PMID- 18594849
OWN - NLM
STAT- MEDLINE
DCOM- 20090331
LR  - 20211020
IS  - 0937-9827 (Print)
IS  - 0937-9827 (Linking)
VI  - 122
IP  - 6
DP  - 2008 Nov
TI  - Cardiac oxidative stress determination and myocardial morphology after a single 
      ecstasy (MDMA) administration in a rat model.
PG  - 461-9
LID - 10.1007/s00414-008-0262-2 [doi]
AB  - 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 Ca(2 +) homeostasis. The depression in Ca(2+) 
      regulatory mechanism by reactive oxygen species ultimately results in 
      intracellular Ca(2 +) overload, CBN and cell death.
FAU - Cerretani, Daniela
AU  - Cerretani D
AD  - Department of Pharmacology, University of Siena, Siena, Italy.
FAU - Riezzo, Irene
AU  - Riezzo I
FAU - Fiaschi, Anna Ida
AU  - Fiaschi AI
FAU - Centini, Fabio
AU  - Centini F
FAU - Giorgi, Giorgio
AU  - Giorgi G
FAU - D'Errico, Stefano
AU  - D'Errico S
FAU - Fiore, Carmela
AU  - Fiore C
FAU - Karch, Steven B
AU  - Karch SB
FAU - Neri, Margherita
AU  - Neri M
FAU - Pomara, Cristoforo
AU  - Pomara C
FAU - Turillazzi, Emanuela
AU  - Turillazzi E
FAU - Fineschi, Vittorio
AU  - Fineschi V
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080702
PL  - Germany
TA  - Int J Legal Med
JT  - International journal of legal medicine
JID - 9101456
RN  - 0 (Hallucinogens)
RN  - 0 (Myoglobin)
RN  - 0 (Troponin C)
RN  - 0 (Troponin I)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - EC 1.8.1.7 (Glutathione Reductase)
RN  - GAN16C9B8O (Glutathione)
RN  - KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
RN  - PQ6CK8PD0R (Ascorbic Acid)
RN  - ULW86O013H (Glutathione Disulfide)
SB  - IM
MH  - Animals
MH  - Ascorbic Acid/metabolism
MH  - Calcinosis/pathology
MH  - Forensic Toxicology
MH  - Glutathione/metabolism
MH  - Glutathione Disulfide/metabolism
MH  - Glutathione Peroxidase/metabolism
MH  - Glutathione Reductase/metabolism
MH  - Hallucinogens/blood/*pharmacology
MH  - Macrophages/pathology
MH  - Male
MH  - Malondialdehyde/metabolism
MH  - Microscopy, Confocal
MH  - Models, Animal
MH  - Myocardium/*metabolism/*pathology
MH  - Myocytes, Cardiac/pathology
MH  - Myoglobin/metabolism
MH  - N-Methyl-3,4-methylenedioxyamphetamine/blood/*pharmacology
MH  - Necrosis
MH  - Oxidative Stress/*drug effects
MH  - Rats
MH  - Superoxide Dismutase/metabolism
MH  - Time Factors
MH  - Troponin C/metabolism
MH  - Troponin I/metabolism
EDAT- 2008/07/03 09:00
MHDA- 2009/04/01 09:00
CRDT- 2008/07/03 09:00
PHST- 2007/11/15 00:00 [received]
PHST- 2008/05/30 00:00 [accepted]
PHST- 2008/07/03 09:00 [pubmed]
PHST- 2009/04/01 09:00 [medline]
PHST- 2008/07/03 09:00 [entrez]
AID - 10.1007/s00414-008-0262-2 [doi]
PST - ppublish
SO  - Int J Legal Med. 2008 Nov;122(6):461-9. doi: 10.1007/s00414-008-0262-2. Epub 2008 
      Jul 2.