Database : MEDLINE
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PMID:28336439
Author:Morgan AM; Ibrahim MA; Noshy PA
Address:Toxicology and Forensic Medicine Department, Faculty of Veterinary Medicine, Cairo University, Egypt.
Title:Reproductive toxicity provoked by titanium dioxide nanoparticles and the ameliorative role of Tiron in adult male rats.
Source:Biochem Biophys Res Commun; 486(2):595-600, 2017 Apr 29.
ISSN:1090-2104
Country of publication:United States
Language:eng
Abstract:Titanium dioxide nanoparticles (TDN) are widely used in paints, plastics, ceramics, cosmetics, printing ink, rubber and paper. Tiron is a water soluble metal chelator and antioxidant. This study was designed to investigate the reproductive toxicity of TDN in male albino rats and the ameliorative role of Tiron to minimize such toxic effects. Eighty adult male albino rats were assigned into 4 equal groups, group 1: control; group 2: received TDN at 100 mg/kg/day orally for 8 weeks; group 3: received Tiron at 470 mg/kg/day intraperitoneally for 2 weeks (the last 2 weeks of the experimental period); group 4: received both TDN and Tiron by the same previously mentioned dose, route and duration. The results revealed that TDN provoked reproductive toxicity which was proved by the deteriorated spermogram picture, high incidence of micronucleated RBCs, elevated oxidative stress parameters and up regulation of Testin gene. Whereas, Tiron co-treatment ameliorated most of these toxic alterations. Our findings highlighted the protective role of tiron against TDN intoxication.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Antioxidants); 0 (Proteins); 0 (testin protein, rat); 15FIX9V2JP (titanium dioxide); 4X87R5T106 (1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt); D1JT611TNE (Titanium)


  2 / 270 MEDLINE  
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PMID:27828984
Author:Tang B; Wang K; Jia YP; Zhu P; Fang Y; Zhang ZJ; Mao XH; Li Q; Zeng DZ
Address:Department of Clinical Microbiology and Immunology, Southwest Hospital & College of Medical Laboratory Science, Third Military Medical University, Chongqing, China.
Title:Fusobacterium nucleatum-Induced Impairment of Autophagic Flux Enhances the Expression of Proinflammatory Cytokines via ROS in Caco-2 Cells.
Source:PLoS One; 11(11):e0165701, 2016.
ISSN:1932-6203
Country of publication:United States
Language:eng
Abstract:Fusobacterium nucleatum (F. nucleatum) plays a critical role in gastrointestinal inflammation. However, the exact mechanism by which F. nucleatum contributes to inflammation is unclear. In the present study, it was revealed that F. nucleatum could induce the production of proinflammatory cytokines (IL-8, IL-1ß and TNF-α) and reactive oxygen species (ROS) in Caco-2 colorectal) adenocarcinoma cells. Furthermore, ROS scavengers (NAC or Tiron) could decrease the production of proinflammatory cytokines during F. nucleatum infection. In addition, we observed that autophagy is impaired in Caco-2 cells after F. nucleatum infection. The production of proinflammatory cytokines and ROS induced by F. nucleatum was enhanced with either autophagy pharmacologic inhibitors (3-methyladenine, bafilomycin A1) or RNA interference in essential autophagy genes (ATG5 or ATG12) in Caco-2 cells. Taken together, these results indicate that F. nucleatum-induced impairment of autophagic flux enhances the expression of proinflammatory cytokines via ROS in Caco-2 Cells.
Publication type:JOURNAL ARTICLE
Name of substance:0 (ATG12 protein, human); 0 (ATG5 protein, human); 0 (Autophagy-Related Protein 12); 0 (Autophagy-Related Protein 5); 0 (Free Radical Scavengers); 0 (IL1B protein, human); 0 (Interleukin-1beta); 0 (Interleukin-8); 0 (Macrolides); 0 (RNA, Small Interfering); 0 (Reactive Oxygen Species); 0 (Tumor Necrosis Factor-alpha); 4X87R5T106 (1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt); 5142-23-4 (3-methyladenine); 88899-55-2 (bafilomycin A1); JAC85A2161 (Adenine); WYQ7N0BPYC (Acetylcysteine)


  3 / 270 MEDLINE  
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PMID:27486852
Author:Lu J; Guo JH; Tu XL; Zhang C; Zhao M; Zhang QW; Gao FH
Address:Institute of Oncology, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Title:Tiron Inhibits UVB-Induced AP-1 Binding Sites Transcriptional Activation on MMP-1 and MMP-3 Promoters by MAPK Signaling Pathway in Human Dermal Fibroblasts.
Source:PLoS One; 11(8):e0159998, 2016.
ISSN:1932-6203
Country of publication:United States
Language:eng
Abstract:Recent research found that Tiron was an effective antioxidant that could act as the intracellular reactive oxygen species (ROS) scavenger or alleviate the acute toxic metal overload in vivo. In this study, we investigated the inhibitory effect of Tiron on matrix metalloproteinase (MMP)-1 and MMP-3 expression in human dermal fibroblast cells. Western blot and ELISA analysis revealed that Tiron inhibited ultraviolet B (UVB)-induced protein expression of MMP-1 and MMP-3. Real-time quantitative PCR confirmed that Tiron could inhibit UVB-induced mRNA expression of MMP-1 and MMP-3. Furthermore, Tiron significantly blocked UVB-induced activation of the MAPK signaling pathway and activator protein (AP)-1 in the downstream of this transduction pathway in fibroblasts. Through the AP-1 binding site mutation, it was found that Tiron could inhibit AP-1-induced upregulation of MMP-1 and MMP-3 expression through blocking AP-1 binding to the AP-1 binding sites in the MMP-1 and MMP-3 promoter region. In conclusion, Tiron may be a novel antioxidant for preventing and treating skin photoaging UV-induced.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Antioxidants); 0 (Transcription Factor AP-1); 4X87R5T106 (1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt); EC 3.4.24.17 (MMP3 protein, human); EC 3.4.24.17 (Matrix Metalloproteinase 3); EC 3.4.24.7 (MMP1 protein, human); EC 3.4.24.7 (Matrix Metalloproteinase 1)


  4 / 270 MEDLINE  
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PMID:27485290
Author:El-Sherbeeny NA; Hassan ZA; Ateyya H
Address:Department of Clinical Pharmacology, Faculty of Medicine, Suez canal University, Egypt. Electronic address: n_elsherbeeny@hotmail.com.
Title:Tiron ameliorates oxidative stress and inflammation in a murine model of airway remodeling.
Source:Int Immunopharmacol; 39:172-180, 2016 Oct.
ISSN:1878-1705
Country of publication:Netherlands
Language:eng
Abstract:Airway remodeling includes lung structural changes that have a role in the irreversibility of pulmonary dysfunction shown in chronic bronchial asthmatics. The current experiment investigated the effect of the mitochondrial antioxidant, tiron in comparison with dexamethasone (DEXA) on airway remodeling in chronic asthma. Sensitized BALB/c mice were challenged with ovalbumin (OVA) aerosol for 8weeks, OVA sensitized-challenged mice were treated with either DEXA or tiron, respectively. After that, lung tissue and bronchoaveolar lavage fluid (BALF) were used for measurement of different biological markers. Lungs were examined for histopathological changes and immunohistochemistry. Upon comparing with vehicle treated animals, trion or DEXA treatment significantly reduced eosinophils, lymphocytes, neutrophils and macrophages count in the BALF. Both drugs significantly alleviated chronic OVA-induced oxidative stress as illustrated by decreased pulmonary malondialdenhyde (MDA) and increased glutathione (GSH) and superoxide dismutase (SOD) levels. Asthmatic mice exhibited elevated levels of NOx, IL-13 and TGF-ß1 that were reduced by DEXA and tiron. Histopathological changes and increased immunoreactivity of nuclear factor-Kappa B (NF-κ B) in OVA-challenged mice were minimized by tiron and DEXA treatment. In conclusion, in this model of chronic asthma DEXA and tiron ameliorated airway remodeling and inflammation in experimental chronic asthma with no difference between the effect of tiron and DEXA. Tiron has a potential role as adjuvant treatment in chronic asthma.
Publication type:COMPARATIVE STUDY; JOURNAL ARTICLE
Name of substance:0 (NF-kappa B); 0 (Transforming Growth Factor beta); 4X87R5T106 (1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt); 7S5I7G3JQL (Dexamethasone); EC 1.15.1.1 (Superoxide Dismutase)


  5 / 270 MEDLINE  
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PMID:27389323
Author:Yasuda Y; Feng GG; Li J; Nakamura E; Hayashi H; Sato M; Fujiwara Y; Kinoshita H
Address:Department of Anesthesiology, Aichi Medical University School of Medicine, 1-1 Yazako Karimata, Nagakute, Aichi, 480-1195, Japan.
Title:High oxygen modifies vasodilator effect of cysteine via enhanced oxidative stress and thromboxane production in the rat mesenteric artery.
Source:Pflugers Arch; 468(9):1555-64, 2016 Sep.
ISSN:1432-2013
Country of publication:Germany
Language:eng
Abstract:Whether high oxygen is harmful to the vascular function is unclear. The present study examined if high oxygen modifies vasodilator effect of cysteine via enhanced oxidative stress and thromboxane production. Rat mesenteric arteries with endothelium at 95 or 50 % oxygen were subjected to isometric force recordings, measurement of thromboxane B2 levels, determination of superoxide and peroxynitrite levels and evaluation of NADPH oxidase subunit protein expression, respectively. L-cysteine (0.01-3 mM) constricted or dilated arteries at 95 and 50 % oxygen, respectively. Thromboxane receptor antagonist SQ-29,548 (1 µM) abolished the constriction at 95 % oxygen. L-cysteine (3 mM) increased levels of thromboxane B2 in arteries upon 95 % oxygen application. L-cysteine relaxed arteries treated with superoxide inhibitor tiron (2 mM) or NADPH oxidase inhibitor gp91ds-tat (1 µM) irrespective of the oxygen concentration while ATP-sensitive K(+) channel inhibitor glibenclamide (1 µM) and cystathionine-γ-lyase (CSE) inhibitor DL-propargylglycine (10 mM) similarly abolished the relaxation. L-cysteine (3 mM) with 95 % oxygen augmented levels of superoxide as well as nitrotyrosine within the artery, concomitantly with enhanced membrane protein expression of NADPH oxidase subunit p47phox. The higher concentration of oxygen attenuates L-cysteine-induced vasodilation via superoxide production mediated by NADPH oxidase along with thromboxane A2 production, resulting in vasoconstriction. The increased levels of superoxide, as well as peroxynitrite, coexist with the impaired vasodilation related to ATP-sensitive K(+) channels and CSE. Higher oxygen with plasma cysteine may cause oxidative stress and vasoconstrictor prostanoid production in blood vessels.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Alkynes); 0 (Glycoproteins); 0 (Thromboxanes); 0 (gp91ds-tat protein, chimeric); 11062-77-4 (Superoxides); 14691-52-2 (Peroxynitrous Acid); 4X87R5T106 (1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt); 64165-64-6 (propargylglycine); EC 1.6.3.- (NADPH Oxidases); K848JZ4886 (Cysteine); S88TT14065 (Oxygen); SX6K58TVWC (Glyburide); TE7660XO1C (Glycine)


  6 / 270 MEDLINE  
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PMID:27243905
Author:Habener A; Chowdhury A; Echtermeyer F; Lichtinghagen R; Theilmeier G; Herzog C
Address:Department of Anesthesiology and Intensive Care Medicine, Hannover Medical School, Hannover, Germany.
Title:MitoNEET Protects HL-1 Cardiomyocytes from Oxidative Stress Mediated Apoptosis in an In Vitro Model of Hypoxia and Reoxygenation.
Source:PLoS One; 11(5):e0156054, 2016.
ISSN:1932-6203
Country of publication:United States
Language:eng
Abstract:The iron-sulfur cluster containing protein mitoNEET is known to modulate the oxidative capacity of cardiac mitochondria but its function during myocardial reperfusion injury after transient ischemia is unknown. The purpose of this study was to analyze the impact of mitoNEET on oxidative stress induced cell death and its relation to the glutathione-redox system in cardiomyocytes in an in vitro model of hypoxia and reoxygenation (H/R). Our results show that siRNA knockdown (KD) of mitoNEET caused an 1.9-fold increase in H/R induced apoptosis compared to H/R control while overexpression of mitoNEET caused a 53% decrease in apoptosis. Necrosis was not affected. Apoptosis of both, mitoNEET-KD and control cells was diminished to comparable levels by using the antioxidants Tiron and glutathione compound glutathione reduced ethyl ester (GSH-MEE), indicating that mitoNEET-dependent apoptosis is mediated by oxidative stress. The interplay between mitoNEET and glutathione redox system was assessed by treating cardiomyocytes with 2-acetylamino-3-[4-(2-acetylamino-2-carboxyethylsulfanylthio-carbonylamino) phenylthiocarbamoylsulfanyl] propionic acid (2-AAPA), known to effectively inhibit glutathione reductase (GSR) and to decrease the GSH/GSSG ratio. Surprisingly, inhibition of GSR-activity to 20% by 2-AAPA decreased apoptosis of control and mitoNEET-KD cells to 23% and 25% respectively, while at the same time mitoNEET-protein was increased 4-fold. This effect on mitoNEET-protein was not accessible by mitoNEET-KD but was reversed by GSH-MEE. In conclusion we show that mitoNEET protects cardiomyocytes from oxidative stress-induced apoptosis during H/R. Inhibition of GSH-recycling, GSR-activity by 2-AAPA increased mitoNEET-protein, accompanied by reduced apoptosis. Addition of GSH reversed these effects suggesting that mitoNEET can in part compensate for imbalances in the antioxidative glutathione-system and therefore could serve as a potential therapeutic approach for the oxidatively stressed myocardium.
Publication type:JOURNAL ARTICLE
Name of substance:0 (2-acetylamino-3-(4-(2-acetylamino-2-carboxyethylsulfanylthiocarbonylamino)phenylthiocarbamoylsulfanyl)propionic acid); 0 (Antioxidants); 0 (Iron-Binding Proteins); 0 (Membrane Proteins); 0 (RNA, Small Interfering); 0 (Reactive Oxygen Species); 0 (Thiocarbamates); 0 (mitoNEET protein, mouse); 4X87R5T106 (1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt); 7W95D60F4J (S-ethyl glutathione); EC 1.8.1.7 (Glutathione Reductase); GAN16C9B8O (Glutathione); WYQ7N0BPYC (Acetylcysteine)


  7 / 270 MEDLINE  
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PMID:27118662
Author:Ateyya H; Wagih HM; El-Sherbeeny NA
Address:College of Pharmacy, Taibah University, El-Madinah, El-Munawarah, Saudi Arabia. hayamatya@hotmail.com.
Title:Effect of tiron on remote organ injury in rats with severe acute pancreatitis induced by L-arginine.
Source:Naunyn Schmiedebergs Arch Pharmacol; 389(8):873-85, 2016 Aug.
ISSN:1432-1912
Country of publication:Germany
Language:eng
Abstract:Acute pancreatitis (AP) is an acute inflammatory disorder of the pancreas that can be complicated by involvement of other remote organs. Oxidative stress is known to have a crucial role in the development of pancreatic acinar damage and one of the main causes in multisystem organ failure in experimental AP. The aim of the study was to determine the effect of tiron on pancreas and remote organ damage in L-arginine (L-Arg) induced AP rat model. Thirty-two male rats were divided in random into four groups: control, tiron, L-Arg, and tiron with L-Arg. At the end of the experiment, blood samples were withdrawn for biochemical analysis. The pancreas, lung, kidney, and liver were collected for histopathological examination. Estimation of pancreatic water content was done. Analysis of pulmonary, hepatic, renal, and pancreatic lipid peroxide levels (MDA), superoxide dismutase (SOD), and reduced glutathione (GSH) were carried out. Finally, nuclear factor kappa B (NF-κB) and transforming growth factor ß1 (TGF-ß1) expression in pancreatic tissue was determined. Results indicated that treatment with tiron significantly decreased lipid peroxide levels and markedly increased both SOD activity and GSH level. Moreover, histopathological analysis further confirmed that administration of tiron relatively ameliorates pancreatic acinar cells and remote organ damage. Increased immunoreactivity of NF-κB and TGF-ß1 were reduced also by tiron treatment. These findings pointed out the protective role of the mitochondrial antioxidant, tiron against AP induced by L-Arg.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Antioxidants); 0 (Biomarkers); 0 (NF-kappa B); 0 (Tgfb1 protein, rat); 0 (Transforming Growth Factor beta1); 31C4KY9ESH (Nitric Oxide); 4X87R5T106 (1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt); 4Y8F71G49Q (Malondialdehyde); 94ZLA3W45F (Arginine); EC 1.15.1.1 (Superoxide Dismutase); GAN16C9B8O (Glutathione)


  8 / 270 MEDLINE  
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PMID:26636617
Author:Chen Y; Dong H; Zhang H
Address:Department of Civil and Environmental Engineering, Temple University , Philadelphia, Pennsylvania 19122, United States.
Title:Experimental and Computational Evidence for the Reduction Mechanisms of Aromatic N-oxides by Aqueous Fe(II)-Tiron Complex.
Source:Environ Sci Technol; 50(1):249-58, 2016 Jan 05.
ISSN:1520-5851
Country of publication:United States
Language:eng
Abstract:A combined experimental-theoretical approach was taken to elucidate the reduction mechanisms of five representative aromatic N-oxides (ANOs) by Fe(II)-tiron complex and to identify the rate-limiting step. Based on the possible types of complexes formed with the reductant, three groups of ANOs were studied: type I refers to those forming 5-membered ring complexes through the N and O atoms on the side chain; type II refers to those forming 6-membered ring complexes through the N-oxide O atom and the O atom on the side chain; and type III refers to complexation through the N-oxide O atom only. Density functional theory calculations suggested that the elementary reactions, including protonation, N-O bond cleavage, and the second electron transfer processes, are barrierless, indicating that the first electron transfer is rate-limiting. Consistent with the theoretical results, the experimental solvent isotope effect, KIEH, for the reduction of quinoline N-oxide (a type III ANO) was obtained to be 1.072 ± 0.025, suggesting protonation was not involved in the rate-limiting step. The measured nitrogen kinetic isotope effect, KIEN, for the reduction of pyridine N-oxide (a type III ANO) (1.022 ± 0.006) is in good agreement with the calculated KIEN for its first electron transfer (1.011-1.028), confirming that the first electron transfer is rate-limiting. Electrochemical cell experiments demonstrated that the electron transfer process can be facilitated significantly by type I complexation with FeL2(6-) (1:2 Fe(II)-tiron complex), to some extent by type II complexation with free Fe(II), but not by weak type III complexation.
Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
Name of substance:0 (Ferrous Compounds); 0 (Oxides); 0 (Pyridines); 4X87R5T106 (1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt); 91F12JJJ4H (pyridine N-oxide)


  9 / 270 MEDLINE  
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PMID:26371849
Author:Vorobjeva NV; Pinegin BV
Address:Biology Faculty, Lomonosov Moscow State University, Lenin Hills 1/12, 119991 Moscow, Russia. Electronic address: nvvorobjeva@mail.ru.
Title:Effects of the antioxidants Trolox, Tiron and Tempol on neutrophil extracellular trap formation.
Source:Immunobiology; 221(2):208-19, 2016 Feb.
ISSN:1878-3279
Country of publication:Netherlands
Language:eng
Abstract:Neutrophils can entrap and kill pathogens by releasing of neutrophil extracellular traps (NETs), in addition to their routine functions such as phagocytosis and degranulation. NETs consist of a DNA backbone supplemented by multiple bactericidal proteins from the nucleus, the cytoplasm and the granules. Neutrophils release NETs after their activation by a number of physiological and pharmacological stimuli. In addition to the antimicrobial function, NETs are involved in the pathogenesis of various autoimmune and inflammatory diseases. Since NET formation predominantly depends on the generation of reactive oxygen species (ROS), all substances that are capable of scavenging ROS or inhibiting the enzymes responsible for their synthesis should prevent ROS-associated NET release. The aim of this study was to test substances with an antioxidant activity, such as Trolox, Tiron, and Tempol, for their capacity to inhibit NET formation by primary human neutrophils in vitro. We revealed for the first time an inhibitory effect of Trolox on ROS-dependent NET release. We also established a suppressive effect of Tempol on NET formation that manifested itself in a wide range of concentrations. In this study, no inhibitory influence of Tiron on NET release was revealed. All tested substances exerted a significant dose-dependent antioxidative effect on ROS generation induced by phorbol 12-myristate 13-acetate (PMA). We suggest that the antioxidants Trolox and Tempol should be recommended for treating autoimmune and inflammatory diseases that implicate ROS-dependent NET release.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Antioxidants); 0 (Chromans); 0 (Cyclic N-Oxides); 0 (Reactive Oxygen Species); 0 (Spin Labels); 4X87R5T106 (1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt); NI40JAQ945 (Tetradecanoylphorbol Acetate); S18UL9710X (6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid); U78ZX2F65X (tempol)


  10 / 270 MEDLINE  
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PMID:26554245
Author:Wang X; Li J; Li L; Li X
Title:Photodynamic Therapy-Induced Apoptosis of Keloid Fibroblasts is Mediated by Radical Oxygen Species In Vitro.
Source:Clin Lab; 61(9):1257-66, 2015.
ISSN:1433-6510
Country of publication:Germany
Language:eng
Abstract:BACKGROUND: It has been demonstrated that photodynamic therapy (PDT) is a promising treatment approach for hyperplastic dermatosis and results in a beneficial outcome. In the present study, PDT involving hematoporphyrin monomethyl ether (HMME) was applied to keloid fibroblasts (KFB), and the effects and the mechanism of action were explored. METHODS: Keloid fibroblastic cells were divided into four groups (PDT group, light alone group, HMME alone group, normal cultured group). Cell proliferation and apoptosis were observed. Radical oxygen species (ROS) were detected by means of dihydroethidium (DHE) and dihydrorhodamine (DHR123). ROS in the PDT group were also assessed after addition of tiron. RESULTS: Cell proliferation was inhibited in the PDT group (p < 0.05), while the rate of apoptosis was also clearly increased (p < 0.05). The levels of ROS were significantly higher in the PDT group than was observed in the other three groups (p < 0.05). With the addition of tiron the damaging effects were reduced. CONCLUSIONS: Our data indicated that HMME-mediated PDT could inhibit keloid fibroblast proliferation and could also induce apoptosis. This process was associated with the production of ROS.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Hematoporphyrins); 0 (Reactive Oxygen Species); 0 (hematoporphyrin monomethyl ether); 11062-77-4 (Superoxides); 4X87R5T106 (1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt)



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