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Insong J. Lee

University of Maryland, Baltimore

2 papers in the library · 135 citations · publishing 2008-2010

Papers

Mechanisms of MDMA (Ecstasy)-Induced Oxidative Stress, Mitochondrial Dysfunction, and Organ Damage

Current Pharmaceutical Biotechnology June 27, 2010 Byoung‐joon Song, Kwan–hoon Moon, Vijay Upreti et al. 73 citations

MDMA (ecstasy) causes organ damage partly through increased oxidative and nitrosative stress. This review focuses on how oxidative modifications of mitochondrial proteins lead to mitochondrial dysfunction. It describes a method using biotin-N-maleimide as a sensitive probe to identify oxidatively-modified mitochondrial proteins in rats exposed to MDMA, and discusses applications and limitations of this Cys-targeted proteomics approach. The review also covers synergistic drug interactions between MDMA and alcohol, and the potential of this redox-based proteomics method for developing preventive and therapeutic agents against MDMA-induced organ damage.

Mechanism of 3,4‐methylenedioxymethamphetamine (MDMA, ecstasy)‐mediated mitochondrial dysfunction in rat liver

PROTEOMICS September 1, 2008 Kwan–hoon Moon, Vijay Upreti, Li‐rong Yu et al. 62 citations

MDMA (ecstasy) causes liver damage, but the mechanism was poorly understood. In rats, MDMA exposure led to abnormal liver histology, elevated plasma transaminases, nitric oxide synthase, and hydrogen peroxide. Oxidatively modified mitochondrial proteins were labeled with a sensitive probe and identified via mass spectrometry. These included proteins involved in energy supply, fat metabolism, antioxidant defense, and chaperone activities. The activities of mitochondrial aldehyde dehydrogenase, 3-ketoacyl-CoA thiolases, and ATP synthase were significantly inhibited. The data show that MDMA causes oxidative inactivation of key mitochondrial enzymes, likely contributing to mitochondrial dysfunction and subsequent liver damage.