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and NF-
B in
perinatal lung epithelium requires glutathione
biosynthesis
Oxygen Signalling Group, Tayside Institute of Child Health, Ninewells Hospital and Medical School, University of Dundee, Dundee DD1 9SY, United Kingdom
To test the genetic
capacity of the perinatal lung to respond to O2 shifts that
coincide with the first respiratory movements, rat fetal alveolar type
II (fATII) epithelial cells were cultured at fetal distal lung
PO2 (23 Torr) and then exposed to postnatal (23 
76 Torr; mild hyperoxic shift), moderate (23 152 Torr; moderate hyperoxic shift), or severe (23 722 Torr; severe hyperoxic shift) oxygenation. Nuclear abundance and
consensus binding characteristics of hypoxia-inducible factor
(HIF)-1
and nuclear factor (NF)-
B (Rel A/p65) plus glutathione
biosynthetic capacity were determined. Maximal HIF-1 activation at
23 Torr was sustained over the postnatal shift in (
)
PO2 and was elevated in vivo
throughout late gestation. NF-B was activated by the acute postnatal
PO2 in fATII cells, becoming maximal with moderate and severe oxygenation in vitro and within 6 h of
birth in vivo, declining thereafter. fATII cell and whole lung
glutathione and GSH-to-GSSG ratio increased fourfold with a postnatal
PO2 and were matched by threefold
activity increases in 
-glutamylcysteine synthetase and glutathione
synthase. GSH concentration depletion by
L-buthionine-(S,R)-sulfoximine abrogated both
HIF-1 and NF-B activation, with HIF-1 showing a heightened
sensitivity to GSH concentration. We conclude that O2-linked genetic regulation in perinatal lung epithelium
is responsive to developmental changes in glutathione biosynthetic capacity.
hypoxia-inducible factor-1; nuclear factor-B; lung
development; L-buthionine-(S,R)-sulfoximine; transcription factor; antioxidant; bronchopulmonary
dysplasia
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