L. A. Fletcher

Exercise training reduces myocardial lipid peroxidation following short-term ischemia-reperfusion

PURPOSE The purpose of these experiments was to test the hypothesis that endurance exercise training will reduce myocardial lipid peroxidation following short-term ischemia and reperfusion (I-R). METHODS Female Sprague-Dawley rats (4 months old) were randomly assigned to either a sedentary control group (N = 13) or to an exercise training group (N = 13). The exercise trained animals ran 4 d.wk-1 (90 min.d-1) at approximately 75% V02max. Following a 10-wk training program, animals were anesthetized, mechanically ventilated, and the chest was opened by thoracotomy. Coronary occlusion was achieved by a ligature around the left coronary artery; occlusion was maintained for 5 min followed by a 10-min period of reperfusion. RESULTS Although training did not alter (P > 0.05) myocardial activities of antioxidant enzymes (superoxide dismutase and glutathione peroxidase), training was associated with significant increase (P > 0.05) in heat shock protein (HSP72) in the left ventricle. Compared with controls, trained animals exhibited significantly lower levels (P < 0.05) of myocardial lipid peroxidation following I-R. CONCLUSION These data support the hypothesis that exercise training provides protection against myocardial lipid peroxidation induced by short-term I-R in vivo.

Cyclosporine A induced changes to plasma and erythrocyte antioxidant defences

Abstract Organ transplant recipients develop pronounced cardiovascular disease, and decreased antioxidant capacity in plasma and erythrocytes is associated with the pathogenesis of this disease. These experiments tested the hypothesis that the immunosuppressant cyclosporine A (CsA) alters erythrocyte redox balance and reduces plasma antioxidant capacity. Female Sprague-Dawley rats were randomly assigned to a control or CsA treated group. Treatment animals received 25 mg/kg/day of CsA via intraperitoneal injection for 18 days. Control rats were injected with the same volume of the vehicle. Three hours after the final CsA injection, rats were exsanguinated and plasma analysed for total antioxidant status (TAS), α-tocopherol, malondialdehyde (MDA), and creatinine. Erythrocytes were analysed for superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and glucose-6-phosphate dehydrogenase (G6PD) activities, α-tocopherol, and MDA. CsA administration resulted in a significant (P < 0.05) decrease in plasma TAS and significant increases (P < 0.05) in plasma creatinine and MDA. Erythrocyte CAT was significantly (P < 0.05) increased in CsA treated rats compared to controls. There were no significant differences (P > 0.05) in erythrocyte SOD, GPX, G6PD, α-tocopherol or MDA between groups. In summary, CsA alters erythrocyte antioxidant defence and decreases plasma total antioxidant capacity.