UMMS Affiliation

Department of Pediatrics

Date

11-2004

Document Type

Article

Medical Subject Headings

Adolescent; Asthma; Biological Markers; Case-Control Studies; Child; Chronic Disease; Female; Glutathione Peroxidase; Granulocytes; Humans; Male; Monocytes; Superoxide Dismutase; Time Factors

Disciplines

Hematology | Oncology | Pediatrics

Abstract

Asthma is an inflammatory condition characterized by the involvement of several mediators, including reactive oxygen species. The aim of the present study was to investigate the superoxide release and cellular glutathione peroxidase (cGPx) activity in peripheral blood granulocytes and monocytes from children and adolescents with atopic asthma. Forty-four patients were selected and classified as having intermittent or persistent asthma (mild, moderate or severe). The spontaneous or phorbol myristate acetate (PMA, 30 nM)-induced superoxide release by granulocytes and monocytes was determined at 0, 5, 15, and 25 min. cGPx activity was assayed spectrophotometrically. The spontaneous superoxide release by granulocytes from patients with mild (N = 15), moderate (N = 12) or severe (N = 6) asthma was higher at 25 min compared to healthy individuals (N = 28, P andlt; 0.05, Duncan test). The PMA-induced superoxide release by granulocytes from patients with moderate (N = 12) or severe (N = 6) asthma was higher at 15 and 25 min compared to healthy individuals (N = 28, P andlt; 0.05 in both times of incubation, Duncan test). The spontaneous or PMA-induced superoxide release by monocytes from asthmatic patients was similar to healthy individuals (P > 0.05 in all times of incubation, Duncan test). cGPx activity of granulocytes and monocytes from patients with persistent asthma (N = 20) was also similar to healthy individuals (N = 10, P > 0.05, Kruskal-Wallis test). We conclude that, under specific circumstances, granulocytes from children with persistent asthma present a higher respiratory burst activity compared to healthy individuals. These findings indicate a risk of oxidative stress, phagocyte auto-oxidation, and the subsequent release of intracellular toxic oxidants and enzymes, leading to additional inflammation and lung damage in asthmatic children.

Comments

Citation: Braz J Med Biol Res. 2004 Nov;37(11):1607-13. Epub 2004 Oct 26. doi: 10.1590/S0100-879X2004001100003. Link to article on publisher's site

All the contents of this journal, except where otherwise noted, are licensed under a Creative Commons Attribution License, http://creativecommons.org/licenses/by-nc/3.0/

Related Resources

Link to article in PubMed

PubMed ID

15517074

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