PMID- 23681166
OWN - NLM
STAT- MEDLINE
DCOM- 20140610
LR  - 20211021
IS  - 1432-2072 (Electronic)
IS  - 0033-3158 (Linking)
VI  - 230
IP  - 1
DP  - 2013 Nov
TI  - Cocaine potentiates MDMA-induced oxidative stress but not dopaminergic 
      neurotoxicity in mice: implications for the pathogenesis of free radical-induced 
      neurodegenerative disorders.
PG  - 125-35
LID - 10.1007/s00213-013-3142-5 [doi]
AB  - RATIONALE: The drugs of abuse 3,4-methylenedioxymethamphetamine (MDMA; "ecstasy") 
      and cocaine both increase the generation of free radicals, and in the case of 
      MDMA, this increase in oxidative stress is involved in the dopaminergic 
      neurotoxicity produced by the drug in mice. Oxidative stress processes are also 
      involved in the pathogenesis of several neurodegenerative diseases. OBJECTIVES: 
      We aimed to determine the consequences of the combined administration of MDMA and 
      cocaine on oxidative stress and dopaminergic neurotoxicity. METHODS: Mice 
      received MDMA (20 mg/kg, i.p.; two doses separated by 3 h) followed by cocaine 1, 
      3, 6, or 24 h after the second MDMA dose. Mice were killed between 1 h and 7 days 
      after cocaine injection. RESULTS: MDMA decreased dopamine transporter density and 
      dopamine concentration 7 days later. Cocaine did not alter this neurotoxicity. 
      MDMA produced an increase in the concentration of 2,3-dihydroxybenzoic acid in 
      striatal microdialysis samples and an increase in lipid peroxidation in the 
      striatum which were potentiated by cocaine. MDMA and cocaine given together also 
      increased nitrate and 3-nitrotyrosine levels compared with either drug given 
      alone. On the other hand, MDMA increased superoxide dismutase activity and 
      decreased catalase activity, changes which were prevented by cocaine 
      administration. In addition, cocaine administration produced an increase in 
      glutathione peroxidase (GPx) activity in both saline-treated and MDMA-treated 
      mice. CONCLUSIONS: Cocaine potentiates MDMA-induced oxidative stress but does not 
      produce an increase in the neurotoxicity produced by MDMA, and this lack of 
      potentiation may involve an increase in GPx activity.
FAU - Peraile, Ines
AU  - Peraile I
AD  - Departamento de Farmacologia, Facultad de Medicina, Universidad Complutense, 
      Madrid, 28040, Spain.
FAU - Granado, Noelia
AU  - Granado N
FAU - Torres, Elisa
AU  - Torres E
FAU - Gutierrez-Lopez, M Dolores
AU  - Gutierrez-Lopez MD
FAU - Moratalla, Rosario
AU  - Moratalla R
FAU - Colado, M Isabel
AU  - Colado MI
FAU - O'Shea, Esther
AU  - O'Shea E
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130517
PL  - Germany
TA  - Psychopharmacology (Berl)
JT  - Psychopharmacology
JID - 7608025
RN  - 0 (Dopamine Plasma Membrane Transport Proteins)
RN  - 0 (Free Radicals)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - I5Y540LHVR (Cocaine)
RN  - KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Animals
MH  - Cocaine/administration & dosage/*toxicity
MH  - Corpus Striatum/drug effects/metabolism
MH  - Dopamine/metabolism
MH  - Dopamine Plasma Membrane Transport Proteins/metabolism
MH  - Free Radicals/metabolism
MH  - Glutathione Peroxidase/metabolism
MH  - Lipid Peroxidation/drug effects
MH  - Male
MH  - Mice
MH  - Microdialysis
MH  - N-Methyl-3,4-methylenedioxyamphetamine/administration & dosage/*toxicity
MH  - Neurotoxicity Syndromes/*etiology/physiopathology
MH  - Oxidative Stress/*drug effects
MH  - Time Factors
EDAT- 2013/05/18 06:00
MHDA- 2014/06/11 06:00
CRDT- 2013/05/18 06:00
PHST- 2013/01/31 00:00 [received]
PHST- 2013/04/30 00:00 [accepted]
PHST- 2013/05/18 06:00 [entrez]
PHST- 2013/05/18 06:00 [pubmed]
PHST- 2014/06/11 06:00 [medline]
AID - 10.1007/s00213-013-3142-5 [doi]
PST - ppublish
SO  - Psychopharmacology (Berl). 2013 Nov;230(1):125-35. doi: 
      10.1007/s00213-013-3142-5. Epub 2013 May 17.