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-mediated oxidative stress and
apoptosis in rat type II cells
Departments of 1 Pediatrics and 2 Medicine, Emory University School of Medicine and Atlanta Veterans Affairs Medical Center, Atlanta, Georgia 30322
In septic patients,
chronic alcohol abuse increases the incidence of the acute respiratory
distress syndrome (ARDS). Because alveolar type II cell viability is
critical for epithelial repair, our objective was to determine if
chronic ethanol ingestion increased the sensitivity of type II cells to
the inflammatory mediators upregulated during sepsis. In rats
chronically fed ethanol, type II cell mitochondrial GSH was depleted,
and tumor necrosis factor-
(TNF-)-induced generation of
mitochondrial reactive oxygen species (ROS) and apoptosis were
potentiated. When added to the ethanol diet, the GSH precursor
(
)-2-oxo-4-thiazolidinecarboxylic acid (Procysteine; Pro) but not
N-acetylcysteine (NAC) normalized type II cell mitochondrial
GSH. Likewise, Pro but not NAC normalized TNF--induced mitochondrial
ROS and apoptosis. This suggested that chronic ethanol
ingestion potentiated TNF--induced apoptosis in type II
cells via mitochondrial GSH depletion. This may be particularly
relevant in ARDS when type II cell viability is critical to repair of
the damaged alveolar epithelium and may have important ramifications
for the treatment of ARDS patients with a history of alcohol abuse.
acute respiratory distress syndrome; alcohol; sepsis; mitochondria
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