Discordant extracellular superoxide dismutase expression and activity in neonatal hyperoxic lung.


Journal Article

Antioxidant defenses in the neonatal lung are required to adapt to the oxygen (O(2))-rich postnatal environment, and oxidant/antioxidant imbalance is a predisposition to lung injury when high concentrations of inspired O(2) 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 a doubling of lung EC-SOD protein in newborn rats exposed to 95% O(2) for 1 week. Furthermore, EC-SOD protein secretion increased, but EC-SOD enzyme activity did not change with O(2) 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 O(2) showed strong increases in protein nitrotyrosine and variable, nonsignificant 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 O(2)-exposed neonatal lung.

Full Text

Duke Authors

Cited Authors

  • Mamo, LB; Suliman, HB; Giles, B-L; Auten, RL; Piantadosi, CA; Nozik-Grayck, E

Published Date

  • August 1, 2004

Published In

Volume / Issue

  • 170 / 3

Start / End Page

  • 313 - 318

PubMed ID

  • 15117745

Pubmed Central ID

  • 15117745

International Standard Serial Number (ISSN)

  • 1073-449X

Digital Object Identifier (DOI)

  • 10.1164/rccm.200309-1282OC


  • eng

Conference Location

  • United States