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Articles in PresS, published online ahead of print April 19, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00018.2002
Submitted on January 15, 2002
Accepted on April 12, 2002
1 Pediatrics, University of Manitoba, Winnipeg, Manitoba, Canada
2 Medicine, Duke University Medical Center, Durham, NC, USA
3 Pediatrics, Duke University Medical Center, Durham, NC, USA
4 Pathology, University of Pittsburgh, Pittsburgh, PA, USA
* To whom correspondence should be addressed. E-mail: grayc001{at}mc.duke.edu.
Extracellular superoxide dismutase (EC-SOD), which scavenges extracellular superoxide (.O2-) is highly regulated in the developing lung. In the prenatal rabbit, EC-SOD is predominantly intracellular and inactive, and postnatally, active EC-SOD is secreted. We hypothesized that prenatal hypoxia would delay the normal postnatal secretion of active EC-SOD in the lung. Pregnant NZ rabbits were exposed to hypobaric hypoxia (15,000 ft x 36 hours) to alter fetal O2 tension or maintained in room air. Lungs were harvested from preterm (28 days), term (30 ± 1 days) and week old kits. Following prenatal hypobaric hypoxia, EC-SOD mRNA expression was significantly decreased in lungs of full term kits while EC-SOD protein decreased at all ages. Immunohistochemical staining for EC-SOD showed that hypoxia delayed secretion of the isoenzyme in the airways and pulmonary vasculature. Furthermore, pulmonary EC-SOD enzyme activity was significantly decreased in the one week old kits exposed to prenatal hypoxia. We conclude that prenatal hypoxia down-regulates EC-SOD expression at both the transcriptional and post-translational levels. Furthermore, prenatal hypoxia delays secretion of active EC-SOD enzyme. These findings have important implications for the effects of prenatal asphyxia on post-natal response to oxidant stress.
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