ArticleCardiovascular toxicology2009
Metabolites of MDMA induce oxidative stress and contractile dysfunction in adult rat left ventricular myocytes.
Article in Cardiovascular toxicology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 32 citations in OpenAlex.
- Subthreshold Thermal Stress Aggravates Methamphetamine-Induced Cardiomyocyte Pyroptosis via the Mitochondrial ROS/BAX/mtDNA/NLRP3 Pathway.International journal of molecular sciences · 2026Article
- Protective effects of vitamin E and quercetin against MDMA-induced cardiac and hematological dysfunction in male wistar rats.Pflugers Archiv : European journal of physiology · 2026Article
- MDMA for the Treatment of Negative Symptoms in Schizophrenia.Journal of clinical medicine · 2022Review
- Role of nitric oxide in psychostimulant-induced neurotoxicity.AIMS neuroscience · 2019Review
- Case of Cardiac Arrest Treated with Extra-Corporeal Life Support after MDMA Intoxication.Case reports in critical care · 2019Article
- Dark Classics in Chemical Neuroscience: 3,4-Methylenedioxymethamphetamine.ACS chemical neuroscience · 2018Review
- Comprehensive review of cardiovascular toxicity of drugs and related agents.Medicinal research reviews · 2018Review
- Environmentally Persistent Free Radicals Cause Apoptosis in HL-1 Cardiomyocytes.Cardiovascular toxicology · 2017Article
- Ecstasy (MDMA) Alters Cardiac Gene Expression and DNA Methylation: Implications for Circadian Rhythm Dysfunction in the Heart.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
- Rapidly reversible multiorgan failure after ingestion of "Molly" (pure 3,4-methylenedioxymethamphetamine): a case report.Journal of medical case reports · 2014Article
- AT1 receptor-mediated augmentation of angiotensinogen, oxidative stress, and inflammation in ANG II-salt hypertension.American journal of physiology. Renal physiology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Repeated administration of 3,4-methylenedioxymethamphetamine (MDMA) (ecstasy) produces eccentric left ventricular (LV) dilation and diastolic dysfunction. While the mechanism(s) underlying this toxicity are unknown, oxidative stress plays an important role. MDMA is metabolized into redox cycling metabolites that produce superoxide. In this study, we demonstrated that metabolites of MDMA induce oxidative stress and contractile dysfunction in adult rat left ventricular myocytes. Metabolites of MDMA used in this study included alpha-methyl dopamine, N-methyl alpha-methyl dopamine and 2,5-bis(glutathion-S-yl)-alpha-MeDA. Dihydroethidium was used to detect drug-induced increases in reactive oxygen species (ROS) production in ventricular myocytes. Contractile function and changes in intracellular calcium transients were measured in paced (1 Hz), Fura-2 AM loaded, myocytes using the IonOptix system. Production of ROS in ventricular myocytes treated with MDMA was not different from control. In contrast, all three metabolites of MDMA exhibited time- and concentration-dependent increases in ROS that were prevented by N-acetyl-cysteine (NAC). The metabolites of MDMA, but not MDMA alone, significantly decreased contractility and impaired relaxation in myocytes stimulated at 1 Hz. These effects were prevented by NAC. Together, these data suggest that MDMA-induced oxidative stress in the left ventricle can be due, at least in part, to the metabolism of MDMA to redox active metabolites.
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Registered trials
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