Superoxide production by peripheral polymorphonuclear leukocytes in patients with COPD
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Updated: Sep 26, 2026

Fast and Specific Assessment of the Halogenating Peroxidase Activity in Leukocyte-enriched Blood Samples
Published on: July 28, 2016
W J C van Beurden1, P L M L Wielders, P J T Scheepers
1Department of Pulmonary Diseases, Catharina Hospital, Eindhoven, The Netherlands. wendy@beurdenvan.myweb.nl
Abstract:
Polymorphonuclear leukocytes (PMNs) have been implicated in the pathogenesis of COPD, partly because of the release of oxidants, like superoxide anion (SA). The goal of this study was to measure the spontaneous and stimulated release of SA by peripheral PMN in stable COPD compared with healthy controls. Seventeen patients with stable moderate COPD and 17 healthy age-matched controls were included. SA release from peripheral PMN was measured spectrophotometrically as the superoxide dismutase (SOD) inhibitable reduction of cytochrome c. PMNs were stimulated with phorbol myristate acetate (PMA, 1 and 10 ng/ml), diesel exhaust particles (DEPs), carbon black (CB) and ultrafine CB (ufCB, 125, 250 and 500 microg/ml). The spontaneous SA release (PMA-0) between patients and control subjects was not significantly different. After stimulation with PMA, SA release increased in both patients and controls. The SA release did not increase after stimulation with DEP and CB in patients nor in controls. There was only an increase after stimulation with ufCB in the patient group. The increased SA release in COPD patients after stimulation with ufCB may suggest that PMN of COPD patients are more prone to stimulation and that the smaller particle size of ufCB might be a crucial factor.
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