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Published ahead of print on April 29, 2004, doi:10.1164/rccm.200309-1282OC

Am. J. Respir. Crit. Care Med., Volume 170, Number 3, August 2004, 313-318

A more recent version of this article appeared on August 1, 2004
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Submitted on September 15, 2003
Accepted on April 25, 2004

Discordant Extracellular Superoxide Dismutase Expression and Activity in Neonatal Hyperoxic Lungs

Lisa B Mamo1, Hagir B Suliman2, Brenda-Louise Giles3, Richard L Auten1, Claude A Piantadosi2, and Eva Nozik-Grayck1*

1 Department of Pediatrics, Duke University Medical Center, Durham, NC, USA, 2 Department of Medicine, Duke University Medical Center, Durham, NC, USA, 3 Department of Pediatrics, Manitoba Institute of Child Health and University of Manitoba, Winnipeg, Manitoba, Canada

* To whom correspondence should be addressed. E-mail: grayc001{at}mc.duke.edu.

Antioxidant defenses in the neonatal lung are required to adapt to the oxygen (O2)-rich post-natal environment, and oxidant/antioxidant imbalance predisposes to lung injury when high inspired O2 concentrations are used in neonatal lung diseases. The lung's main extracellular enzymatic defense against superoxide, extracellular superoxide dismutase (EC-SOD), is closely regulated during development. In testing the hypothesis that developmental change in EC-SOD expression and activity in the immature lung would be disrupted by hyperoxia we found doubling of lung EC-SOD protein in newborn rats exposed to 95% O2 for 1 week. Furthermore, EC-SOD protein secretion increased but EC-SOD enzyme activity did not change with O2 exposure. EC-SOD mRNA did not change at multiple points between 6 hours and 8 days. Lung EC-SOD recovered by immunoprecipitation after 1 week of O2 showed strong increases in protein nitrotyrosine and variable, non-significant differences in protein carbonyl content. These data provide the first direct evidence that EC-SOD is itself a target of nitration in hyperoxia, and offer a plausible explanation for low EC-SOD activity despite its increased secretion by O2-exposed neonatal lung.
Key words: nitrotyrosine, protein carbonyl, antioxidant, oxygen




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