Correlation between cardiac oxidative stress and myocardial pathology due to acute and chronic norepinephrine administration in rats

Autor: Daniela Cerretani, Angela Bruna Maffione, Carmela Fiore, Cristoforo Pomara, Pasini Franco Laghi, Cristina Nencini, Lucia Micheli, Stefano D'Errico, Anna Ida Fiaschi, Emanuela Turillazzi, Giorgio Giorgi, Pietro Euea Lazzerini, Margherita Neri, Irene Riezzo, Giancarlo Bruni, Vittorio Fineschi
Přispěvatelé: Neri, M, Cerretani, D, Fiaschi, Ai, Laghi, Pf, Lazzaroni, Pe, Mafiose, Ab, Micheli, L, Bruni, G, Nencini, C, Giorgi, G, D'Errico, S, Fiore, C, Pomara, C, Riezzo, I, Turillazzi, E, Fineschi, V
Jazyk: angličtina
Rok vydání: 2007
Předmět:
Male
Glutathione reductase
Apoptosis
medicine.disease_cause
chemistry.chemical_compound
Electrocardiography
cardiac antioxidant cellular defence system
Malondialdehyde
chemistry.chemical_classification
Glutathione Disulfide
Glutathione peroxidase
Articles
Immunohistochemistry
Glutathione Reductase
Molecular Medicine
Cardiac antioxidant cellular defence system
oxidative stress
myocardial pathology
norepinephrine
Adrenergic alpha-Agonists
medicine.medical_specialty
β1-adrenergic receptors
Cytokines
Norepinephrine
Animals
Drug Administration Schedule
Glutathione Peroxidase
Lipid Peroxidation
Myocardium
Oxidative Stress
Rats
Rats
Wistar
Reactive Oxygen Species
Receptor Cross-Talk
Receptors
Adrenergic
beta-1
Superoxide Dismutase
Biochemistry
Genetics and Molecular Biology (all)
Biochemistry
β
Socio-culturale
Biology
Superoxide dismutase
Internal medicine
medicine
adrenergic receptors
Reactive oxygen species
1
Cell Biology
Glutathione
norepinephrine
cardiac antioxidant cellular defence system
β1-adrenergic receptors
cytokines
cytokines
Endocrinology
chemistry
biology.protein
Glutathione disulfide
Oxidative stress
Zdroj: Journal of Cellular and Molecular Medicine
ISSN: 1582-4934
1582-1838
Popis: Background: To investigate the cardiotoxic role of reactive oxygen species (ROS) and of products derived from catecholamines auto-oxidation, we studied: (1) the response of antioxidant cardiac cellular defence systems to oxidative stress induced by norepinephrine (NE) administration, (2) the effect of NE administration on cardiac β1-adrenergic receptors by means of receptor binding assay, (3) the cellular morphological alterations related to the biologically cross-talk between the NE administration and cytokines [tumor necrosis factor-alpha (TNF-α), monocyte chemotactic protein-1 (MCP-1), interleukins IL6, IL8, IL10]Methods and Results: A total of 195 male rats was used in the experiment. All animals underwent electrocardiogram (EKG) before being sacrificed. The results obtained show that NE administration influences the antioxidant cellular defence system significantly increasing glutathione peroxidase (GPx) activity, glutathione reductase (GR) and superoxide dismutase (SOD). The oxidized glutathione (GSH/GSSG) ratio significantly decreases and malondialdehyde (MDA) levels increase showing a state of lipoperoxidation of cardiac tissue. We describe a significant apoptotic process randomly sparse in the damaged myocardium and the effect of ROS on the NE-mediated TNF-α, MCP-1, and IL6, IL8, IL10 production. Conclusions: Our results support the hypothesis that catecholamines may induce oxidative damage through reactive intermediates resulting from their auto-oxidation, irrespective of their interaction with adrenergic receptors, thus representing an important factor in the pathogenesis of catecholamines-induced cardiotoxicity. The rise of the cardioinhibitory cytokines may be interpreted as the adaptive response of jeopardized myocardium with respect to the cardiac dysfunction resulting from NE injection.
Databáze: OpenAIRE
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