Toxicology
January 5, 2005
Helena Carmo, Jan G Hengstler, Douwe De Boer et al.
85 citations
The psychoactive designer drug 2C-B is broken down by liver cells from humans, monkeys, dogs, rabbits, rats, and mice through oxidative deamination and demethylation, producing several metabolites. A previously unknown metabolite, 4-bromo-2,5-dimethoxy-phenol (BDMP), appeared only in mouse cells, while another metabolite, 2-(4-bromo-2-hydroxy-5-methoxyphenyl)-ethanol (B-2-HMPE), formed in human, monkey, and rabbit cells but not in dog, rat, or mouse cells. Toxic effects on liver cells varied little across species but showed large differences among cells from three human donors, indicating that individual human variation may be more important than species differences in determining 2C-B toxicity.
Chemical Research in Toxicology
April 27, 2004
Márcia Carvalho, Fernando Remião, Nuno Milhazes et al.
77 citations
MDMA (ecstasy) and its major metabolite MDA did not directly damage heart cells from adult rats in the lab, but two further metabolites, N-Me-alpha-MeDA and alpha-MeDA, caused significant toxicity. These catechol metabolites triggered a loss of normal cell shape, depletion of the antioxidant glutathione, sustained increases in intracellular calcium, drops in ATP, and reduced activity of antioxidant enzymes. N-Me-alpha-MeDA was the most toxic. The findings suggest that MDMA must be metabolized into these catechol compounds for cardiotoxicity to occur in isolated heart cells.
JOURNAL OF HEALTH SCIENCE
January 1, 2007
Carla Macedo, Paula S. Branco, Luı́sa M. Ferreira et al.
36 citations
The neurotoxic effects of MDMA (Ecstasy) may depend heavily on how the body metabolizes the drug in the liver. Metabolism produces highly reactive compounds, including catechols, catechol thioethers, and quinones. Researchers used cyclic voltammetry to measure the electrochemical oxidation-reduction processes of chemically synthesized human MDMA metabolites. They then correlated the redox potentials of α-methyldopamine, N-methyl-α-methyldopamine, and 5-(glutathion-S-yl)-α-methyldopamine with their toxicity to rat cortical neurons. The data demonstrated that the lower oxidation potential of the catecholic thioether of α-MeDA correlated with its higher toxicity, supporting the use of voltammetry data to predict the toxicity of MDMA metabolites.
PLoS ONE
June 14, 2016
João Martins, Miguel Castelo-Branco, Ana Batista et al.
10 citations
A single dose of MDMA (ecstasy) given to rats temporarily alters retinal function, as measured by electroretinograms. Three hours after administration, both MDMA-treated and high-temperature control rats showed larger and faster retinal responses, suggesting that the acute effects are partly due to MDMA-induced hyperthermia. After 24 hours, MDMA-treated animals still had increased responses in the outer retinal layers (photoreceptors and bipolar cells), even after temperature effects subsided, indicating a direct subacute effect of the drug. These changes returned to normal within seven days. The findings provide direct evidence that MDMA can enhance outer retinal activity, which may help explain visual disturbances reported by human users.