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Oxidative Medicine and Cellular Longevity - Volume 2016 2016, Article ID 8470394, 12 pages -

Research Article

Department of Pathophysiology -Victor Babeș- University of Medicine and Pharmacy, 2 Eftimie Murgu Square, 300041 Timișoara, Romania

Center for Translational Research and Systems Medicine -Victor Babeș- University of Medicine and Pharmacy, 2 Eftimie Murgu Square, 300041 Timișoara, Romania

Department of Parasitology -Victor Babeș- University of Medicine and Pharmacy, 2 Eftimie Murgu Square, 300041 Timișoara, Romania

Department of Histology -Victor Babeș- University of Medicine and Pharmacy, 2 Eftimie Murgu Square, 300041 Timișoara, Romania

Department of Morphopathology -Victor Babeș- University of Medicine and Pharmacy, 2 Eftimie Murgu Square, 300041 Timișoara, Romania

Department of Cardiovascular Surgery -Victor Babeș- University of Medicine and Pharmacy, 2 Eftimie Murgu Square, 300041 Timișoara, Romania

Department of Cardiology, 2nd Cardiology Clinic -Victor Babeș- University of Medicine and Pharmacy, 2 Eftimie Murgu Square, 300041 Timișoara, Romania

Received 25 September 2015; Revised 26 January 2016; Accepted 11 February 2016

Academic Editor: Katsutaro Morino

Copyright © 2016 O. M. Duicu 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.

Abstract

Mitochondria-related oxidative stress is a pathomechanism causally linked to coronary heart disease CHD and diabetes mellitus DM. Recently, mitochondrial monoamine oxidases MAOs have emerged as novel sources of oxidative stress in the cardiovascular system and experimental diabetes. The present study was purported to assess the mitochondrial impairment and the contribution of MAOs-related oxidative stress to the cardiovascular dysfunction in coronary patients with-without DM. Right atrial appendages were obtained from 75 patients randomized into 3 groups: 1 Control CTRL, valvular patients without CHD; 2 CHD, patients with confirmed CHD; and 3 CHD-DM, patients with CHD and DM. Mitochondrial respiration was measured by high-resolution respirometry and MAOs expression was evaluated by RT-PCR and immunohistochemistry. Hydrogen peroxide H2O2 emission was assessed by confocal microscopy and spectrophotometrically. The impairment of mitochondrial respiration was substrate-independent in CHD-DM group. MAOs expression was comparable among the groups, with the predominance of MAO-B isoform but no significant differences regarding oxidative stress were detected by either method. Incubation of atrial samples with MAOs inhibitors significantly reduced the H2O2 in all groups. In conclusion, abnormal mitochondrial respiration occurs in CHD and is more severe in DM and MAOs contribute to oxidative stress in human diseased hearts with-without DM.





Autor: O. M. Duicu, R. Lighezan, A. Sturza, R. Balica, A. Vaduva, H. Feier, M. Gaspar, A. Ionac, L. Noveanu, C. Borza, D. M. Mu

Fuente: https://www.hindawi.com/



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