Ann Clin Biochem 2008;45:508-512
doi:10.1258/acb.2008.008030
© 2008 Association for Clinical Biochemistry
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Original Articles
Afaf M Hassan
South Manchester University Hospital, South Moor Road, Wythenshawe, Manchester M23 9LT, UK
Corresponding author: Afaf M Hassan. Email: afaf.hassan{at}smuht.nwest.nhs.uk
Background: Platelets are involved in the pathogenesis of aspirin-inducedasthma (AIA). AIA patients suffer from an active disease despiteavoidance of aspirin, and it has been suggested that administrationof aspirin to these patients increases the generation of immediateoxygen products of arachidonic acid, 12-hydroperoxyeicosatetraenoicacid (12-HPETE), in their platelets. 12-HPETE further activatesthe 5-lipoxygenase of leukotriene B4-producing inflammatorymacrophages precipitating an acute asthmatic attack. Glutathioneperoxidase (GPX) has the antioxidant capacity to reduce 12-HPETE,and thus modulate the arachidonic acid metabolic cascade. Thereis evidence that selenium (Se) nutrition can influence asthmabut Se status in AIA patients has not received much attention.
Methods: We measured Se concentrations and GPX activities in plateletsand plasma from 13 patients with AIA. Age- and sex-matched healthyindividuals served as the control group.
Results: Patients with AIA had significantly higher median platelet Se concentration (102 ng/mg platelet protein) when compared with controls (49 ng/mg platelet protein, P = 0.003). Plasma Se concentrations in patients with AIA and controls were not significantly different (P = 0.59). Median platelet GPX activity was significantly higher in patients with AIA (102.7 mU/mg platelet protein) than in controls (66 mU/mg protein) (P = 0.05). The patient and control groups when combined showed weak, but significant correlation between platelet Se concentration and platelet GPX activity (r = 0.44; P = 0.03).
Conclusion: It is proposed that the higher platelet Se concentration observedin AIA patients contributed to the higher platelet GPX activityseen in these patients. Such an enhanced antioxidant defencesystem might represent an adaptive response to protect againstincreasing free radical production by inflammatory cells inAIA and help decelerate ongoing respiratory hypersensitivity.
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