Human Psychopharmacology Clinical and Experimental
May 1, 2017
Daniel Martins, Monica J. Barratt, Cristiana Vale Pires et al.
76 citations
At the 2014 Boom Festival in Portugal, a drug-checking service analyzed 245 samples that users believed to be LSD. Only 67.3% actually contained LSD alone; 24.1% contained another psychoactive substance instead, including 11.4% that were DOx derivatives and 9.8% that were 25x-NBOMe derivatives. Among users who received unexpected results, 74.2% said they did not intend to consume the drug they actually had. After alerts were disseminated on the second day, a larger proportion of all tests conducted were for LSD compared to the 2012 festival, where no such alert was issued. The authors suggest these findings support integrated drug-checking services in party settings.
Pharmaceuticals
August 15, 2023
Daniel Martins, Eva Gil-Martins, Fernando Cagide et al.
13 citations
Adding an N-2-methoxybenzyl group to mescaline and related 2C phenethylamine drugs to create NBOMe compounds significantly increases their in vitro toxicity to both brain (SH-SY5Y) and liver (HepG2) cell lines. The NBOMe drugs had lower EC50 values, indicating greater potency, and were able to cross the blood–brain barrier. The increased toxicity was linked to higher lipophilicity, disruption of mitochondrial membrane potential, and depletion of glutathione and ATP levels. Inhibition of cytochrome P450 enzymes, particularly CYP3A4 and CYP2D6, influenced the drugs' toxicity, suggesting these enzymes play a role in detoxification or bioactivation. No reactive oxygen species overproduction was detected.
Journal of xenobiotics
June 5, 2024
Eva Gil-Martins, Fernando Cagide-Fagín, Daniel Martins et al.
2 citations
Substituted phenethylamines, including 2C and NBOMe drugs, are potent psychoactive substances with unknown toxicity. In laboratory experiments using rat brain cells and a human cell line, six such drugs (2C-T-2, 2C-T-4, 2C-T-7 and their NBOMe versions) caused concentration-dependent cell death. NBOMe drugs were more toxic than their 2C counterparts, a difference linked to their lipophilicity. The cell damage involved mitochondrial dysfunction, shown by loss of mitochondrial membrane potential and lower ATP levels. Two drugs, 2C-T-7 and 25T7-NBOMe, also disrupted calcium regulation. Although reactive oxygen species did not increase, total glutathione levels fell, indicating oxidative stress. These findings clarify the mechanisms behind these drugs' neurotoxicity.