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First Department of Medicine, Tokyo Women's Medical University, Shinjuku-ku, Tokyo 162-8666, Japan
Alveolar macrophages (AMs) may play a critical role
in cigarette smoke (CS)-related pulmonary diseases. This study was
designed to determine whether CS induces apoptosis of AMs. In
in vitro studies, mouse, rat, and human AMs and human blood
monocyte-derived macrophages cultured with aqueous whole CS extracts
underwent apoptosis that was detected by light and electron
microscopy and terminal deoxynucleotidyltransferase-mediated dUTP nick
end labeling. The gas phase of CSE did not cause apoptosis. The
CS-induced apoptosis was associated with increased oxidative
stress, Bax protein accumulation, mitochondrial dysfunction, and
mitochondrial cytochrome c release but was independent of
p53, Fas, and caspase activation. This apoptosis was inhibited
by antioxidants such as glutathione, ascorbic acid, and 
-tocopherol.
In in vivo studies where rats were exposed to the smoke from 10 cigarettes over 5 h in an exposure chamber, ~3% of AMs obtained
by bronchoalveolar lavage after 24 h showed apoptosis.
These results suggest that acute CS exposure is capable of inducing
apoptosis of AMs.
oxidative stress; Bax; mitochondria; p53; caspase
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