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

Neri M, Cerretani D, Fiaschi AI, Laghi PF, Lazzerini PE, Maffione AB, Micheli L, Bruni G, Nencini C, Giorgi G, D'Errico S, Fiore C, Pomara C, Riezzo I, Turillazzi E, Fineschi V - J. Cell. Mol. Med. (2007 Jan-Feb)

Bottom Line: 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-alpha, MCP-1, and IL6, IL8, IL10 production.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Forensic Pathology, University of Foggia, Italy.

ABSTRACT

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 beta1-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-alpha), 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-alpha, 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.

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Related in: MedlinePlus

Effect of norepinephrine exposure (3 mg/kg i.p.) on cardiac antioxidant cellular systems. Values are presented as the mean (S.D.) of nine rats • p < 0.05, ♦ p < 0.01 and ★ p < 0.001 compared with control group.
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fig01: Effect of norepinephrine exposure (3 mg/kg i.p.) on cardiac antioxidant cellular systems. Values are presented as the mean (S.D.) of nine rats • p < 0.05, ♦ p < 0.01 and ★ p < 0.001 compared with control group.

Mentions: The results obtained (Fig. 1) showed that NE administration influences the antioxidant cellular defence system significantly increasing, compared to controls, GPx activity starting from 4 hrs up to 30 days after administration (Fig. 1A).


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

Neri M, Cerretani D, Fiaschi AI, Laghi PF, Lazzerini PE, Maffione AB, Micheli L, Bruni G, Nencini C, Giorgi G, D'Errico S, Fiore C, Pomara C, Riezzo I, Turillazzi E, Fineschi V - J. Cell. Mol. Med. (2007 Jan-Feb)

Effect of norepinephrine exposure (3 mg/kg i.p.) on cardiac antioxidant cellular systems. Values are presented as the mean (S.D.) of nine rats • p < 0.05, ♦ p < 0.01 and ★ p < 0.001 compared with control group.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4401229&req=5

fig01: Effect of norepinephrine exposure (3 mg/kg i.p.) on cardiac antioxidant cellular systems. Values are presented as the mean (S.D.) of nine rats • p < 0.05, ♦ p < 0.01 and ★ p < 0.001 compared with control group.
Mentions: The results obtained (Fig. 1) showed that NE administration influences the antioxidant cellular defence system significantly increasing, compared to controls, GPx activity starting from 4 hrs up to 30 days after administration (Fig. 1A).

Bottom Line: 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-alpha, MCP-1, and IL6, IL8, IL10 production.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Forensic Pathology, University of Foggia, Italy.

ABSTRACT

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 beta1-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-alpha), 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-alpha, 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.

Show MeSH
Related in: MedlinePlus