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Department of Sports Medicine, Medical Clinic, University of Heidelberg, 69115 Heidelberg, Germany
In
oxygen-sensitive excitable cells, responses to hypoxia are initiated by
membrane depolarization due to closing of the K channels that is
thought to be mediated by a decrease in reactive oxygen species (ROS).
Because the mechanisms of hypoxic inhibition of ion transport of
alveolar epithelial cells (Planes C, Friedlander G, Loiseau A, Amiel C,
and Clerici C. Am J Physiol Lung Cell Mol Physiol 271:
L70-L78, 1996; Mairbäurl H, Wodopia R, Eckes S, Schulz S,
and Bärtsch P. Am J Physiol Lung Cell Mol Physiol 273: L797-L806, 1997) are not yet understood, we tested the possible involvement of a hypoxia-induced change in ROS that might control transport activity. Transport was measured as 86Rb and
22Na uptake in A549 cells exposed to normoxia, hyperoxia,
or hypoxia together with ROS donors and scavengers.
H2O2 < 1 mM did not affect transport,
whereas 1 mM H2O2 activated
22Na uptake (+200%) but inhibited 86Rb uptake
(
30%). Also hyperoxia, aminotriazole plus menadione, and
diethyldithiocarbamate inhibited 86Rb uptake.
N-acetyl-L-cysteine, diphenyleneiodonium, and
tetramethylpiperidine-N-oxyl, used to reduce ROS, inhibited
86Rb uptake, thus mimicking the hypoxic effects, whereas
deferoxamine, superoxide dismutase, and catalase were ineffective.
Also, hypoxic effects on ion transport were not prevented in the
presence of H2O2, diethyldithiocarbamate, and
N-acetyl-L-cysteine. These results indicate that
ion transport of A549 cells is significantly affected by decreasing or
increasing cellular ROS levels and that it is possible that certain
species of ROS might mediate the hypoxic effects on ion transport of
alveolar epithelial cells.
cation transport; sodium/potassium pump; sodium/potassium/2 chloride cotransport; hyperoxia; reactive oxygen species; superoxide anion; A549 cells; oxygen sensing; pulmonary edema
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