Biomedical Engineering Reference
In-Depth Information
Figure 4
Model of potential pathways used by circulating cells for the generation of
NO-derived reactive oxygen species and reactive halogen species.
The physiological consequences of EPO-dependent formation of
brominated oxidants such as HOBr in vivo are unknown. HOBr reacts
rapidly with a variety of nucleophilic targets such as thiols, thiol ethers,
amines, unsaturated groups, and aromatic compounds.
Several transition metal salts react with H
2
O
2
to form
OH. Most
attention in vivo for the generation of
OH has focused on the role of iron.
Iron is a critical element in many oxidative reactions. Free iron in the
ferrous form catalyzes the Fenton reaction and the superoxide driven
Haber-Weiss reaction, which generate the
OH, an ROS which damages
tissues, particularly cell membranes by lipid peroxidation (Fig. 5).
IV.
INHALED OXIDANTS AND CIGARETTE SMOKE
Cigarette smoking, inhalation of airborne pollutants, either oxidant gases
[such as ozone, nitrogen dioxide (NO
2
), sulfur dioxide SO
2
] or particulate
air pollution results in direct lung damage as well as in the activation of
inflammatory responses in the lungs. These environmental noxious agents
are implicated in the pathogenesis and exacerbations of COPD. Cigarette
smoke is a complex mixture of over 4700 chemical compounds, including
high concentrations of oxidants
=
free radicals (
>
10
15
molecules
=
puff) (7).
Short-lived oxidants such as O
2
-
and nitric oxide (NO) are predominantly
