Endogenous Nitric Oxide Can Enhance Oxidative Stress Caused by Air Pollutants and Explain Higher Susceptibility of Individuals with Inflammatory Disorders.
Steven LelieveldJos LelieveldAshmi MishraAndreas DaiberAndrea PozzerUlrich PöschlThomas BerkemeierPublished in: Environmental science & technology (2024)
Air pollution causes morbidity and excess mortality. In the epithelial lining fluid of the respiratory tract, air pollutants trigger a chemical reaction sequence that causes the formation of noxious hydroxyl radicals that drive oxidative stress. For hitherto unknown reasons, individuals with pre-existing inflammatory disorders are particularly susceptible to air pollution. Through detailed multiphase chemical kinetic analysis, we show that the commonly elevated concentrations of endogenous nitric oxide in diseased individuals can increase the production of hydroxyl radicals via peroxynitrite formation. Our findings offer a molecular rationale of how adverse health effects and oxidative stress caused by air pollutants may be exacerbated by inflammatory disorders.
Keyphrases
- oxidative stress
- nitric oxide
- air pollution
- respiratory tract
- diabetic rats
- ischemia reperfusion injury
- dna damage
- induced apoptosis
- heavy metals
- particulate matter
- nitric oxide synthase
- lung function
- hydrogen peroxide
- clinical trial
- cardiovascular events
- cardiovascular disease
- risk assessment
- risk factors
- signaling pathway
- single molecule
- chronic obstructive pulmonary disease
- heat shock
- fluorescent probe
- amino acid