Does the Oxidative Stress in Chronic Obstructive Pulmonary Disease Cause Thioredoxin/Peroxiredoxin Oxidation?

Department of Internal Medicine, University of Oulu and Oulu University Hospital, Oulu, Finland.
Antioxidants and Redox Signaling (Impact Factor: 7.41). 05/2008; 10(4):813-9. DOI: 10.1089/ars.2007.1952
Source: PubMed

ABSTRACT The thioredoxin/peroxiredoxin system comprises a redox-regulated antioxidant family in human lung; its significance, regulation, or oxidation has not been evaluated in smoking-related lung diseases. Here, we present the expression of the thioredoxin/peroxiredoxin system in lung biopsies from normal lung (n = 14), smokers (n = 21), and patients with chronic obstructive pulmonary disease (COPD, n = 38), and assess the possible inactivation/oxidation of this system by nonreducing Western blotting, two-dimensional gel electrophoresis, and mass spectrometry. Our study shows that the thiol status of the Trx/Prx-system can be modulated in vitro, but it appears to have high resistance against the oxidative stress in COPD.

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    • "Also implicated in bacterial survival in the lung was the pgdX gene encoding a hybrid peroxiredoxin/thioredoxin glutathione-dependent peroxidase (Pauwels et al., 2003). Peroxiredoxin and thioredoxin are ubiquitous anti-oxidant enzymes present in all known organisms and have been implicated in defense against reactive oxygen species in bacteria (Zeller and Klug, 2006) and in mammalian airways (Rahman et al., 2006; Lehtonen et al., 2008). "
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