Related Experiment Videos
Reduced platelet glutathione peroxidase activity and serum selenium concentration in atopic asthmatic patients
N L Misso1, K A Powers, R L Gillon
1Department of Medicine, University of Western Australia, Queen Elizabeth II Medical Centre, Perth, Australia.
Background:
Asthmatic inflammation results in increased oxygen free radical generation and assessment of the activity of the selenium (Se) dependent anti-oxidant enzyme, glutathione peroxidase (GSH-Px) in asthma may therefore be important.
Objective:
To test the hypothesis that reduced GSH-Px activity and Se intake contribute to asthmatic inflammation, platelet and whole blood GSH-Px activities and serum and whole blood Se concentrations were measured and compared in atopic and non-atopic asthmatic patients and non-asthmatic control subjects.
Methods:
GSH-Px activities of whole blood and isolated platelets were assessed in 41 asthmatic patients (33 atopic) and 41 age- and sex-matched non-asthmatic subjects (15 atopic) by spectrophotometric assay based on the oxidation of NADPH. Se concentrations were determined by semi-automated fluorimetric assay.
Results:
Mean (+/-SD) platelet GSH-Px activity was lower in asthmatic (89.5 +/- 45.7 mumol NADPH oxidized min-1 g-1 of protein) than in non-asthmatic subjects (109.9 +/- 41.9; P = 0.038) and in atopic (89.7 +/- 45.1, n = 48) compared with non-atopic subjects (113.7 +/- 40.9, n = 34; P = 0.016). Mean whole blood GSH-Px activity was also lower in atopic (12.2 +/- 5.2 mumol NADPH oxidized min-1 g-1 of Hb) than in non-atopic subjects (14.5 +/- 4.2; P = 0.038). In non-asthmatic subjects, the mean whole blood GSH-Px activity was lower in men (9.9 +/- 3.5) than in women (14.5 +/- 3.7; P = 0.0004) and was positively correlated with age (r = 0.51; P = 0.0006). Mean serum Se was lower in asthmatic (1.07 +/- 0.12 mumol/L) than in non-asthmatic subjects (1.16 +/- 0.31; P = 0.036). Using multiple linear regression, asthma was an independent predictor of decreased platelet GSH-Px after gender, age and serum Se were taken into account (P = 0.048) while atopy was a significant predictor of low whole blood GSH-Px independent of asthma, gender, age and whole blood Se (P = 0.033).
Conclusions:
In addition to Se status, atopy, gender and age all appear to influence GSH-Px activity, although the relative importance of these factors may differ in asthmatic and non-asthmatic populations. It seems likely that the reduced activity of this enzyme in platelets and blood may reflect mechanisms associated with the pathogenesis and severity of asthma.