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Oxidative Medicine and Cellular Longevity
Volume 2015 (2015), Article ID 429713, 7 pages
Research Article

Endogenous Estrogen-Mediated Heme Oxygenase Regulation in Experimental Menopause

1Department of Physiology, Anatomy and Neuroscience, Faculty of Science and Informatics, University of Szeged, Kozep Fasor 52, Szeged 6726, Hungary
2Faculty of Dentistry and Department of Orthodontics and Pediatric Dentistry, University of Szeged, Szeged 6720, Hungary
3Department of Cardiology, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria

Received 25 April 2014; Accepted 4 July 2014

Academic Editor: Narasimham L. Parinandi

Copyright © 2015 Anikó Pósa et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Estrogen deficiency is one of the main causes of age-associated diseases in the cardiovascular system. Female Wistar rats were divided into four experimental groups: pharmacologically ovariectomized, surgically ovariectomized, and 24-month-old intact aging animals were compared with a control group. The activity and expression of heme oxygenases (HO) in the cardiac left ventricle, the concentrations of cardiac interleukin-6 (IL-6) and tumor necrosis factor- (TNF-), the myeloperoxidase (MPO) activity in the cardiac left ventricle, and the effects of heme oxygenase blockade (by 24-hour and 1-hour pretreatment with tin-protoporphyrin IX, SnPP) on the epinephrine and phentolamine-induced electrocardiogram ST segment changes in vivo were investigated. The cardiac HO activity and the expression of HO-1 and HO-2 were significantly decreased in the aged rats and after ovariectomy. Estrogen depletion was accompanied by significant increases in the expression of IL-6 and TNF-. The aged and ovariectomized animals exhibited a significantly elevated MPO activity and a significant ST segment depression. After pretreatment with SnPP augmented ST segment changes were determined. These findings demonstrate that the sensitivity to cardiac ischemia in estrogen depletion models is associated with suppression of the activity and expression of the HO system and increases in the secretion of proinflammatory cytokines and biomarkers.