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Biosynthetic Pathway of Psilocybes: Presence of phenylethylamine in Hall. Psilocybes

Jabberwocky

Jabberwocky

Frumious Bandersnatch
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Presence of phenylethylamine in hallucinogenic Psilocybe mushroom : Possible role in adverse reactions
by: BECK O. (1) ; HELANDER A. (2) ; KARLSON-STIBER C. (3) ; STEPHANSSON N.

Abstract: The use of mushrooms containing the hallucinogenic substance psilocybin for intentional intoxication is relatively common. Occasionally, this results in adverse reactions with typical tachycardia that is not evidently caused by psilocybin. This study demonstrates the presence of phenylethylamine in the species Psilocybe semilanceata using gas chromatography-mass spectrometry and shows that the amount of this substance may vary much more than that of psilocybin. The highest amount of phenylethylamine (146 μg/g wet weight) was observed in mushrooms from a case of three young men hospitalized because of adverse reactions. Comparison of the symptoms observed in clinical cases of magic mushroom intoxication with those after intake of pure psilocybin or phenylethylamine suggests that phenylethylamine might have a role in the development of adverse reactions to Psilocybe mushroom intake.

OK, I have a couple questions....as this is new information to me...I figured somebody in here would be able to answer.

1) What possible biosynthetic pathway does the mushroom body utilize to produce phenethylamine?

2) What is the reason for the adverse reaction (ie where does the contradiction lay)?

3) Is it possible for the mushroom fruit to hydroxylate the phenethylamine into tyramine (4-ho-pea)?

I think I have more questions, but those are the ones I'm most curious about. Thanks!
 
also, how is PEA absorbed without being destroyed by MAO-B? Is it PEA itself or a metabolite of PEA (after being broken from MAO)?
 
Nobody has any comments on this....I can't believe this is not interesting to some knowledgeable folks. Mushrooms synthing PEAs! Think of the possibilities!
 
1) What possible biosynthetic pathway does the mushroom body utilize to produce phenethylamine?
Click to expand...
Chorismic acid is the precursor to both, the PEAs and the tryps.
The chorismate mutase converts the chorismic acid into prephenic acid which yields within several steps in tyrosin and phenylalanin and so, in phens.
The enzyme anthranilate synthase converts chorismic acid into anthranilic acid, which is the bio-precursor for tryptophane and so for the tryps.
When the organism has both enzyms, it could make both.
2) What is the reason for the adverse reaction (ie where does the contradiction lay)?
Click to expand...
No idea!
3) Is it possible for the mushroom fruit to hydroxylate the phenethylamine into tyramine (4-ho-pea)?
Click to expand...
maybe?
 
bump this old thread. I have been wondering about this lately again. I was discussing this with a friend and cited this (nobody has heard about this pretty much).

The question still remains, how is the PEA active? It *must* (lol rhetoric not a logical necessity) be the case that PEA is being hydroxylated or otherwise converted to an orally active compound? Right?

They have to be wrong in their assumption that it is the PEA interacting with the psiloc(yb)in to produce the negative effects since PEA is not itself orally active (it is destroyed by MAO-b).

It amazes me that mushrooms are capable of synthesizing PEA!!! How much do we not know about these magnificent organisms?

Am I alone in wondering about this???? Come on...I don't know enough to solve this puzzle! Help please from what I have called ya'll before in previous threads (chem whizzes!)!!! =D

peace and respect,
samadhi
 
For question #2, I have some mere conjecture to offer:

It seems that there must be something else going on here that we're as yet unaware of.

Say your dry weight dose of the p. semilanceata with the highest PEA content of the samples that they analyzed is 2 grams, and assuming that the dry weight is about 10% of the wet weight, then the PEA content of a 2 gram dose is still less than 3 milligrams. Certainly, this is a negligible amount, as previously stated, MAO-B would render inactive any but the highest oral dose of phenethylamine. Less than three milligrams shouldn't have any effect at all on the user. But the literature does suggest a relationship between PEA content and adverse reactions involving tachycardia and hypertension among others.

"One case of Psilocybe semilanceata intoxication resulting in seizures, cardiopulmonary arrest and myocardial infarction is reported."-Psilocybe and others (Group PIM G027)

Apparently, the enzyme pathways involved in the biosynthesis of psilocybe alkaloids have not been thoroughly elucidated. According to the data, PEA is occasionally produced by psilocybe mushrooms so maybe there is an MAO-inhibiting factor that is also produced?

There was recently discovered an MAO-inhibiting factor in mimosa hostilis that is said to be responsible for it's oral activity as a standalone source of DMT and 5-MeO-DMT. Possibly, there is an analogous factor in psilocybe mushrooms that has evaded discovery.

If that were the case, then the researchers' assumption that interactions between PEA and psiloc(yb)in are responsible for the negative effects would be plausible. Aside from that, it seems a mystery.

I can't find any info stating the presence of chorismate mutase in psilocybe, but that begs the question of how phenylethylamine ended up in a sample of p. semilanceata.

Could it be that the phenylethylamine-attributed effects in the cases in question are brought about by some neurochemical effect exerted secondary to the central action of psilocin? It seems prima facie more plausible that the tachycardia and hypertensive effects (supposedly PEA-related) are a consequence of the 5-HT agonism or some other effect by/of psilocin; as opposed to the idea that the orally administered miniscule dose of PEA exhibits some central action when it is administered concurrently with psilocin, psilocybin, baeocystin, and/or norbaeocystin.

You're not alone s_s, these are intriguing questions. If only researchers could get more funding to pursue answers to these types of questions!
 
So, three dudes had a bad response to mushrooms and these mushrooms were found to have 146 ug/g of phenethylamine in them. Therefore, the guys ingested what, like 500 ug of PEA per person. Am I missing something here?
 
Strange! When I check PIHKAL, PEA is given as completly inactive in doses up to 1.6 g, even 50 mg i.v. are not active. How can this be explained?!?! I would say, the adverse reactions occured due to something different...

About your 3rd question: Possibly yes! Indeed quite probable. But just guessing here.

Peace! Murphy
 
samadhi_smiles said:
1) What possible biosynthetic pathway does the mushroom body utilize to produce phenethylamine?
Click to expand...
i highly suspect some sort of phenylalanine decarboxylase to convert phenylalanine into phenethylamine. that would be the simplest solution as phenylalanine is ubiquitious and the whole reaction is completely homologous to 5-HTP -> 5-HT. i don't know if that enzyme has been found in shrooms though...
 
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