Natl Acad Sci U S A 2018 Jun 5;115(23):5839-5848.PMID:29802228DOI:10.1073/pnas.1804932115.
Oxygen-derived free radicals and related oxidants are ubiquitous and short-lived intermediates formed in aerobic organisms throughout life. These reactive species participate in redox reactions leading to oxidative modifications in biomolecules, among which proteins and lipids are preferential targets. Despite a broad array of enzymatic and nonenzymatic antioxidant systems in mammalian cells and microbes, excess oxidant formation causes accumulation of new products that may compromise cell function and structure leading to cell degeneration and death. Oxidative events are associated with pathological conditions and the process of normal aging. Notably, physiological levels of oxidants also modulate cellular functions via homeostatic redox-sensitive cell signaling cascades. On the other hand, nitric oxide (•NO), a free radical and weak oxidant, represents a master physiological regulator via reversible interactions with heme proteins. The bioavailability and actions of •NO are modulated by its fast reaction with superoxide radical ([Formula: see text]), which yields an unusual and reactive peroxide, Peroxynitrite, representing the merging of the oxygen radicals and •NO pathways. In this Inaugural Article, I summarize early and remarkable developments in free radical biochemistry and the later evolution of the field toward molecular medicine; this transition includes our contributions disclosing the relationship of •NO with redox intermediates and metabolism. The biochemical characterization, identification, and quantitation of Peroxynitrite and its role in disease processes have concentrated much of our attention. Being a mediator of protein oxidation and nitration, lipid peroxidation, mitochondrial dysfunction, and cell death, Peroxynitrite represents both a pathophysiologically relevant endogenous cytotoxin and a cytotoxic effector against invading pathogens.
Peroxynitrite: cellular pathology and implications in autoimmunity
J Immunoassay Immunochem 2019;40(2):123-138.PMID:30843753DOI:10.1080/15321819.2019.1583109.
In inflamed tissues, the reaction of nitric oxide and superoxide leads to the formation of an extremely reactive Peroxynitrite (ONOO-), which is a well known oxidizing and nitrating agent that exhibits high reactivity at physiological pH. The Peroxynitrite formed can attack a wide range of biomolecules via direct oxidative reactions or indirect radical-mediated mechanisms thus triggering cellular responses leading to cell signaling, oxidative injury, committing cells to necrosis or apoptosis. Cellular DNA is an important target for ONOO- attack, and can react with deoxyribose, nucleobases or induces single strand breaks. The free radical-mediated damage to proteins results in the modification of amino acid residues, cross-linking of side chains and fragmentation. Free/protein-bound tyrosines are attacked by various reactive nitrogen species (RNS), including Peroxynitrite, to form free/protein-bound nitrotyrosine (NT). The formation of NT represents a specific peroxynitrite-mediated protein modification, and the detection of NT in proteins is considered as a biomarker for endogenous Peroxynitrite activity. The peroxynitrite-driven oxidation and nitration of biomolecules may lead to autoimmunity and age-related neurodegenerative diseases. Hence, Peroxynitrite modified DNA and nitrated proteins can act as neoantigens and lead to the generation of autoantibodies against self-components in autoimmune disorders.
Peroxynitrite-An ugly biofactor?
Biofactors 2010 Jul-Aug;36(4):264-73.PMID:20645283DOI:10.1002/biof.103.
Cellular damage occurring under oxidative conditions has been ascribed mainly to the formation of Peroxynitrite (ONOOH/ONOO(-)) that originates from the reaction of NO(*) with O(2) (*-). The detrimental effects of Peroxynitrite are exacerbated by the reaction with CO(2) that leads to ONOOC(O)O(-), which further decays to the strong oxidant radicals NO(2) (*) and CO(3) (*-). The reaction with CO(2), however, may redirect Peroxynitrite specificity. An excessive formation of Peroxynitrite represents an important mechanism contributing to the DNA damage, the inactivation of metabolic enzymes, ionic pumps, and structural proteins, and the disruption of cell membranes. Because of its ability to oxidize biomolecules, Peroxynitrite is implicated in an increasing list of diseases, including neurodegenerative and cardiovascular disorders, inflammation, pain, autoimmunity, cancer, and aging. However, Peroxynitrite displays also protective activities: (i) at high concentrations, it shows anti-viral, anti-microbial, and anti-parasitic actions; and (ii) at low concentrations, it stimulates protective mechanisms in the cardiovascular, nervous, and respiratory systems. The detrimental effects of Peroxynitrite and related reactive species are impaired by (pseudo-) enzymatic systems, mainly represented by heme-proteins (e.g., hemoglobin and myoglobin). Here, we report biochemical aspects of Peroxynitrite actions being at the root of its biomedical effects.
Peroxynitrite: From interception to signaling
Arch Biochem Biophys 2016 Apr 1;595:153-60.PMID:27095233DOI:10.1016/j.abb.2015.06.022.
Peroxynitrite is a strong oxidant and nitrating species that mediates certain biological effects of superoxide and nitrogen monoxide. These biological effects include oxidative damage to proteins as well as the formation of 3-nitrotyrosyl moieties in proteins. As a consequence, such proteins may lose their activity, gain altered function, or become prone to proteolytic degradation - resulting in modulation of cellular protein turnover and in the modulation of signaling cascades. In analogy to hydrogen peroxide, Peroxynitrite may be scavenged by selenoproteins like glutathione peroxidase-1 (GPx-1) or by selenocompounds with a GPx-like activity, such as ebselen; in further analogy to H2O2, peroxiredoxins have also been established as contributors to Peroxynitrite reduction. This review covers three aspects of Peroxynitrite biochemistry, (i) the interaction of selenocompounds/-proteins with Peroxynitrite, (ii) peroxynitrite-induced modulation of cellular proteolysis, and (iii) peroxynitrite-induced modulation of cellular signaling.
Peroxynitrite and drug-dependent toxicity
Toxicology 2005 Mar 15;208(2):273-88.PMID:15691591DOI:10.1016/j.tox.2004.11.023.
Peroxynitrite is the product of the diffusion-controlled termination reaction between two radicals, nitric oxide and superoxide and is a strong oxidant and nitrating intermediate. Critical biomolecules like proteins, lipids and DNA react with Peroxynitrite via direct or radical-mediated mechanisms, resulting in alterations in enzyme activities and signaling pathways. The biological consequences of peroxynitrite-mediated oxidative modifications depend on the levels of oxidant achieved in vivo and its cellular site of production. High and prolonged fluxes of Peroxynitrite that overcome the endogenous antioxidant mechanisms, end up in disruption of cell homeostasis leading to apoptotic or necrotic cell death. Several drugs used in modern medicine and agriculture can exert their toxic side effects through mechanisms involving the formation of toxic levels of Peroxynitrite, via redox cycling, uncoupling of nitric oxide synthase, stimulation of the endogenous formation of nitric oxide and superoxide or lowering of the antioxidant defenses. Experimental evidence point to Peroxynitrite participation in the toxicity of doxorubicin, paraquat, acetaminophen and MPTP (N-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine). The pharmacology against peroxynitrite-mediated toxicity could be oriented towards decreasing the levels of the precursor radicals (i.e. using NOS or oxidases inhibitors, SOD mimetics) or reducing the levels of Peroxynitrite itself (Peroxynitrite scavengers or decomposition catalysts) and serve to attenuate or neutralize drug-dependent toxicity linked to enhanced Peroxynitrite formation.