Smoking during pregnancy is a major source of fetal exposure to
numerous harmful agents present in tobacco smoke. Lung development involves
complex biochemical processes resulting in dramatic changes which continue even
after birth. In addition to type I cells which form the blood-air barrier, type
II alveolar epithelial (AE) cells have important and diverse functions related
to immunological protection and stabilization of the alveolus through synthesis
and secretion of the pulmonary surfactant. Apoptosis or programmed cells death
is an important physiological process during lung embryogenesis and for the
proper maintenance of homeostasis. Caspases are proteases that play important roles
in regulating apoptosis. Caspase-3 is the key executioner caspase in the
cascade of events leading to cell death by apoptosis. We explored the
hypothesis that cigarette smoke extract (CSE) induces apoptosis in fetal rat
lung type II AE cells by activation of caspase-3. To analyze these factors,
isolated fetal rat lung type II AE cells were used. The cells were exposed to
different concentrations of CSE (5%, 10% or 15%) (v/v) for 60 min. The results
of the present study showed that CSE induced apoptosis in fetal rat lung type
II AE cells with a significant increase (p<0.05) in
caspase-3 activity and decrease in cell proliferation at CSE concentrations of
10% and 15% (v/v). These observations indicate that cigarette smoke extract
induces apoptosis by activation of caspase-3
in fetal rat lung type II AE cells in a dose-dependent manner
and may potentially alter the regulated development of the lung and the
appearance of the surfactant-producing type II alveolar cells which are
critical for the establishment of adequate gas exchange at birth.
Cite this paper
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