Inflammation and Lung Cancer: Roles of Reactive Oxygen/Nitrogen Species
Abstract
The lung is a highly specialized organ that facilitates uptake of oxygen and release of carbon dioxide. Due to its unique structure providing enormous surface area to outside ambient air, it is vulnerable to numerous pathogens, pollutants, oxidants, gases, and toxicants that are inhaled continuously from air, which makes the lung susceptible to varying degrees of oxidative injury. To combat these unrelenting physical, chemical, and biological insults, the respiratory epithelium is covered with a thin layer of lining fluid containing several antioxidants and surfactants. Inhaled toxic agents stimulate the generation of reactive oxygen/nitrogen species (ROS/RNS), which in turn provoke inflammatory responses resulting in the release of proinflammatory cytokines and chemokines. These subsequently stimulate the influx of polymorphonuclear leukocytes (PMNs) and monocytes into the lung so as to combat the invading pathogens or toxic agents. In addition to the beneficial effects, persistent inhalation of the invading pathogens or toxic agents may result in overwhelming production of ROS/RNS, producing chronic inflammation and lung injury. During inflammation, enhanced ROS/RNS production may induce recurring DNA damage, inhibition of apoptosis, and activation of proto-oncogenes by initiating signal transduction pathways. Therefore, it is conceivable that chronic inflammation-induced production of ROS/RNS in the lung may predispose individuals to lung cancer. This review describes the complex relationship between lung inflammation and carcinogenesis, and highlights the role of ROS/RNS in cancer development.
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ROS from different sources causes DNA damage which enhances genomic instability in lung cancer.
“ROS from different sources causes DNA damage which in turn enhances genomic instability in lung cancer (Azad et al. 2008).”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Azad et al. 2008
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- Authors
- Azad, N., Rojanasakul, Y., & Vallyathan, V.
- Affiliations
- West Virginia University (US)
- National Institute for Occupational Safety and Health (US)
- Corresponding author
- Vallyathan, Val
- Venue
- Journal of Toxicology and Environmental Health, Part B
- Publisher
- Informa UK Limited
- Published
- 2008-01-02
- Volume
- 11
- Issue
- 1
- Pages
- 1-15
- ISSN
- 1093-7404 (ISSN-L)
- 1521-6950
- OpenAlex
- W2021149374
- Cited by
- 409
- References
- 142
- Citations by year
- 2026: 8 · 2025: 16 · 2024: 16 · 2023: 23 · 2022: 32 · 2021: 32 · 2020: 22 · 2019: 25 · 2018: 18 · 2017: 21 · 2016: 13 · 2015: 24 · 2014: 29 · 2013: 21 · 2012: 27
- FWCI
- 11.40
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Toxicology and Environmental Health Part B (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Keywords
- lung cancer, lung inflammation, reactive oxygen species, reactive nitrogen species, oxidative stress, chronic inflammation, carcinogenesis, inflammatory cytokines, chemokines, polymorphonuclear leukocytes, monocytes, DNA damage, apoptosis inhibition, proto-oncogene activation, signal transduction, inhaled toxicants, respiratory epithelium, lung injury
- MeSH terms
- Humans, Inflammation, Lung Neoplasms, Reactive Oxygen Species, Reactive Nitrogen Species
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