ArticleThe Journal of pharmacology and experimental therapeutics2013
A novel nontoxic inhibitor of the activation of NADPH oxidase reduces reactive oxygen species production in mouse lung.
Article in The Journal of pharmacology and experimental therapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 51 citations in OpenAlex.
- Circadian Control of Pulmonary Endothelial Signaling Occurs via the NADPH Oxidase 2-NLRP3 Pathway.Journal of biological rhythms · 2025Article
- Vitexin's Role in Colon Cancer Apoptosis: AMPK/mTOR Pathway Modulation Explored Through Experimental and Computational Approaches.Recent patents on anti-cancer drug discovery · 2025Article
- Decreased LPS-induced lung injury in pigs treated with a lung surfactant protein A-derived nonapeptide that inhibits peroxiredoxin 6 activity and subsequent NOX1,2 activation.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Role of Oxygen and Its Radicals in Peripheral Nerve Regeneration: From Hypoxia to Physoxia to Hyperoxia.International journal of molecular sciences · 2024Review
- Structure Activity Relationship and Molecular Docking of Some Quinazolines Bearing Sulfamerazine Moiety as New 3CLpro, cPLA2, sPLA2 Inhibitors.Molecules (Basel, Switzerland) · 2023Article
- Anti-Oxidant and Pro-Oxidant Effects of Peroxiredoxin 6: A Potential Target in Respiratory Diseases.Cells · 2023Review
- Inhibition of Peroxiredoxin 6 PLA2 Activity Decreases Oxidative Stress and the Severity of Acute Lung Injury in the Mouse Cecal Ligation and Puncture Model.Antioxidants (Basel, Switzerland) · 2021Article
- A Peptide Inhibitor of Peroxiredoxin 6 Phospholipase AAntioxidants (Basel, Switzerland) · 2021Article
- Regulation of Prdx6 by Nrf2 Mediated Through aiPLA2 in White Matter Reperfusion Injury.Molecular neurobiology · 2021Article
- Ischemia-reperfusion Injury in the Transplanted Lung: A Literature Review.Transplantation direct · 2021Review
- Article
- Bioengineering of Pulmonary Epithelium With Preservation of the Vascular Niche.Frontiers in bioengineering and biotechnology · 2020Review
- Peroxiredoxins and Beyond; Redox Systems Regulating Lung Physiology and Disease.Antioxidants & redox signaling · 2019Review
- A Peptide Inhibitor of NADPH Oxidase (NOX2) Activation Markedly Decreases Mouse Lung Injury and Mortality Following Administration of Lipopolysaccharide (LPS).International journal of molecular sciences · 2019Article
- Genetic inactivation of the phospholipase AAmerican journal of physiology. Lung cellular and molecular physiology · 2019Article
- Identification of Small Peptides that Inhibit NADPH Oxidase (Nox2) Activation.Antioxidants (Basel, Switzerland) · 2018Article
- The Role of Peroxiredoxin 6 in Cell Signaling.Antioxidants (Basel, Switzerland) · 2018Review
- Detection of hydrogen peroxide production in the isolated rat lung using Amplex red.Free radical research · 2018Article
- The phospholipase AJournal of lipid research · 2018Review
- Peroxiredoxin 6 mediates Gαi protein-coupled receptor inactivation by cJun kinase.Nature communications · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
1-Hexadecyl-3-trifluoroethylglycero-sn-2-phosphomethanol (MJ33) is a fluorinated phospholipid analog that inhibits the phospholipase A2 (PLA2) activity of peroxiredoxin 6 (Prdx6). Prdx6 PLA2 activity is required for activation of NADPH oxidase 2 and subsequent generation of reactive oxygen species (ROS). In vitro, MJ33 inhibited agonist-stimulated production of ROS by the isolated perfused mouse lung, lung microvascular endothelial cells, and polymorphonuclear leukocytes. MJ33 (0.02-0.5 µmol MJ33/kg body weight) in mixed unilamellar liposomes was administered to C57BL/6 mice by either intratracheal (i.t.) or i.v. routes. Lung MJ33 content, measured by liquid chromatography/mass spectroscopy, showed uptake of 67-87% of the injected dose for i.t. and 23-42% for i.v. administration at 4 hours postinjection. PLA2 activity of lung homogenates was markedly inhibited (>85%) at 4 hours postadministration. Both MJ33 content and PLA2 activity gradually returned to near control levels over the subsequent 24-72 hours. Mice treated with MJ33 at 12.5-25 µmol/kg did not show changes (compared with control) in clinical symptomatology, body weight, hematocrit, and histology of lung, liver, and kidney during a 30- to 50-day observation period. Thus, the toxic dose of MJ33 was >25 µmol/kg, whereas the PLA2 inhibitory dose was approximately 0.02 µmol/kg, indicating a high margin of safety. MJ33 administered to mice prior to lung isolation markedly reduced ROS production and tissue lipid and protein oxidation during ischemia followed by reperfusion. Thus, MJ33 could be useful as a therapeutic agent to prevent ROS-mediated tissue injury associated with lung inflammation or in harvested lungs prior to transplantation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.