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L-Glutathione, oxidized (sodium salt) Sale

(Synonyms: L-氧化型谷胱苷肽钠,L-Glutathione oxidized disodium; GSSG disodium; Oxiglutatione disodium) 目录号 : GC44060

An oxidized form of GSH

L-Glutathione, oxidized (sodium salt) Chemical Structure

Cas No.:103239-24-3

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Sample solution is provided at 25 µL, 10mM.

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产品描述

Glutathione can occur in reduced (GSH), oxidized (GSSG), or in mixed disulfide forms and is ubiquitous in multiple biological systems serving as the major thiol-disulfide redox buffer of the cell. GSSG is the oxidized form of GSH . It can be reduced back to GSH through the NADPH-dependent enzyme glutathione reductase. GSSG functions as a hydrogen acceptor in the enzymatic determination of NADP+ and NADPH and can be a proximal donor in S-glutathionylation post translational modifications. The ratio of reduced glutathione to oxidized glutathione within cells is often used as an indicator of oxidative stress, with higher concentrations of GSSG predicting increased oxidative stress.

Chemical Properties

Cas No. 103239-24-3 SDF
别名 L-氧化型谷胱苷肽钠,L-Glutathione oxidized disodium; GSSG disodium; Oxiglutatione disodium
Canonical SMILES O=C([C@@H](NC(CC[C@@H](C([O-])=O)N)=O)CSSC[C@H](NC(CC[C@@H](C([O-])=O)N)=O)C(NCC(O)=O)=O)NCC(O)=O.[Na+].[Na+]
分子式 C20H30N6O12S2•2Na 分子量 656.6
溶解度 PBS (pH 7.2): 10 mg/ml 储存条件 Store at -20°C
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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。
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1 mg 5 mg 10 mg
1 mM 1.523 mL 7.615 mL 15.23 mL
5 mM 0.3046 mL 1.523 mL 3.046 mL
10 mM 0.1523 mL 0.7615 mL 1.523 mL
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Research Update

Glutathione sodium salt as a novel adjunctive treatment for acute myocardial infarction

Med Hypotheses 2017 May;102:48-50.PMID:28478830DOI:10.1016/j.mehy.2017.03.010.

Timely recanalization of infarct related artery along with effective myocardial cell reperfusion represents a major challenge in the management of STEMI. The reperfusion of coronary arteries can induce further cardiomyocyte death by generating oxidative stress, which itself can mediate myocardial damage through a number of different mechanisms. Based on experimental and clinical studies, interventions to treat reperfusion injury by antioxidants were considered to be an appropriate therapeutic option. We emphasize the hypothesis that glutathione sodium salt, a physiologic antioxidant, may be of value when administered to STEMI patients both at an early stage of myocardial reperfusion by primary angioplasty and for up to three days after the procedure, in addition to standard treatment.

Protective Biomolecular Mechanisms of Glutathione sodium salt in Ischemia-Reperfusion Injury in Patients with Acute Coronary Syndrome-ST-Elevation Myocardial Infarction

Cells 2022 Dec 8;11(24):3964.PMID:36552727DOI:10.3390/cells11243964.

Ischemia-Reperfusion Injury (IRI) is responsible for adverse outcomes in patients with ST-Elevation Myocardial Infarction (STEMI). Oxidative stress, resulting from the production of Reactive Oxygen Species (ROS) and low availability of Glutathione (GSH), are the two main mediators of IRI. The effectiveness of exogenous antioxidant therapy in this scenario is still debated, since the encouraging results obtained in animal models have not been fully reproduced in clinical studies. In this review we focus on the role of GSH, specifically on the biomolecular mechanisms that preserve myocardial cells from damage due to reperfusion. In this regard, we provide an extensive discussion about GSH intrinsic antioxidant properties, its current applications in clinical practice, and the future perspectives.

Nitroalkane oxidation by streptomycetes

J Bacteriol 1979 Feb;137(2):916-24.PMID:33965DOI:10.1128/jb.137.2.916-924.1979.

Crude cell-free extracts of nine strains of Streptomyces tested for nitroalkane-oxidizing activity showed production of nitrous acid from 2-nitropropane, 1-nitropropane, nitroethane, nitromethane, and 3-nitropropionic acid. These substrates were utilized in most strains but to a decreasing extent in the order given, and different strains varied in their relative efficiency of oxidation. p-Nitrobenzoic acid, p-aminobenzoic acid, enteromycin, and omega-nitro-l-arginine were not attacked. d-Amino acid oxidase, glucose oxidase, glutathione S-transferase, and xanthine oxidase, enzymes potentially responsible for the observed oxidations in crude cellfree extracts, were present at concentrations too low to play any significant role. A nitroalkane-oxidizing enzyme from streptozotocin-producing Streptomyces achromogenes subsp. streptozoticus was partially purified and characterized. It catalyzes the oxidative denitrification of 2-nitropropane as follows: 2CH(3)CH(NO(2))CH(3) + O(2) --> 2CH(3)COCH(3) + 2HNO(2). At the optimum pH of 7.5 of the enzyme, 2-nitropropane was as good a substrate as its sodium salt; t-nitrobutane was not a substrate. Whereas Tiron, oxine, and nitroxyl radical acted as potent inhibitors of this enzyme, superoxide dismutase was essentially without effect. Sodium peroxide abolished a lag phase in the progress curve of the enzyme and afforded stimulation, whereas sodium superoxide did not affect the reaction. Reducing agents, such as glutathione, reduced nicotinamide adenine dinucleotide, and nicotinamide adenine dinucleotide phosphate, reduced form, as well as thiol compounds, were strongly inhibitory, but cyanide had no effect. The S. achromogenes enzyme at the present stage of purification is similar in many respects to the enzyme 2-nitropropane dioxygenase from Hansenula mrakii. The possible involvement of the nitroalkane-oxidizing enzyme in the biosynthesis of antibiotics that contain a nitrogen-nitrogen bond is discussed.

Influence of water-soluble flavonoids, quercetin-5'-sulfonic acid sodium salt and morin-5'-sulfonic acid sodium salt, on antioxidant parameters in the subacute cadmium intoxication mouse model

Exp Toxicol Pathol 2010 Mar;62(2):105-8.PMID:19297139DOI:10.1016/j.etp.2009.02.118.

Water-soluble quercetin-5'-sulfonic acid sodium salt (NaQSA) and morin-5'-sulfonic acid sodium salt (NaMSA) could exert an antagonistic effect on cadmium intoxication. The aim of the study was to examine the influence of these substances on superoxide dismutase (SOD) and glutathione (GSH) levels in the mouse liver in the subacute cadmium intoxication model. NaQSA and NaMSA significantly counteracted cadmium-induced decreases in SOD and GSH levels. No significant differences in SOD and GSH levels between groups exposed to cadmium receiving NaQSA or/and NaMSA were observed.