Selenium levels and glutathione peroxidase activities in patients with acute myocardial infarction

Abstract

Objective: Selenium (Se) is part of the enzyme glutathione peroxidase (GSH-Px) that plays an important role in the antioxidant defence of the body, including the myocardium, against the deleterious actions of free radicals and lipid peroxides. In order to evaluate the Se status and the GSH-Px activity in ischaemic heart disease, plasma, erythrocyte and urinary Se concentrations together with plasma and erythrocyte GSH-Px activities were determined in 27 patients diagnosed as acute myocardial infarction (AMI). The control group consisted of 24 age-matched healthy individuals.

Methods and results: Fasting blood and urine samples were collected within 24 hours after the onset of chest pain. Mean plasma, erythrocyte and urine Se concentrations were significantly lower in the patient groups (63.7 +/- 12 micrograms/l, 0.48 +/- 0.04 microgram/g Hb and 49.6 +/- 27.7 micrograms/g creatinine, respectively), compared to controls (82.2 +/- 14.6 micrograms/l, 0.51 +/- 0.03 microgram/g Hb and 93.4 +/- 62.6 micrograms/g creatinine, p < 0.001, p < 0.02 and p < 0.003, respectively). No statistically significant difference was found between mean plasma GSH-Px activity in patients (0.36 +/- 0.1 U/ml) and controls (0.35 +/- 0.09 U/ml), whereas erythrocyte GSH-Px activity was higher in patients (48.1 +/- 10.2 U/g Hb) than in the controls (35.3 +/- 9.1 U/g Hb, p < 0.001).

Conclusion: Our findings confirm the previous studies and demonstrate that patients suffering from AMI exhibit lower plasma, erythrocyte and urinary Se than the controls. Since the erythrocyte Se level represents a measure of the Se status over a period of several weeks due to its long biological half-life, low Se levels observed in the patient group might have been present before the acute event, thereby suggesting an aetiologic relevance. The presence of increased erythrocyte GSH-Px activity in these patients may be interpreted as an antioxidant defence against the chronic oxidant stress present before the AMI, presumably due to the process of coronary atherosclerosis.