Cited by 918Nitric Oxide and Endothelin EffectsAsthma and respiratory diseasesRedox biology and oxidative stress

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The Biology of Nitrogen Oxides in the Airways

Gaston, B, Drazen, J M, Loscalzo, J, Stamler, J S·1994·American Journal of Respiratory and Critical Care Medicine

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Abstract

Nitrogen oxides (NOx), regarded in the past primarily as toxic air pollutants, have recently been shown to be bioactive species formed endogenously in the human lung. The relationship between the toxicities and the bioactivities of NOx must be understood in the context of their chemical interactions in the pulmonary microenvironment. Nitric oxide synthase (NOS) is a newly identified enzyme system active in airway epithelial cells, macrophages, neutrophils, mast cells, autonomic neurons, smooth muscle cells, fibroblasts, and endothelial cells. The chemical products of NOS in the lung vary with disease states, and are involved in pulmonary neurotransmission, host defense, and airway and vascular smooth muscle relaxation. Further, certain patients with pulmonary hypertension, adult respiratory distress syndrome and asthma may experience physiologic improvement with NOx therapy, including inhalation of nitric oxide (NO.) gas. Both endogenous and exogenous NOx react readily with oxygen, superoxide, water, nucleotides, metalloproteins, thiols, amines, and lipids to form products with biochemical actions ranging from bronchodilation and bacteriostasis (S-nitrosothiols) to cytotoxicity and pulmonary capillary leak (peroxynitrite), as well as those with frank mutagenic potential (nitrosamines). Recent discoveries demonstrating the relevance of these species to the lung have provided new insights into the pathophysiology of pulmonary disease, and they have opened a new horizon of therapeutic possibilities for pulmonary medicine.

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Items 201–300 of 917

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Background
S -nitrosothiol repletion by an inhaled gas regulates pulmonary function
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Self-citation
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Background
Distinct Protein Kinase A Anchoring Proteins Direct Prostaglandin E2 Modulation of Toll-like Receptor Signaling in Alveolar Macrophages
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“…epithelium, endothelial cells of the pulmonary vasculature, bronchial and vascular smooth muscle cells, macrophages, mast cells, fibroblasts, eosinophils, basophils and neutrophils (Hamid et al., 1993; Asano et al., 1994; Gaston et al., 1994; Kharitonov and Barnes, 2001; Ricciardolo et al., 2004).”
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Background
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Background
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Background
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Background
NO in the lung
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“(2) of extracellular calcium (Ca21), under basal conditions or with 1028 M E2b added for 60 min.”
BackgroundMethodInfluential
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Background
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BackgroundInfluential
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Background
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“Evidence does exist that NO attenuates leukocyte adhesion and recruitment into the lung in certain models of lung inflammation (Gaston et al., 1994; Hickey & Kubes, 1997; Lin et al., 2001; Sato et al., 1999).”
Background
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Blau, H., Riklis, S., van Iwaarden, J. F., McCormack, F. X., & Kalina, M. (1997) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.1997.272.6.l1198 · Cited by 62
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Gravesande, K. S. V., Wechsler, M. E., Grasemann, H., et al. (2003) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.200212-1491bc · Cited by 61
“of FENO was performed according to the guidelines for off-line measurements ( 25 ).”
BackgroundMethodSelf-citation
Peroxynitrite in airway diseases
Sadeghi‐Hashjin, Folkerts, Henricks, P. A. J., Muijsers, & Nijkamp (1998) · Clinical & Experimental Allergy · doi:10.1046/j.1365-2222.1998.00428.x · Cited by 61
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“When oxygen reacts to the NO surplus produced during the inflammatory process, generates nitrogen oxides byproducts such as peroxynitrite, N2O3 and N2O4, which are powerful nitrosating agents [61].”
Background
Silencing of caspase-8 and caspase-3 by RNA interference prevents vascular endothelial cell injury in mice with endotoxic shock
Matsuda, N., Takano, Y., Kageyama, S., HATAKEYAMA, N., Shakunaga, K., Kitajima, I., YAMAZAKI, M., & Hattori, Y. (2007) · Cardiovascular Research · doi:10.1016/j.cardiores.2007.05.024 · Cited by 60
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“In the lungs NO is produced by several cell types, including airway epithelium, macrophages, and intrapulmonary vascular endothelium ( 12 ).”
Background
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Artlich, A., Busch, T., Lewandowski, K., Jonas, S., Gortner, L., & Kj, F. (1999) · European Respiratory Journal · doi:10.1183/09031936.99.13614029 · Cited by 58
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Background
Role of L ‐arginine in the deficiency of nitric oxide and airway hyperreactivity after the allergen‐induced early asthmatic reaction in guinea‐pigs
de Boer, J., Duyvendak, M., Schuurman, F. E., et al. (1999) · British Journal of Pharmacology · doi:10.1038/sj.bjp.0702882 · Cited by 60
“Endogenous nitric oxide (NO) plays a central role in the regulation of airway tone as well as in asthmatic airway in¯ammation (Barnes & Belvisi, 1993; Gaston et al., 1994; Barnes & Liew, 1995), and may be importantly involved in the development of allergen-induced AHR (De Boer et al., 1996;…”
Background
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Background
Inhaled Nitric Oxide Primes Lung Macrophages to Produce Reactive Oxygen and Nitrogen Intermediates
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“However, in contrast to inhaled ozone or nitrogen dioxide, which induce marked inflammatory responses (7, 9), we did not observe increased numbers of macrophages or neutrophils in the lung after nitric oxide exposure.”
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“…regulations, which are suggested to include those of vascular tone, bronchial tone, neurotransmission, or immune defense (Moncada et al., 1991; Gaston et al., 1994), impairment of expression and activity of eNOS, if any, may contribute to tissue injury in sepsis by hindrance of physiologic…”
Background
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BackgroundInfluential
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Self-citation
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Background
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“NO has a very short half-life in physiologic systems, of 0.1 s to 5 s ( 13 ), and labeling studies show that plasma [NO32 1 NO22] reflects a large fraction of NO metabolites or adducts in the body (27, 28).”
BackgroundInfluential
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Proteolytic Cleavage Confers Nitric Oxide Synthase Inducing Activity upon Prolactin
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Nitric oxide synthase activity is inducible in rat, but not rabbit alveolar macrophages, with a concomitant reduction in arginase activity
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“In the respiratory tract, NO is produced by a variety of cells, including, neurons, epithelial cells, macrophages, and inflammatory cells (6), and NO may play a crucial role in inflammatory airway diseases such as asthma.”
Background
The role of apoptosis in pulmonary fibrosis.
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“ROS and their reactions with lung epithelial cells participate in the pathophysiology of several lung diseases, including IPF, ARDS, and lung cancer (Gaston et al., 1994; Shi et al., 2001).”
Background
Characterization of reactive nitrogen species in allergic asthma
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“Nitrites and nitrates are stable end-products of the nitric oxide (NO) metabolism and their levels reflect activity of inducible nitric oxide synthetase expressed by neutrophils, eosinophils, and other inflammatory cells in the respiratory tract [35].”
Background
Nitric Oxide: Perspectives and Emerging Studies of a Well Known Cytotoxin
Paradise, W. A., Vesper, B. J., Goel, A., Waltonen, J. D., Altman, K. W., Haines, G. K., & Radosevich, J. A. (2010) · International Journal of Molecular Sciences · doi:10.3390/ijms11072715 · Cited by 55
“Exogenous sources of NO, such as cigarette smoke, contribute to subcellular damage through the formation of N-nitrosoamines and N-nitrosamides, contributing to elevated expression of head and neck cancers [7,33-36].”
Background
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Authors: Gaston, B., Drazen, J. M., Loscalzo, J., & Stamler, J. S.
Affiliations: Boston Children's Hospital (US)
ORCID: Gaston, B
Drazen, J M
Loscalzo, J
Stamler, J S
Venue: American Journal of Respiratory and Critical Care Medicine
Publisher: Oxford University Press (OUP)
Published: 1994-02-01
Volume: 149
Issue: 2
Pages: 538-551
ISSN: 1073-449X (ISSN-L)
1535-4970
DOI: 10.1164/ajrccm.149.2.7508323
OpenAlex: W2054510493
Cited by: 918
References: 0
Citations by year: 2025: 6 · 2024: 4 · 2023: 4 · 2022: 10 · 2021: 13 · 2020: 5 · 2019: 6 · 2018: 10 · 2017: 9 · 2016: 15 · 2015: 16 · 2014: 19 · 2013: 27 · 2012: 16
FWCI: 37.13
Type: journal article
Language: en
Open access: closed
Licence: academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations: American Journal of Respiratory and Critical Care Medicine (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (5r01hl040411-02, 5p50hl019170-20, 5r01hl043344-04)
National Heart, Lung, and Blood Institute (HL43344, HL-40411, HL 19170)
Topics: Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Asthma and respiratory diseases
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Keywords: nitrogen oxides, nitric oxide, nitric oxide synthase, airway epithelial cells, S-nitrosothiols, peroxynitrite, nitrosamines, pulmonary hypertension, acute respiratory distress syndrome, asthma, nitric oxide inhalation therapy, bronchodilation, host defense, smooth muscle relaxation
MeSH terms: Amino Acid Oxidoreductases, Animals, Humans, Lung, Lung Diseases, Nitric Oxide, Nitrogen Oxides, Nitrous Oxide, Nitric Oxide Synthase

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The Biology of Nitrogen Oxides in the Airways

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