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  6. Keywords
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We began analyzing https://link.springer.com/article/10.1007/s00414-008-0262-2, but it redirected us to https://link.springer.com/article/10.1007/s00414-008-0262-2. The analysis below is for the second page.

Title[redir]:
Cardiac oxidative stress determination and myocardial morphology after a single ecstasy (MDMA) administration in a rat model | International Journal of Legal Medicine
Description:
Experimental and clinical data indicate that 3,4-methylenedioxy-N-methylamphetamine (MDMA) abuse can produce significant cardiovascular toxicity. A mechanism may be a direct toxic effect of redox active metabolites of MDMA. To evaluate the effect of a single MDMA dose on cellular antioxidant defence system and to investigate the morphology in male albino rats, total glutathione (GSH), oxidised glutathione (GSSG), ascorbic acid (AA), glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD) and malondialdehyde (MDAL) were studied. The effects were evaluated at 3, 6, 16 and 24 h after MDMA administration. Antioxidant enzymes activity was significantly reduced: GPx (−24%) and SOD (−50%) after 3 h and GR (−19%) after 6 h from treatment. AA levels decrease (−37%) after 3 h and (−30%) after 6 h; MDAL level increased (+119%) after 3 h; GSH levels decreased after 3 (31.3%) and 6 h (37.9%) from MDMA treatment. GSSG content was not affected by ecstasy administration. Myocardial contraction band necrosis (CBN) was already visible in rats killed at 6 h. After 16 h, macrophagic monocytes around the necrotic myocardial cells were observed, and within 24 h, this infiltrate became more widespread with an early removal of the necrotic material. Calcium deposits were observed within ventricular cardiomyocytes with intact nuclei and sarcomeres. Single administration of MDMA can significantly alter the cellular antioxidant defence system and produce oxidative stress which may result in lipid peroxidation and disruption of Ca2 + homeostasis. The depression in Ca2+ regulatory mechanism by reactive oxygen species ultimately results in intracellular Ca2 + overload, CBN and cell death.

Matching Content Categories {📚}

  • Education
  • Health & Fitness
  • Science

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

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Traffic Estimate {📈}

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


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Keywords {🔍}

article, google, scholar, pubmed, cas, mdma, legal, med, glutathione, oxidative, stress, rat, carvalho, int, ecstasy, administration, fineschi, cardiac, myocardial, content, determination, riezzo, rats, effects, res, forensic, university, siena, italy, privacy, cookies, journal, research, morphology, cerretani, fiaschi, neri, turillazzi, acid, access, chem, toxicol, remiao, bastos, postmortem, methylenedioxymethamphetamine, author, data, publish, search,

Topics {✒️}

rat involve alpha-adrenoceptors month download article/chapter cardiac oxidative stress high-performance liquid chromatography piperazine-derived designer drugs margherita neri author information authors vittorio fineschi gas chromatography/mass spectrometry cu2+-induced isoproterenol oxidation n-methyl-alpha-methyldopamine produce oxidative stress rat heart cells article international journal rat model author correspondence full article pdf ecstasy-induced cardiotoxicity related subjects anna ida fiaschi privacy choices/manage cookies myocardial morphology isoproterenol oxidation products sudden cardiac death ischemia-reperfusion injury necrotic myocardial cells myocardial pathology due animal research perspective legal medicine aims check access instant access 4-methylenedioxyamphetamine-induced hepatotoxicity oxidative stress methylenedioxyamphetamine-mediated neurotoxicity tissue selenium levels antioxidant enzymes activity increases intracellular calcium european economic area redox active metabolites vivo potential involvement van bocxlaer jf post-mortem redistribution vivo intravenous infusion post-mortem infusion intraperitoneal cocaine injection optimum methamphetamine profiling solid-phase microextraction placebo-controlled trial folin phenol reagent 8-tetrachlorodibenzo-p-dioxin

Schema {🗺️}

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         headline:Cardiac oxidative stress determination and myocardial morphology after a single ecstasy (MDMA) administration in a rat model
         description:Experimental and clinical data indicate that 3,4-methylenedioxy-N-methylamphetamine (MDMA) abuse can produce significant cardiovascular toxicity. A mechanism may be a direct toxic effect of redox active metabolites of MDMA. To evaluate the effect of a single MDMA dose on cellular antioxidant defence system and to investigate the morphology in male albino rats, total glutathione (GSH), oxidised glutathione (GSSG), ascorbic acid (AA), glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD) and malondialdehyde (MDAL) were studied. The effects were evaluated at 3, 6, 16 and 24 h after MDMA administration. Antioxidant enzymes activity was significantly reduced: GPx (−24%) and SOD (−50%) after 3 h and GR (−19%) after 6 h from treatment. AA levels decrease (−37%) after 3 h and (−30%) after 6 h; MDAL level increased (+119%) after 3 h; GSH levels decreased after 3 (31.3%) and 6 h (37.9%) from MDMA treatment. GSSG content was not affected by ecstasy administration. Myocardial contraction band necrosis (CBN) was already visible in rats killed at 6 h. After 16 h, macrophagic monocytes around the necrotic myocardial cells were observed, and within 24 h, this infiltrate became more widespread with an early removal of the necrotic material. Calcium deposits were observed within ventricular cardiomyocytes with intact nuclei and sarcomeres. Single administration of MDMA can significantly alter the cellular antioxidant defence system and produce oxidative stress which may result in lipid peroxidation and disruption of Ca2 + homeostasis. The depression in Ca2+ regulatory mechanism by reactive oxygen species ultimately results in intracellular Ca2 + overload, CBN and cell death.
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      headline:Cardiac oxidative stress determination and myocardial morphology after a single ecstasy (MDMA) administration in a rat model
      description:Experimental and clinical data indicate that 3,4-methylenedioxy-N-methylamphetamine (MDMA) abuse can produce significant cardiovascular toxicity. A mechanism may be a direct toxic effect of redox active metabolites of MDMA. To evaluate the effect of a single MDMA dose on cellular antioxidant defence system and to investigate the morphology in male albino rats, total glutathione (GSH), oxidised glutathione (GSSG), ascorbic acid (AA), glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD) and malondialdehyde (MDAL) were studied. The effects were evaluated at 3, 6, 16 and 24 h after MDMA administration. Antioxidant enzymes activity was significantly reduced: GPx (−24%) and SOD (−50%) after 3 h and GR (−19%) after 6 h from treatment. AA levels decrease (−37%) after 3 h and (−30%) after 6 h; MDAL level increased (+119%) after 3 h; GSH levels decreased after 3 (31.3%) and 6 h (37.9%) from MDMA treatment. GSSG content was not affected by ecstasy administration. Myocardial contraction band necrosis (CBN) was already visible in rats killed at 6 h. After 16 h, macrophagic monocytes around the necrotic myocardial cells were observed, and within 24 h, this infiltrate became more widespread with an early removal of the necrotic material. Calcium deposits were observed within ventricular cardiomyocytes with intact nuclei and sarcomeres. Single administration of MDMA can significantly alter the cellular antioxidant defence system and produce oxidative stress which may result in lipid peroxidation and disruption of Ca2 + homeostasis. The depression in Ca2+ regulatory mechanism by reactive oxygen species ultimately results in intracellular Ca2 + overload, CBN and cell death.
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      name:Department of Forensic Pathology, University of Foggia, Foggia, Italy
      name:Department of Forensic Pathology, University of Foggia, Foggia, Italy
      name:Department of Forensic Pathology, University of Foggia, Foggia, Italy
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