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1 Section of Pulmonary and
Critical Care Medicine,
Findings in recent years strongly suggest that
the stress-inducible gene heme oxygenase (HO)-1 plays an important role
in protection against oxidative stress. Although the mechanism(s) by
which this protection occurs is poorly understood, we hypothesized that
the gaseous molecule carbon monoxide (CO), a major by-product of heme
catalysis by HO-1, may provide protection against oxidative stress. We
demonstrate here that animals exposed to a low concentration of CO
exhibit a marked tolerance to lethal concentrations of hyperoxia in
vivo. This increased survival was associated with highly significant attenuation of hyperoxia-induced lung injury as assessed by the volume
of pleural effusion, protein accumulation in the airways, and
histological analysis. The lungs were completely devoid of lung airway
and parenchymal inflammation, fibrin deposition, and pulmonary edema in
rats exposed to hyperoxia in the presence of a low concentration of CO.
Furthermore, exogenous CO completely protected against
hyperoxia-induced lung injury in rats in which endogenous HO enzyme
activity was inhibited with tin protoporphyrin, a selective inhibitor
of HO. Rats exposed to CO also exhibited a marked attenuation of
hyperoxia-induced neutrophil infiltration into the airways and total
lung apoptotic index. Taken together, our data demonstrate, for the
first time, that CO can be therapeutic against oxidative stress such as
hyperoxia and highlight possible mechanism(s) by which CO may mediate
these protective effects.
oxidative stress; acute respiratory distress syndrome; heme oxygenase; gaseous molecule; apoptosis
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