The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Ibuprofen prevents oxidant lung injury and in vitro lipid peroxidation by chelating iron.
Open accessAbstract
Because ibuprofen protects from septic lung injury, we studied the effect of ibuprofen in oxidant lung injury from phosgene. Lungs from rabbits exposed to 2,000 ppm-min phosgene were perfused with Krebs-Henseleit buffer at 50 ml/min for 60 min. Phosgene caused no increase in lung generation of cyclooxygenase metabolites and no elevation in pulmonary arterial pressure, but markedly increased transvascular fluid flux (delta W = 31 +/- 5 phosgene vs. 8 +/- 1 g unexposed, P less than 0.001), permeability to albumin (125I-HSA) lung leak index 0.274 +/- 0.035 phosgene vs. 0.019 +/- 0.001 unexposed, P less than 0.01; 125I-HSA lavage leak index 0.352 +/- 0.073 phosgene vs. 0.008 +/- 0.001 unexposed, P less than 0.01), and lung malondialdehyde (50 +/- 7 phosgene vs. 24 +/- 0.7 mumol/g dry lung unexposed, P less than 0.01). Ibuprofen protected lungs from phosgene (delta W = 10 +/- 2 g; lung leak index 0.095 +/- 0.013; lavage leak index 0.052 +/- 0.013; and malondialdehyde 16 +/- 3 mumol/g dry lung, P less than 0.01). Because iron-treated ibuprofen failed to protect, we studied the effect of ibuprofen in several iron-mediated reactions in vitro. Ibuprofen attenuated generation of .OH by a Fenton reaction and peroxidation of arachidonic acid by FeCl3 and ascorbate. Ibuprofen also formed iron chelates that lack the free coordination site required for iron to be reactive. Thus, ibuprofen may prevent iron-mediated generation of oxidants or iron-mediated lipid peroxidation after phosgene exposure. This suggests a new mechanism for ibuprofen's action.
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Ibuprofen chelates iron in a stable form without a free Fenton-reactive coordination site and protects from lipid peroxidation in vitro and phosgene-induced septic lung injury in rabbits.
“ibuprofen, a widely used synthetic anti-inflammatory agent, has been shown to chelate iron in a stable form without a free Fenton-reactive coordination site and to protect from lipid peroxidation in vitro and phosgene-induced septic lung injury in rabbits [48].”
From The utility of iron chelators in the management of inflammatory disorders (2015) · cites this paper as [48]
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Cites
Shock and Tissue Injury Induced by Recombinant Human Cachectin
Tracey, K. J., Beutler, B., Lowry, S. F., Merryweather, J., Wolpe, S., Milsark, I. W., Hariri, R. J., Fahey, T. J., Zentella, A., Albert, J. D., et al. (1986) · Science · doi:10.1126/science.3764421 · Cited by 2,549
Iron-catalyzed hydroxyl radical formation. Stringent requirement for free iron coordination site.
Graf, E., Mahoney, J. R., Bryant, R. G., & Eaton, J. W. (1984) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)43139-5 · Cited by 855
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Research works printed but not linked: 4
- Spiro, T. G., and P. Saltman. 1974. Inorganic chemistry. In Iron in Biochemistry and Medicine. A. Jacobs, and M. Worwood, editors. Academic Press, Inc., New York. 1-28.
- Cohen, G. 1985. The Fenton reaction. In Handbook of Methods for Oxygen Radical Research. R. A. Greenwald, editor. CRC Press, Inc., Boca Raton, FL. 55-69.
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The utility of iron chelators in the management of inflammatory disorders
Lehmann, C., Islam, S., Jarosch, S., Zhou, J., Hoskin, D., Greenshields, A., Al-Banna, N., Sharawy, N., Sczcesniak, A., Kelly, M., et al. (2015) · Mediators of Inflammation · doi:10.1155/2015/516740 · Cited by 54
“As to synthetic agents with antiinflammatory activity, ibuprofen, a widely used synthetic anti-inflammatory agent, has been shown to chelate iron in a stable formwithout a free Fenton-reactive coordination site and to protect from lipid peroxidation in vitro and phosgeneinduced septic lung injury in rabbits [48].”
Background
Metadata
- Authors
- Kennedy, T. P., Rao, N. V., Noah, W., Michael, J. R., Jafri, M. H., Gurtner, G. H., & Hoidal, J. R.
- Affiliations
- Duke University (US)
- Venue
- Journal of Clinical Investigation
- Published
- 1990-11-01
- Volume
- 86
- Issue
- 5
- Pages
- 1565-1573
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC296904
- OpenAlex
- W2017222748
- Cited by
- 72
- References
- 2
- Citations by year
- 2025: 1 · 2024: 1 · 2023: 1 · 2022: 2 · 2021: 3 · 2020: 1 · 2018: 2 · 2017: 2 · 2016: 1 · 2015: 3 · 2014: 1 · 2013: 3 · 2012: 1
- FWCI
- 4.87
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute for Occupational Safety and Health (OHO2264)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Respiratory Support and Mechanisms
- Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Paraquat toxicity studies and treatments
- Keywords
- ibuprofen, phosgene, lipid peroxidation, iron chelation, Fenton reaction, hydroxyl radicals, malondialdehyde, lung permeability, cyclooxygenase metabolites, sepsis-induced acute lung injury, arachidonic acid peroxidation
- MeSH terms
- Animals, Chlorides, Ferric Compounds, Hydroxides, Ibuprofen, Iron Chelating Agents, Lung, Oxidation-Reduction, Perfusion, Phosgene, Prostaglandin-Endoperoxide Synthases, Rabbits, Lipid Peroxidation, Hydroxyl Radical
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