ArticleFree radical biology & medicine2012
Free radical-operated proteotoxic stress in macrophages primed with lipopolysaccharide.
Article in Free radical biology & medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The trial behind it
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
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- Development of Diclofenac Acid Encapsulated Transferosomal gel with Enhanced Antioxidant and Anti-Inflammatory Activities for the Management of Musculoskeletal Pain.AAPS PharmSciTech · 2026Article
- Dendranthema oreastrum (Hance) Y.Ling Attenuates Oxidative Stress and Airway Inflammation in a Murine Model of Lipopolysaccharide-Induced Acute Lung Injury.Environmental toxicology · 2025Article
- Trapping DNA Radicals With DMPO Reduces Hypochlorous Acid-Induced 8-oxo-7,8-dihydro-2'-deoxyguanosine and Mutagenesis in Lung Epithelial Cells.Oxidative medicine and cellular longevity · 2025Article
- Review
- Exploring the Mechanism of Asiatic Acid against Atherosclerosis Based on Molecular Docking, Molecular Dynamics, and Experimental Verification.Pharmaceuticals (Basel, Switzerland) · 2024Article
- The inflammation and reactive oxygen species regulated by Nrf2 and NF-κB signaling pathways in 630-nm light-emitting diode irradiation treated THP-1 monocytes/macrophages.Lasers in medical science · 2021Article
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- Pharmacologic Activities of Plant-Derived Natural Products on Respiratory Diseases and Inflammations.BioMed research international · 2021Review
- The nitrone spin trap 5,5-dimethyl-1-pyrroline N-oxide dampens lipopolysaccharide-induced transcriptomic changes in macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Article
- Triptriolide Alleviates Lipopolysaccharide-Induced Liver Injury by Nrf2 and NF-κB Signaling Pathways.Frontiers in pharmacology · 2018Article
- Vitexin attenuates lipopolysaccharide-induced acute lung injury by controlling the Nrf2 pathway.PloS one · 2018Article
- The Neuroprotective Effects of Muscle-Derived Stem Cells via Brain-Derived Neurotrophic Factor in Spinal Cord Injury Model.BioMed research international · 2017Article
- Radicalization of Glyceraldehyde-3-Phosphate Dehydrogenase by HOCl in Living Cells.Enzyme engineering (Los Angeles, Calif.) · 2015Article
- Punicalagin Induces Nrf2/HO-1 Expression via Upregulation of PI3K/AKT Pathway and Inhibits LPS-Induced Oxidative Stress in RAW264.7 Macrophages.Mediators of inflammation · 2015Article
- LPS preconditioning ameliorates intestinal injury in a rat model of hemorrhagic shock.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Article
- Inducible nitric oxide synthase is key to peroxynitrite-mediated, LPS-induced protein radical formation in murine microglial BV2 cells.Free radical biology & medicine · 2014Article
- Immuno-spin trapping from biochemistry to medicine: advances, challenges, and pitfalls. Focus on protein-centered radicals.Biochimica et biophysica acta · 2014Review
- The nitrone spin trap 5,5-dimethyl-1-pyrroline N-oxide affects stress response and fate of lipopolysaccharide-primed RAW 264.7 macrophage cells.Inflammation · 2013Article
- Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
The free-radical-operated mechanism of death of activated macrophages at sites of inflammation is unclear, but it is important to define it in order to find targets to prevent further tissue dysfunction. A well-defined model of macrophage activation at sites of inflammation is the treatment of RAW 264.7 cells with lipopolysaccharide (LPS), with the resulting production of reactive oxygen species (ROS). ROS and other free radicals can be trapped with the nitrone spin trap 5,5-dimethyl-1-pyrroline N-oxide (DMPO), a cell-permeable probe with antioxidant properties, which thus interferes with free-radical-operated oxidation processes. Here we have used immuno-spin trapping to investigate the role of free-radical-operated protein oxidation in LPS-induced cytotoxicity in macrophages. Treatment of RAW 264.7 cells with LPS resulted in increased ROS production, oxidation of proteins, cell morphological changes and cytotoxicity. DMPO was found to trap protein radicals to form protein-DMPO nitrone adducts, to reduce protein carbonyls, and to block LPS-induced cell death. N-Acetylcysteine (a source of reduced glutathione), diphenyleneiodonium (an inhibitor of NADPH oxidase), and 2,2'-dipyridyl (a chelator of Fe(2+)) prevented LPS-induced oxidative stress and cell death and reduced DMPO-nitrone adduct formation, suggesting a critical role of ROS, metals, and protein-radical formation in LPS-induced cell cytotoxicity. We also determined the subcellular localization of protein-DMPO nitrone adducts and identified some candidate proteins for DMPO attachment by LC-MS/MS. The LC-MS/MS data are consistent with glyceraldehyde-3-phosphate dehydrogenase, one of the most abundant, sensitive, and ubiquitous proteins in the cell, becoming labeled with DMPO when the cell is primed with LPS. This information will help find strategies to treat inflammation-associated tissue dysfunction by focusing on preventing free radical-operated proteotoxic stress and death of macrophages.
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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.