HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (26) Citing Articles via Google Scholar Google Scholar Articles by Kim, H.-S. Articles by Fisher, A. B. Search for Related Content PubMed PubMed Citation Articles by Kim, H.-S. Articles by Fisher, A. B.

Induction of 1-cys peroxiredoxin expression by oxidative stress in lung epithelial cells

¹Institute for Environmental Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104; and ²Institute of Chemical Toxicology, Wayne State University, Detroit, Michigan 48202

Submitted 17 March 2003 ; accepted in final form 4 April 2003

1-Cys peroxiredoxin (1-cysPrx), a member of the peroxiredoxin family that contains a single conserved cysteine residue, reduces a broad spectrum of hydroperoxides. We studied changes in 1-cysPrx expression in rat lungs and lung cell lines in response to oxidative stress due to hyperoxia, H₂O₂, or paraquat. After 60 h of hyperoxia (>95% O₂), mRNA and protein levels of 1-cysPrx and peroxidase activity were significantly elevated in rat lungs by 1.5- to 2-fold compared with the control (P < 0.05). A similar induction of 1-cysPrx was observed in mouse lungs following exposure to O₂ for 63 or 72 h; enzyme induction in mouse lungs was similar for wild-type and glutathione peroxidase 1 gene-targeted mice. H₂O₂ and paraquat treatment induced 1-cysPrx gene expression in L2 cells. Enzyme induction was attenuated by pretreatment with Trolox or N-acetylcysteine. Actinomycin D treatment showed that stability of 1-cysPrx mRNA was not altered in the presence of H₂O₂ or paraquat, indicating that increased expression with oxidative stress is regulated at the transcriptional level. These data indicate that the antioxidant enzyme 1-cysPrx is induced in lung cells by oxidative stress.

antioxidant enzyme; reactive oxygen species; gene regulation; lung injury

This article has been cited by other articles:

				N. Nagy, G. Malik, A. B. Fisher, and D. K. Das Targeted disruption of peroxiredoxin 6 gene renders the heart vulnerable to ischemia-reperfusion injury Am J Physiol Heart Circ Physiol, December 1, 2006; 291(6): H2636 - H2640. [Abstract] [Full Text] [PDF]

				Y. Wang, S. A. Phelan, Y. Manevich, S. I. Feinstein, and A. B. Fisher Transgenic Mice Overexpressing Peroxiredoxin 6 Show Increased Resistance to Lung Injury in Hyperoxia Am. J. Respir. Cell Mol. Biol., April 1, 2006; 34(4): 481 - 486. [Abstract] [Full Text] [PDF]

				S. T. Lehtonen, P. M. H. Markkanen, M. Peltoniemi, S. W. Kang, and V. L. Kinnula Variable overoxidation of peroxiredoxins in human lung cells in severe oxidative stress Am J Physiol Lung Cell Mol Physiol, May 1, 2005; 288(5): L997 - L1001. [Abstract] [Full Text] [PDF]

				G. Leyens, B. Verhaeghe, M. Landtmeters, J. Marchandise, B. Knoops, and I. Donnay Peroxiredoxin 6 Is Upregulated in Bovine Oocytes and Cumulus Cells During In Vitro Maturation: Role of Intercellular Communication Biol Reprod, November 1, 2004; 71(5): 1646 - 1651. [Abstract] [Full Text] [PDF]

				Y. Wang, Y. Manevich, S. I. Feinstein, and A. B. Fisher Adenovirus-mediated transfer of the 1-cys peroxiredoxin gene to mouse lung protects against hyperoxic injury Am J Physiol Lung Cell Mol Physiol, June 1, 2004; 286(6): L1188 - L1193. [Abstract] [Full Text] [PDF]