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Am J Physiol Lung Cell Mol Physiol 280: L1212-L1217, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 6, L1212-L1217, June 2001

Rat lung peroxiredoxins I and II are differentially regulated during development and by hyperoxia

Han-Suk Kim1, Sang Won Kang2, Sue Goo Rhee2, and Linda Biadasz Clerch1

1 Lung Biology Laboratory, Georgetown University Medical Center, Washington, District of Columbia 20007; and 2 Laboratory of Cell Signaling, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892

Peroxiredoxin I (Prx I) and peroxiredoxin II (Prx II) are found in abundance in the cytoplasm of cells and catalyze the reduction of hydrogen peroxide with the use of electrons provided by thioredoxin. Here we examined Prx I and Prx II expression in rat lung during perinatal development and in response to hyperoxia. Prx I protein increased during late gestation and after birth fell to adult levels; conversely, Prx I mRNA increased after birth. Prx II protein concentration was unchanged in the perinatal period, but Prx II mRNA increased after birth. In response to hyperoxia begun on postnatal day 4, there was no change in Prx II expression; however, Prx I mRNA, protein, and enzymatic activity increased significantly. These data show that 1) Prx I and Prx II are developmentally regulated at the level of translational efficiency and 2) Prx I, but not Prx II, is inducible and is upregulated during the late-gestational preparation for the oxidative stress experienced by the lung at birth and during exposure to hyperoxia in the neonatal period.

antioxidant enzyme; thioredoxin peroxidase; thiol-specific antioxidant; perinatal development


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