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Protective Effects of Heme Oxygenase-1 in Acute Lung Injury*

Leo E. Otterbein; Patty J. Lee, MD; Beek Yoke Chin; Irina Petrache, MD; Sharon L. Camhi, MD; Jawed Alam, PhD; Augustine M. K. Choi, MD
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*From the Division of Pulmonary and Critical Care Medicine (Drs. Otterbein, Chin, and Petrache), The Johns Hopkins University School of Medicine, Baltimore, MD; Department of Molecular Genetics (Dr. Alam), Alton Ochsner Medical Foundation and Department of Biochemistry and Molecular Biology, Louisiana State University Medical Center, New Orleans, LA; Section of Pulmonary and Critical Care Medicine (Drs. Otterbein, Lee, Chin, and Choi), Yale University School of Medicine, New Haven, CT, and Connecticut VACHS, West Haven, CT; and Division of Pulmonary and Critical Care Medicine (Dr. Camhi), University of Arizona, Tucson, AZ.

Correspondence to: Augustine M.K. Choi, MD, Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, 333 Cedar St, LCI 105, New Haven, CT 06520; e-mail: augustine.choi@yale.edu



Chest. 1999;116(suppl_1):61S-63S. doi:10.1378/chest.116.suppl_1.61S-a
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Heme oxygenase (HO) catalyzes the first and rate-limiting step in the oxidative degradation of heme to bilirubin12(Fig 1). The binding of HO with the heme molecule leads to the cleavage of a meso carbon bond and results in the production of biliverdin, which is subsequently converted to bilirubin by biliverdin reductase.12 Three isoforms of HO exist; HO-1 is highly inducible, while HO-2 and HO-3 are constitutively expressed.12 Although heme is the major substrate of HO-1, a variety of nonheme products, including heavy metals, cytokines, hormones, endotoxin, and heat shock, are also strong inducers of HO-1 expression.1 In addition, HO-1 is highly induced by a variety of agents causing oxidative stress, including hydrogen peroxide, glutathione depletors, ultraviolet irradiation, endotoxin, and hyperoxia.1,34 This diversity of HO-1 inducers has provided further support for the speculation that HO-1, besides its role in heme degradation, may also serve to play a vital function in maintaining cellular homeostasis. We will review some of the experimental data that support the evolving paradigm that the stress inducible gene HO-1 plays an important functional role in the lung and host’s defense against oxidant-induced lung injury.


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