Journal of Neuroscience Research
October 1, 2009
Irene Riezzo, Daniela Cerretani, Carmela Fiore et al.
47 citations
A single dose of MDMA (20 mg/kg) in rats rapidly disrupts the brain's antioxidant defenses within hours. Reduced and oxidized glutathione ratios decreased, and antioxidant enzyme activities fell significantly after 3 and 6 hours in the frontal cortex. Ascorbic acid levels rose sharply in the striatum, hippocampus, and frontal cortex after 3 and 6 hours. Malonaldehyde, a marker of oxidative damage, increased in the striatum after 3 and 6 hours and in the hippocampus and frontal cortex after 6 hours. Immunohistochemistry revealed strong antivesicular monoamine transporter 2 positivity in frontal sections, basal ganglia, and thalamus, and heat shock protein 70 appeared in the superficial cortical layer after 24 hours, indicating early neurotoxic changes.
Current Pharmaceutical Biotechnology
June 27, 2010
Emanuela Turillazzi, Irene Riezzo, Margherita Neri et al.
43 citations
MDMA (ecstasy) can cause four main types of serious toxicity: liver, heart, brain, and overheating. The exact molecular causes are not fully understood, but oxidative stress, excitotoxicity, and mitochondrial dysfunction appear to be key events leading to damage. Animal studies show that MDMA triggers cardiovascular responses similar to amphetamine, involving both catecholaminergic and non-catecholaminergic mechanisms. While evidence of cardiac and liver toxicity is clear, the mechanisms remain unclear; liver damage may involve MDMA metabolism, neurotransmitter release, oxidation of biogenic amines, and hyperthermia. Overwhelming evidence shows MDMA produces acute and long-lasting toxic effects on brain cells in both animals and humans.
International Journal of Molecular Sciences
March 12, 2019
Stefania Schiavone, Margherita Neri, Angela Bruna Maffione et al.
22 citations
MDMA (ecstasy) neurotoxicity may involve nitrosative stress driven by the enzyme iNOS rather than by NOX enzymes that produce reactive oxygen species. In rats given MDMA, iNOS expression increased, and cells positive for 3-nitrotyrosine (a marker of nitrosative damage) rose in the frontal cortex. No changes occurred in NOX2, NOX1, or NOX4 immunoreactivity or in the oxidative stress marker 8OHdG. MDMA and nitrosative markers colocalized with dopamine-transporter-positive cells, which were neurons, not microglia or astrocytes. The findings indicate that iNOS-derived nitrosative stress, not NOX enzymes, likely contributes to MDMA-induced neurotoxicity.