[Oxygen radicals in the mechanism of lung injury caused by air pollutants].
Ozone and nitrogen oxides are environmental pollutants especially present in smog. They are oxidants potent to cause bronchial hyperreactivity, lung fibrosis, and emphysema. Other occupational hazards are mineral dust particles (asbestos, silica) which may cause the development of inflammation and fibrosis in the lungs. Inflammatory cells (neutrophils, eosinophils, monocytes, macrophages) become activated during inflammation and produce superoxide anion radicals. Reactive oxygen species developed e.g. in smog have been recognized--at least partly--to be responsible for the observed pulmonary tissue damage. Several mechanisms leading to toxicity, including disbalance of vegetative nervous control, damage of bronchial epithelium, role of mediators of inflammation and other issues are discussed. (Fig. 1, Ref. 32.)
Visnovský
P
P
Katedra farmakologie a toxikologie Farmaceutické fakulty University Karlovy v Hradci Králové, Ceská republika. visnovsk@faf.cuni.cz
Suchánková
J
J
Styrandová
M
M
D000393:Air Pollutants / Q000009:adverse effects*; D000818:Animals; D016535:Bronchial Hyperreactivity / Q000209:etiology / Q000378:metabolism; D004391:Dust / Q000009:adverse effects; D005609:Free Radicals / Q000378:metabolism*; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D008168:Lung / Q000378:metabolism / Q000473:pathology*; D011658:Pulmonary Fibrosis / Q000209:etiology* / Q000378:metabolism; D012905:Smog / Q000009:adverse effects
D000393:Air Pollutants; D004391:Dust; D005609:Free Radicals; D018836:Inflammation Mediators; D012905:Smog
Kyslíkové radikály v mechanizmoch poskodenia pl'úc vyvolaného polutantmi ovzdusia.