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Assessment of Mitochondrial Dysfunction and Monoamine Oxidase Contribution to Oxidative Stress in Human Diabetic Hearts

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 presen...

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Autores principales: Duicu, O. M., Lighezan, R., Sturza, A., Balica, R., Vaduva, A., Feier, H., Gaspar, M., Ionac, A., Noveanu, L., Borza, C., Muntean, D. M., Mornos, C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4846770/
https://www.ncbi.nlm.nih.gov/pubmed/27190576
http://dx.doi.org/10.1155/2016/8470394
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author Duicu, O. M.
Lighezan, R.
Sturza, A.
Balica, R.
Vaduva, A.
Feier, H.
Gaspar, M.
Ionac, A.
Noveanu, L.
Borza, C.
Muntean, D. M.
Mornos, C.
author_facet Duicu, O. M.
Lighezan, R.
Sturza, A.
Balica, R.
Vaduva, A.
Feier, H.
Gaspar, M.
Ionac, A.
Noveanu, L.
Borza, C.
Muntean, D. M.
Mornos, C.
author_sort Duicu, O. M.
collection PubMed
description 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 (H(2)O(2)) 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 H(2)O(2) 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.
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spelling pubmed-48467702016-05-17 Assessment of Mitochondrial Dysfunction and Monoamine Oxidase Contribution to Oxidative Stress in Human Diabetic Hearts Duicu, O. M. Lighezan, R. Sturza, A. Balica, R. Vaduva, A. Feier, H. Gaspar, M. Ionac, A. Noveanu, L. Borza, C. Muntean, D. M. Mornos, C. Oxid Med Cell Longev Research Article 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 (H(2)O(2)) 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 H(2)O(2) 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. Hindawi Publishing Corporation 2016 2016-04-13 /pmc/articles/PMC4846770/ /pubmed/27190576 http://dx.doi.org/10.1155/2016/8470394 Text en Copyright © 2016 O. M. Duicu et al. https://creativecommons.org/licenses/by/4.0/ 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.
spellingShingle Research Article
Duicu, O. M.
Lighezan, R.
Sturza, A.
Balica, R.
Vaduva, A.
Feier, H.
Gaspar, M.
Ionac, A.
Noveanu, L.
Borza, C.
Muntean, D. M.
Mornos, C.
Assessment of Mitochondrial Dysfunction and Monoamine Oxidase Contribution to Oxidative Stress in Human Diabetic Hearts
title Assessment of Mitochondrial Dysfunction and Monoamine Oxidase Contribution to Oxidative Stress in Human Diabetic Hearts
title_full Assessment of Mitochondrial Dysfunction and Monoamine Oxidase Contribution to Oxidative Stress in Human Diabetic Hearts
title_fullStr Assessment of Mitochondrial Dysfunction and Monoamine Oxidase Contribution to Oxidative Stress in Human Diabetic Hearts
title_full_unstemmed Assessment of Mitochondrial Dysfunction and Monoamine Oxidase Contribution to Oxidative Stress in Human Diabetic Hearts
title_short Assessment of Mitochondrial Dysfunction and Monoamine Oxidase Contribution to Oxidative Stress in Human Diabetic Hearts
title_sort assessment of mitochondrial dysfunction and monoamine oxidase contribution to oxidative stress in human diabetic hearts
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4846770/
https://www.ncbi.nlm.nih.gov/pubmed/27190576
http://dx.doi.org/10.1155/2016/8470394
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