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Topics {✒️}

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         headline:Markers of cardiac oxidative stress and altered morphology after intraperitoneal cocaine injection in a rat model
         description: This study was designed to assess the parameters of myocardial oxidative stress and related cardiac morphological changes following intraperitoneal cocaine exposure in rats. The cardiac levels of reduced glutathione(GSH), oxidised glutathione(GSSG), ascorbic acid (AA), and the production of malondialdehyde (MDA) were measured, as well as the variations of activity in the enzyme systems involved in cell antioxidant defence, glutathione peroxidase (GSH-Px), glutathione reductase (GR) and superoxide dismutase (SOD). After chronic cocaine administration for 30 days GSH was significantly depleted in the heart from 30 min (P < 0.001) to 24 h (P < 0.001) after exposure, and GSSG was increased for a similar time (P < 0.05 at 30 min and P < 0.01 at 24 h). SOD increased during the first hour (P < 0.001), GR and GSH-Px both increased from 30 min to 24 h, and these increases were statistically significant (P < 0.01 and P < 0.001 at 30 min and P < 0.01 and P < 0.001 at 24 h, respectively). The AA levels increased after 1 h (P < 0.01), remaining significantly so for 24 h (P < 0.001) and MDA increased from 30 min to 24 h, all values being highly significant (P < 0.001). The body weight was significantly (P < 0.001) reduced in both cocaine groups (40 mg/kg × 30 days and 40 mg/kg × 10 days + 60 mg/kg × 20 days). The heart weight (P < 0.01) and its percentage of the body weight (P < 0.001) were significantly higher in these two groups than in the controls. Similarly, in the noradrenaline 4 mg/ kg × 30 days group, the body weight was significantly (P < 0.001) reduced and the heart weight (P < 0.01) and its percentage of body weight (P < 0.001) were significantly higher than in the controls. In comparing the cocaine and noradrenaline experiments, the frequency and extent of cardiac lesions obtained with 40 mg/kg × 10 days + 60 mg/kg × 20 days of cocaine were similar to those with 8 mg/kg of noradrenaline at 24 h. In this experimental model, cocaine administration compromised the antioxidant defence system of the heart associated with a significant increase of heart weight and the percentage of body weight.
         datePublished:
         dateModified:
         pageStart:323
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         keywords:
            Keywords Cocaine
            Myocardial necrosis
            Cardiac oxidative stress
            Parameters
            Contraction band necrosis
            Forensic Medicine
            Medical Law
            Medicine/Public Health
            general
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                     address:
                        name:Institute of Legal Medicine, University of Foggia, Ospedali Riuniti, Via L. Pinto 1, 71100 Foggia, Italy e-mail: [email protected], Fax: +39-0577-287756, , IT
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                     address:
                        name:Institute of Legal Medicine, University of Foggia, Ospedali Riuniti, Via L. Pinto 1, 71100 Foggia, Italy e-mail: [email protected], Fax: +39-0577-287756, , IT
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      headline:Markers of cardiac oxidative stress and altered morphology after intraperitoneal cocaine injection in a rat model
      description: This study was designed to assess the parameters of myocardial oxidative stress and related cardiac morphological changes following intraperitoneal cocaine exposure in rats. The cardiac levels of reduced glutathione(GSH), oxidised glutathione(GSSG), ascorbic acid (AA), and the production of malondialdehyde (MDA) were measured, as well as the variations of activity in the enzyme systems involved in cell antioxidant defence, glutathione peroxidase (GSH-Px), glutathione reductase (GR) and superoxide dismutase (SOD). After chronic cocaine administration for 30 days GSH was significantly depleted in the heart from 30 min (P < 0.001) to 24 h (P < 0.001) after exposure, and GSSG was increased for a similar time (P < 0.05 at 30 min and P < 0.01 at 24 h). SOD increased during the first hour (P < 0.001), GR and GSH-Px both increased from 30 min to 24 h, and these increases were statistically significant (P < 0.01 and P < 0.001 at 30 min and P < 0.01 and P < 0.001 at 24 h, respectively). The AA levels increased after 1 h (P < 0.01), remaining significantly so for 24 h (P < 0.001) and MDA increased from 30 min to 24 h, all values being highly significant (P < 0.001). The body weight was significantly (P < 0.001) reduced in both cocaine groups (40 mg/kg × 30 days and 40 mg/kg × 10 days + 60 mg/kg × 20 days). The heart weight (P < 0.01) and its percentage of the body weight (P < 0.001) were significantly higher in these two groups than in the controls. Similarly, in the noradrenaline 4 mg/ kg × 30 days group, the body weight was significantly (P < 0.001) reduced and the heart weight (P < 0.01) and its percentage of body weight (P < 0.001) were significantly higher than in the controls. In comparing the cocaine and noradrenaline experiments, the frequency and extent of cardiac lesions obtained with 40 mg/kg × 10 days + 60 mg/kg × 20 days of cocaine were similar to those with 8 mg/kg of noradrenaline at 24 h. In this experimental model, cocaine administration compromised the antioxidant defence system of the heart associated with a significant increase of heart weight and the percentage of body weight.
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      pageStart:323
      pageEnd:330
      sameAs:https://doi.org/10.1007/s004140000194
      keywords:
         Keywords Cocaine
         Myocardial necrosis
         Cardiac oxidative stress
         Parameters
         Contraction band necrosis
         Forensic Medicine
         Medical Law
         Medicine/Public Health
         general
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                  address:
                     name:Institute of Legal Medicine, University of Foggia, Ospedali Riuniti, Via L. Pinto 1, 71100 Foggia, Italy e-mail: [email protected], Fax: +39-0577-287756, , IT
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                     name:Institute of Clinical Physiology, National Research Council, Department of Cardiology “De Gasperis”, Niguarda Hospital, 20162 Milan, Italy, , IT
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            name:Fabio Centini
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                  address:
                     name:Division of Forensic Toxicology, University of Siena, Policlinico Le Scotte, 53100 Siena, Italy, , IT
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               name:Institute of Legal Medicine, University of Foggia, Ospedali Riuniti, Via L. Pinto 1, 71100 Foggia, Italy e-mail: [email protected], Fax: +39-0577-287756, , IT
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            address:
               name:Institute of Clinical Physiology, National Research Council, Department of Cardiology “De Gasperis”, Niguarda Hospital, 20162 Milan, Italy, , IT
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               name:Division of Forensic Toxicology, University of Siena, Policlinico Le Scotte, 53100 Siena, Italy, , IT
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            address:
               name:Department of Pharmacology “G. Segre”, University of Siena, Policlinico Le Scotte, 53100 Siena, Italy, , IT
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      name:Anna Ida Fiaschi
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            address:
               name:Department of Pharmacology “G. Segre”, University of Siena, Policlinico Le Scotte, 53100 Siena, Italy, , IT
               type:PostalAddress
            type:Organization
      name:Lucia Micheli
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            address:
               name:Department of Pharmacology “G. Segre”, University of Siena, Policlinico Le Scotte, 53100 Siena, Italy, , IT
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               name:Institute of Clinical Physiology, National Research Council, Department of Cardiology “De Gasperis”, Niguarda Hospital, 20162 Milan, Italy, , IT
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            address:
               name:Institute of Legal Medicine, University of Foggia, Ospedali Riuniti, Via L. Pinto 1, 71100 Foggia, Italy e-mail: [email protected], Fax: +39-0577-287756, , IT
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      name:Institute of Clinical Physiology, National Research Council, Department of Cardiology “De Gasperis”, Niguarda Hospital, 20162 Milan, Italy, , IT
      name:Division of Forensic Toxicology, University of Siena, Policlinico Le Scotte, 53100 Siena, Italy, , IT
      name:Department of Pharmacology “G. Segre”, University of Siena, Policlinico Le Scotte, 53100 Siena, Italy, , IT
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