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Methylenedioxymethamphetamine inhibits mitochondrial complex I activity in mice: a possible mechanism underlying neurotoxicity
Author(s) -
Puerta Elena,
Hervias Isabel,
GoñiAllo Beatriz,
Zhang Steven F,
Jordán Joaquín,
Starkov Anatoly A,
Aguirre Norberto
Publication year - 2010
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.2010.00663.x
Subject(s) - mdma , chemistry , neurotoxicity , dopamine , glutathione , dopaminergic , pharmacology , superoxide dismutase , mitochondrion , biochemistry , oxidative stress , biology , endocrinology , toxicity , enzyme , organic chemistry
3,4-methylenedioxymethamphetamine (MDMA) causes a persistent loss of dopaminergic cell bodies in the substantia nigra of mice. Current evidence indicates that such neurotoxicity is due to oxidative stress but the source of free radicals remains unknown. Inhibition of mitochondrial electron transport chain complexes by MDMA was assessed as a possible source.