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Published ahead of print on October 1, 2004, doi:10.1164/rccm.200311-1516OC

Am. J. Respir. Crit. Care Med., Volume 170, Number 12, December 2004, 1317-1323

A more recent version of this article appeared on December 15, 2004
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Submitted on November 7, 2003
Accepted on September 27, 2004

Myeloperoxidase and Protein Oxidation in the Airways of Young Children with Cystic Fibrosis

Anthony J Kettle1*, Timothy Chan1, Iris Osberg2, Revathy Senthilmohan1, Anna LP Chapman1, Tessa J Mocatta1, and Jeffrey S Wagener2

1 Department of Pathology, Free Radical Research Group, Christchurch School of Medicine and Health Sciences, Christchurch, New Zealand, 2 Department of Pediatrics, University of Colorado Health Science Center and Children's Hospital, Denver, CO, USA

* To whom correspondence should be addressed. E-mail: tony.kettle{at}chmeds.ac.nz.

Cystic fibrosis is characterised by considerable oxidative stress. However, it is not known whether oxidative stress is an important feature early in this disease. We have investigated a group of infants and young children with cystic fibrosis to establish whether oxidants are produced in their airways. Bronchoalveolar lavage fluid (BALF) was assayed for myeloperoxidase as a measure of neutrophilic inflammation, and 3-chlorotyrosine as a biomarker of the potent oxidant hypochlorous acid, which is formed by myeloperoxidase. Protein carbonyls were also measured as a non-specific indicator of reactive oxidant production. Myeloperoxidase and 3-chlorotyrosine levels in BALF from children with cystic fibrosis were 10 and five-fold higher than in disease controls. There was a strong correlation between myeloperoxidase and 3-chlorotyrosine. Myeloperoxidase levels were four-fold higher in children with infections in their airways. Median protein carbonyls were elevated by only two-fold compared to disease controls but some children had extremely high levels of protein oxidation. We conclude that hypochlorous acid is produced early in cystic fibrosis and that it is a candidate for precipitating the fatal decline in lung function associated with this disease. Also, there must be other sources of oxidants because protein carbonyls were not related to either inflammation or infection.
Key words: neutrophil, myeloperoxidase, hypochlorous acid, protein carbonyl, and oxidative stress




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