Carvedilol Increases Copper-Zinc Superoxide Dismutase Activity in Patients with Acute Myocardial Infarction
Authors: Kastratović, Dragana A.1; Vasiljević, Zorana M.2; Spasić, Mihajlo B.3; Perunicić, Jovan P.2; Matić, Mihajlo2; Blagojević, Dusko P.3; Mijalković, Dejan N.3; Antonijević, Nebojsa M.2; Marković, Srdjan Z.4; Gojković-Bukarica, Ljiljana5; Stojiljkovic, Milos P.6; Lasica, Ratko M.2; Jones, David R.3; Nikolić-Kokić, Aleksandra L.3
Source: Basic & Clinical Pharmacology & Toxicology, Volume 101, Number 2, August 2007 , pp. 138-142(5)
Publisher: Blackwell Publishing
Abstract:
: Balanced and coordinated antioxidant defence enzyme activities are of utmost importance for correct physiological function and for shielding against unwelcome pathological conditions. We determined the activities of copper-zinc superoxide dismutase (CuZnSOD), catalase, glutathione peroxidase and glutathione reductase in erythrocytes isolated from patients receiving different therapy (streptokinase alone or in combination with metoprolol or with carvedilol) for up to 168 hr after starting treatment for acute myocardial infarction. We observed increased CuZnSOD activity in erythrocytes isolated from patients treated with streptokinase-carvedilol (after 6, 24 and 168 hr) and in erythrocytes isolated from patients treated with streptokinase-metoprolol (after 24 hr). In addition, positive correlation between CuZnSOD and catalase activities was found in erythrocytes isolated from patients that received streptokinase-carvedilol after 168 hr. As metoprolol does not react directly with hydrogen peroxide, it would appear that combined streptokinase-metoprolol therapy exerted its effects primarily via by β-blockade whereas combined streptokinase-carvedilol therapy appeared to function via both β-blockade and direct antioxidant mechanisms.Document Type: Research article
DOI: 10.1111/j.1742-7843.2007.00094.x
Affiliations: 1: Centre for Clinical Pharmacology, Clinical Centre of Serbia, Belgrade, 2: Coronary Unit, Institute for Cardiovascular Diseases, Clinical Centre of Serbia, Belgrade, 3: Department of Physiology, Institute for Biological Research `Siniša Stankovič', Belgrade, 4: Students Research Group, Medical Faculty University of Belgrade, Belgrade, 5: Institute for Pharmacology, Medical faculty University of Belgrade, Belgrade, and 6: Actavis Trading Ltd., Belgrade Representative Office, Belgrade, Serbia

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