ArticleAmerican journal of respiratory and critical care medicine2010
Aging adversely affects the cigarette smoke-induced glutathione adaptive response in the lung.
Article in American journal of respiratory and critical care medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 72 citations in OpenAlex.
- Protandim does not influence alveolar epithelial permeability or intrapulmonary oxidative stress in human subjects with alcohol use disorders.American journal of physiology. Lung cellular and molecular physiology · 2012Trial
- Short-Term and Long-Term Effects of Electronic Cigarettes on Mouse Lungs Following Nose-Only Exposures.Chemical research in toxicology · 2025Article
- [Physiological and pathophysiological changes of the ageing lung].Zeitschrift fur Gerontologie und Geriatrie · 2025Review
- Impact of electronic cigarette vaping on the cardiovascular function in young and old rats.Scientific reports · 2024Article
- Identification of CD8 T-cell dysfunction associated with symptoms in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and Long COVID and treatment with a nebulized antioxidant/anti-pathogen agent in a retrospective case series.Brain, behavior, & immunity - health · 2024Article
- Review
- How Aging and Oxidative Stress Influence the Cytopathic and Inflammatory Effects of SARS-CoV-2 Infection: The Role of Cellular Glutathione and Cysteine Metabolism.Antioxidants (Basel, Switzerland) · 2022Review
- The role of sulfur compounds in chronic obstructive pulmonary disease.Frontiers in molecular biosciences · 2022Review
- The age-dependent decline of the extracellular thiol-disulfide balance and its role in SARS-CoV-2 infection.Redox biology · 2021Article
- Ursolic acid alleviates airway-vessel remodeling and muscle consumption in cigarette smoke-induced emphysema rats.BMC pulmonary medicine · 2019Article
- Oxidative stress associated with aging activates protein kinase Cε, leading to cilia slowing.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Lung cellular senescence is independent of aging in a mouse model of COPD/emphysema.Scientific reports · 2018Article
- Distribution and characteristics of COPD phenotypes - results from the Polish sub-cohort of the POPE study.International journal of chronic obstructive pulmonary disease · 2018Observational
- Protective effect of autophagy on endoplasmic reticulum stress induced apoptosis of alveolar epithelial cells in rat models of COPD.Bioscience reports · 2017Article
- The pulmonary inflammatory response to multiwalled carbon nanotubes is influenced by gender and glutathione synthesis.Redox biology · 2016Article
- Redox mechanisms in age-related lung fibrosis.Redox biology · 2016Review
- Alpha-1 Antitrypsin Investigations Using Animal Models of Emphysema.Annals of the American Thoracic Society · 2016Review
- The Presence of Chronic Mucus Hypersecretion across Adult Life in Relation to Chronic Obstructive Pulmonary Disease Development.American journal of respiratory and critical care medicine · 2016Article
- POPE study: rationale and methodology of a study to phenotype patients with COPD in Central and Eastern Europe.International journal of chronic obstructive pulmonary disease · 2016Observational
- Oxidative stress response and Nrf2 signaling in aging.Free radical biology & medicine · 2015Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
rationaleCigarette smoke (CS) is the leading cause of chronic obstructive pulmonary disease, accounting for more than 90% of cases. The prevalence of chronic obstructive pulmonary disease is much higher in the elderly, suggesting an age dependency. A prominent defense against the oxidant burden caused by CS is the glutathione (GSH) adaptive response in the lung epithelial lining fluid (ELF) and tissue. However, as one ages the ability to maintain GSH levels declines.
objectivesExamine the effect of aging on the GSH adaptive response to CS and resulting lung sensitization to inflammation and oxidation.
methodsBoth young (2 mo old) and aged (8, 13, 19, and 26 mo old) mice were used to study the effects of age on the GSH adaptive response after an acute exposure to CS. MEASUREMENTS AND MAIN
resultsYoung mice had a robust sixfold increase in ELF GSH after a single exposure to CS. The GSH response to CS decreased as a function of age and diminishes in the older mice to only a twofold increase over air controls. As a consequence, levels of CS-induced tumor necrosis factor-α and nitric oxide synthase, markers of inflammation, and 8-hydroxy-2-deoxyguanosine, a marker of DNA oxidation, were elevated in the aged mice compared with the young mice. Additionally, depletion of ELF GSH with buthionine sulfoximine in young mice recapitulated changes in ELF tumor necrosis factor-α as seen in old mice.
conclusionsThese data suggest that the age-related maladaptive response to CS sensitizes the lung to both inflammation and oxidation potentially contributing to the development of CS-induced chronic obstructive pulmonary disease.
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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.