Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 105, Issue 21, Pages 7365-7369Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0710791105
Keywords
ascorbic acid; oxidative damage; particulate matter; lung; biosurfaces
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The pulmonary epithelium, like most aerial biosurfaces, is naturally protected against atmospheric ozone (O-3) by fluid films that contain ascorbic acid (AH(2)) and related scavengers. This mechanism of protection will fail, however, if specific copollutants redirect AH(2) and O-3(g) to produce species that can transduce oxidative damage to underlying tissues. Here, the possibility that the synergistic adverse health effects of atmospheric O-3(g) and acidic particulate matter revealed by epidemiological studies could be mediated by hitherto unidentified species is investigated by electrospray mass spectrometry of aqueous AH(2) droplets exposed to O-3(g). The products of AH(2) ozonolysis at the relevant air-water interface shift from the innocuous dehydroascorbic acid at biological pH to a C-4-hydroxy acid plus a previously unreported ascorbate ozonide (m/z = 223) below pH approximate to 5. The structure of this ozonide is confirmed,by tandem mass spectrometry and its mechanism of formation delineated by kinetic studies. Present results imply enhanced production of a persistent ozonide in airway-lining fluids acidified by preexisting pathologies or inhaled particulate matter. Ozonides are known to generate cytotoxic free radicals in vivo and can, therefore, transduce oxidative damage.
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