Influences of dietary selenium (Se) deficiency, physical training and an acute bout of exercise on myocardial antioxidant enzyme activity, lipid peroxidation and related biochemical properties were investigated in post-weanling male Sprague- Dawley rats. An experimental group was fed a diet containing <0.01 mg Se/kg and had free access to distilled water (Se- D), whereas control rats were supplemented with 0.5 mg Se/1 in drinking water (Se-A). Se deficiency depleted heart mitochondrial and cytosolic Se-dependent glutathione peroxidase activity to 24 and 3%, respectively, of those in Se-A rats. Heart mitochondrial superoxide dismutase (Mn SOD) activity was 24% higher (p < 0.05) in Se-D than in Se-A rats. Cytosolic (copper-zinc) SOD and catalase activities were not altered, whereas glutathione S-transferase activity was significantly decreased in Se-D (p < 0.01). Myocardial antioxidant enzyme activities were not affected by either training or an acute exercise bout. Heart lipid peroxidation and activities of several enzymes in substrate metabolism were also unaffected by Se or exercise. It is concluded that rat heart has sufficient reserve of antioxidant enzyme capacity in coping with oxidative stress imposed by Se deficiency or exercise. The adaptation of Mn SOD may reveal its potential role in myocardial antioxidant defense. Abbreviations: ANOVA = analysis of variance; CS = citrate synthase; Cu = copper; GPX = glutathione peroxidase; GST = glutathione S-transferase; LDH = lactate dehydrogenase; MDA = malondialdehyde; MDH = malate dehydrogenase; Mn SOD = manganese superoxide dismutase; PFK = phosphofructoki- nase; Se = selenium; Se-A = selenium-adequate controls; Se-D = selenium- deficient group; SOD = superoxide dismutase; VO2 max = maximal oxygen consumption; Zn = zinc.
Bibliographical noteFunding Information:
Supported in part by a grant from the American Heart Association (Illinois affiliate) and by grant AM 10,334 from the National Institutes of Health. We thank Ms.
- Antioxidant enzyme