The Role of Oxidative Stress in Methamphetamine and MDMA-induced Toxicity
Irene Riezzo, Carmela Fiore, Dania De Carlo, Steven B. Karch, Margherita Neri, Turillazzi Emanuela Turillazi and Vittori Fineschi
Affiliation: Department of Forensic Pathology, Ospedale Colonnello D’Avanzo, Viale degli Aviatori 1, 71100 Foggia, Italy.
Keywords: Methamphetamine, MDMA, stress oxidative, neurotoxicity, cardiotoxicity, nephrotoxicity, hepatotoxicity.
Methamphetamine and 3, 4-methylenedioxymethamphetamine are psychoactive recreational hallucinogenic
substances with considerable CNS stimulatory effects. Acute or sub-chronic exposure to METH or MDMA can damage
several organs. Many different organs may be involve. There is evidence for neurotoxicity, cardiotoxicity, hepatotoxicity
and nephrotoxicity. Many of these mechanisms are complex and difficult to explain.
There is emerging consensus that oxidative stress play a paramount role in the molecular toxicity of both METH and
MDMA. Free radicals can arise secondary to oxidative deamination of monoamines, cathecolamines autoxidation,
hypothermia, lipoperoxidation and even cellular death. There is very little doubt that the toxic effects of METH and
MDMA are mediated either by the direct effect of METH and MDMA or by its redox active metabolites. Metabolites
formed in liver cells can reach the others organs (heart, kidney, brain, etc) and produce their own toxic effects inducing
cellular oxidative stress and lipoperoxidation. The present review is aimed to further clarify the mechanisms of METH
and MDMA-induced toxicity, mainly focusing on the role of oxidative stress pathway.
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