Biomedical Engineering Reference
In-Depth Information
Figure 6
Cigarette smoke-derived gas and tar phase showing oxidative stress.
During redox cycling, the cigarette smoke containing semiquinone intermediate
reduces molecular oxygen to the superoxide anion. The cycle can be sustained by
biological reducing equivalents [ascorbate, NAD(P)H, glutathione, etc.] which
reduce the oxidized quinoid substances back to their reduced states, enabling them
to produce again the superoxide radical.
V. OXIDATIVE STRESS IN THE ALVEOLAR SPACE
The oxidant burden in the lungs is enhanced in smokers by the release of
ROS from macrophages and neutrophils. Oxidants present in cigarette
smoke can stimulate alveolar macrophages to produce ROS and to release
a host of mediators, some of which attract neutrophils and other inflamma-
tory cells into the lungs. Both neutrophils and macrophages, which are
known to migrate in increased numbers into the lungs of cigarette smokers,
compared with non-smokers, can generate ROS via the NADPH oxidase
system. Moreover, the lungs of smokers with airway obstruction have more
neutrophils than smokers without airway obstruction. Circulating neutro-
phils from cigarette smokers and patients with exacerbations of COPD
release more O
2
-
(12). Cigarette smoking is associated with increased
