A review on the mitochondrial toxicity of “ecstasy” (3,4-methylenedioxymethamphetamine, MDMA)
Current Research in Toxicology May 27, 2022 João Paulo Capela, Félix Dias Carvalho 17 citations
MDMA (ecstasy) disrupts mitochondria in brain and liver cells. In laboratory models, MDMA depletes ATP, inhibits mitochondrial complexes I and III, reduces mitochondrial membrane potential, and triggers mitochondrial permeability transition. It also causes release of cytochrome c, impairing mitochondrial trafficking and increasing fragmentation of axonal mitochondria. Animal studies show decreased complex I activity, lower ATP levels, and oxidative stress leading to mitochondrial DNA deletions and impaired protein synthesis. These mitochondrial abnormalities partly explain MDMA's neurotoxicity and hepatotoxicity, though concentrations used in some studies may not match human exposure levels.