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Neurotoxicological profile of the hallucinogenic compound 25I-NBOMe.

Monika Herian, Adam Wojtas, Marzena Maćkowiak, Agnieszka Wawrzczak-Bargieła, Anna Solarz, Agnieszka Bysiek, Katarzyna Madej, Krystyna Gołembiowska

Scientific Reports February 21, 2022 DOI: 10.1038/s41598-022-07069-8 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Experimental study Peer reviewed
Population Rats
Intervention 25I-NBOMe
Duration 72 hours after chronic treatment
Citations 15
Key findings 25I-NBOMe crosses the blood-brain barrier, accumulates in the brain, causes DNA damage, and reduces glial cells in the frontal and medial prefrontal cortex without inducing apoptosis.

Abstract

4-Iodo-2,5-dimethoxy-N-(2-methoxybenzyl)phenethylamine (25I-NBOMe) is a new psychoactive substance with strong hallucinogenic properties. Our previous data reported increased release of dopamine, serotonin, and glutamate after acute injections and a tolerance development in the neurotransmitters release and rats' behavior after chronic treatment with 25I-NBOMe. The recreational use of 25I-NBOMe is associated with severe intoxication and deaths in humans. There is no data about 25I-NBOMe in vivo toxicity towards the brain tissue. In this article 25I-NBOMe-crossing through the blood-brain barrier (BBB), the impact on DNA damage, apoptosis induction, and changes in the number of cortical and hippocampal cells were studied. The presence of 25I-NBOMe in several brain regions shortly after the drug administration and its accumulation after multiple injections was found. The DNA damage was detected 72 h after the chronic treatment. On the contrary, at the same time point apoptotic signal was not identified. A decrease in the number of glial but not in neural cells in the frontal (FC) and medial prefrontal cortex (mPFC) was observed. The obtained data indicate that 25I-NBOMe passes easily across the BBB and accumulates in the brain tissue. Observed oxidative DNA damage may lead to the glial cells' death.

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