The effects of aging on pulmonary oxidative damage, protein nitration, and extracellular superoxide dismutase down-regulation during systemic inflammation
Open accessAbstract
Systemic inflammatory response syndrome (SIRS), a serious clinical condition characterized by whole-body inflammation, is particularly threatening for elderly patients, who suffer much higher mortality rates than the young. A major pathological consequence of SIRS is acute lung injury caused by neutrophil-mediated oxidative damage. Previously, we reported an increase in protein tyrosine nitration (a marker of oxidative/nitrosative damage) and a decrease in the antioxidant enzyme extracellular superoxide dismutase (EC-SOD) in the lungs of young mice during endotoxemia-induced SIRS. Here we demonstrate that during endotoxemia, down-regulation of EC-SOD is significantly more profound and prolonged, whereas up-regulation of iNOS is augmented, in aged compared to young mice. Aged mice also showed 2.5-fold higher protein nitration levels, compared to young mice, with particularly strong nitration in the pulmonary vascular endothelium during SIRS. Additionally, by two-dimensional gel electrophoresis, Western blotting, and mass spectrometry, we identified proteins that show increased tyrosine nitration in age- and SIRS-dependent manners; these proteins (profilin-1, transgelin-2, LASP 1, tropomyosin, and myosin) include components of the actin cytoskeleton responsible for maintaining pulmonary vascular permeability. Reduced EC-SOD in combination with increased oxidative/nitrosative damage and altered cytoskeletal protein function due to tyrosine nitration may contribute to augmented lung injury in the aged with SIRS.
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Increased and prolonged neutrophil recruitment in the aged lung can have devastating effects on lung parenchyma.
“Increased and prolonged neutrophil recruitment in the aged lung can have devastating effects on lung parenchyma (125).”
From Aging and Lung Disease (2020) · cites this paper as [125]
Increasing numbers of recruited neutrophils can promote the development of edema, enhanced disease severity, prolonged inflammation, and pulmonary tissue damage.
“Increasing numbers of recruited neutrophils can promote the development of edema, enhanced disease severity, prolonged inflammation, and pulmonary tissue damage (125, 126).”
From Aging and Lung Disease (2020) · cites this paper as [125]
Increased and prolonged neutrophil recruitment in the COPD lung can have devastating effects on lung parenchyma and can enhance disease severity, prolong inflammation, and cause further tissue damage.
“Increased and prolonged neutrophil recruitment in the COPD lung can have devastating effects on lung parenchyma and can enhance disease severity, prolong inflammation, and cause further tissue damage (107, 125, 126).”
From Aging and Lung Disease (2020) · cites this paper as [125]
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- Authors
- Starr, M. E., Ueda, J., Yamamoto, S., Evers, B. M., & Saito, H.
- Affiliations
- University of Kentucky (US)
- The University of Texas Medical Branch at Galveston (US)
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2011-01
- Volume
- 50
- Issue
- 2
- Pages
- 371-380
- ISSN
- 0891-5849 (ISSN-L)
- PMC
- PMC3340560
- OpenAlex
- W1972042561
- Cited by
- 86
- References
- 62
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 3 · 2023: 5 · 2022: 2 · 2021: 3 · 2020: 8 · 2019: 8 · 2018: 6 · 2017: 12 · 2016: 5 · 2015: 5 · 2014: 7 · 2013: 5 · 2012: 10
- FWCI
- 2.20
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- U.S. Public Health Service (P30A6024832)
- National Institute on Aging (R01AG025908, P30AG024832)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- aging, systemic inflammatory response syndrome, endotoxemia, acute lung injury, tyrosine nitration, extracellular superoxide dismutase, inducible nitric oxide synthase, oxidative stress, nitrosative damage, pulmonary vascular endothelium, actin cytoskeleton, profilin-1, TAGLN2, LASP1, tropomyosin, myosin, pulmonary vascular permeability, elderly patients
- MeSH terms
- Aging, Animals, Extracellular Space, Inflammation, Lipopolysaccharides, Male, Mice, Inbred C57BL, Nitrates, RNA, Messenger, Superoxide Dismutase, Tyrosine, Blotting, Western, Electrophoresis, Gel, Two-Dimensional, Down-Regulation, Oxidative Stress, Nitric Oxide Synthase, Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization, Endotoxemia, Reverse Transcriptase Polymerase Chain Reaction, Mice, Lung Injury
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