Toxicity data on the chloro-mda compound would be great, but I don't think much is available as yet sadly
People are also using a crude mixture of aldehydes/ketones (stemming from oxidation of a conspicuously ecstasy-like aldehyde) in reductive amination to yield MDMA as well as "n-methyl piperonylamine" and "n-methyl-helionamine." A quick search for the former didn't bring up any leads, but I'm sure some sort of toxicology study for this compound exists. It is well established as a byproduct of MDMA synthesis from a variety of routes.. For the n-methyl helionamine there is unlikely to be any data available.
As to something I actually can weigh in on: when synthesizing DMT from tryptamine by reductive methylation with formaldehyde,
if special precautions are not taken one will form a substantial amount of pictet-spengler cyclization product 2-methyl tetrahydrobetacarboline. Given the structural similarity between this compound and MPTP, its ability to selectively destroy dopaminergic neurons in the substantia nigra is of utmost concern.
Interestingly, the compound has been isolated from brain and nerve tissue, so it is produced endogenously to some degree.
As with MPTP -> MPP+, the 2-me-thbc needs to be first oxidized in vivo to form the potentially toxic species. While the beta carboline is a poor substrate for MAO (this is good), it CAN be oxidized to the "toxic" compound by heme peroxidases. See
Herraiz, Tomás, Hugo Guillén, and Juan Galisteo. "N-Methyltetrahydro-?-carboline analogs of 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) neurotoxin are oxidized to neurotoxic ?-carbolinium cations by heme peroxidases." Biochemical and biophysical research communications 356.1 (2007): 118-123.Studies using direct intracerebral perfusion of the 2-me-thbc into rat brains suggest that it does NOT destroy dopaminergic neurons in the manner that MPTP or MPP+ does, however perfusion of the pre-oxidized beta-carboline (2-mbc+) is neurotoxic, though to a lesser degree than MPP+. The thought is that the beta-carboline is not efficiently oxidized by MAO, and so toxic levels of 2-mbc+ are never reached (phew). See:
Rollema, Hans, Raymond G. Booth, and Neal Castagnoli. "In vivo dopaminergic neurotoxicity of the 2-?-methylcarbolinium ion, a potential endogenous MPP+ analog." European journal of pharmacology 153.1 (1988): 131-134.More good news: when monkeys were loaded up with 2-me-thbc on a daily basis, they did not get parkinson's disease!
Collins, Michael A., and Edward J. Neafsey. "?-carboline analogues of N-methyl-4-phenyl-1, 2, 5, 6-tetrahydropyridine (MPTP): Endogenous factors underlying idiopathic Parkinsonism?." Neuroscience letters 55.2 (1985): 179-184.So the moral of the story? The impurity from sloppy DMT synthesis will
probably not give you parkinson's disease. But it's still a good idea to keep the temperature low in your methylation and avoid taking any risks
Now some
bad news for methcathinone fans: Trace amounts of permanganate left in the product after oxidation of [pseudo]ephedrine will cause irreversible damage to the basal ganglia, resulting in permanent parkinsons-like symptoms including changes in gait and speech. See
Stepens, Ain?rs, et al. "A Parkinsonian syndrome in methcathinone users and the role of manganese." New England Journal of Medicine 358.10 (2008): 1009-1017.It should be noted that the participants in the study were heavy intravenous users.. But even still, Beeee safe folks. No buzz is worth permanent neurological damage.
