Ah, my mistake, so apparently all of these can occur with sodium carbonate in aqueous:
Na2CO3 + H2O <-> Na+ + OH- + NaHCO3
NaHCO3 + H2O <-> Na+ + OH- + H2CO3
H2CO3(aq) <-> H+ + HCO3-
HCO3− + H+ <-> CO2 + H2O (to completion)
and this would account for all species present in a sodium carbonate solution? Couldn't find this drawn up in longhand in my book or anywhere else, so I would guess at this based on patching up all the info I've collected.

That last one isn't "to completion" per se, but in equilibrium with both carbon dioxide being released and atmospheric carbon dioxide redissolving. Also, the third one is pretty much the same reaction as the second one, just written a different way.

Here's how I'd list the reactions(though much of this is personal preference):
CO3-- + H2O <-> OH- + HCO3-
HCO3- + H2O <-> OH- + H2CO3
H2CO3 <-> CO2(g) + H2O

h the second and the first are never BOTH significant contributory reactions at the same pH. Ie, in any given solution, one or the other is VASTLY predominant (or both are relatively insignificant). That's not to say they couldn't be playing tricksy things with tipping equilibria, though.

My intuition would be that we're barking up the wrong tree examining anions, and that the story's in the cation, but the Merck index specifying re carbonates and hydroxides is both intriguing and contrary to that hypothesis.

I agree. The predominant reaction that provide hydroxides in a solution from carbonate ions is the

The second reaction HCO3- + H2O <-> OH- + H2CO3 is way too insignificant at raising the concentration of hydroxides. And the third reaction H2CO3 <-> CO2(g) + H2O is also too insignificant to play a role since the amount of H2CO3 that dissociate to CO2(gas) and water are going to be too little. It would take ages to deplete the carbonate off a solution via this pathway. Destruction of bufo and psilo on the other hand is (reportedly) destroyed much much faster.

Now I will take my turn at trying to explain the phenomenon. The explanation is based on 69ron/spasticspaz's mentioned fact that phenols have weak acidic properties, i.e their hydroxile can be deprotonated.

Since it has been speculated that both psilocin's and bufo's hydroxile can be deprotonated in high pHs (which is really not too far-fetched) then could it be that the acquired negative ion on the indole ring somehow attract the dimethylated ethanolamine arm of the molecule? I try to demonstrate this on the attached image. Arrows indicate nucleophilic attacks.

So...my thesis is that dehydrobufotenine formation requires deprotonation of the bufo's hydroxile. And this may not happen because of the fine balance of ions in carbonic solutions. That is, as I previously stated the sodium carbonate solution may form a weakly buffered solution.

And a sodium carbonate solution can be technically considered a very weak buffered solution. Just as a solution of sodium carbonate and sodium bicarbonate is a buffered solution.

I therefore propose that sodium carbonate solutions can work as very weak buffers. to weak to withstand the effect of strong bases or acids but strong enough withstand pH changes that can be brought by by such weak acids as a hydroxylated indole.

Very interesting you guys.

The idea of bufotenine forming dehydrobufotenine in strong alkali is not too far fetched. It is after all a hypothesis proposed by Alexander Shulgin himself in TiHKAL.

How would this apply to harmalol?

Hmmmm…if harmalol is deprotonated that should change it’s polarity to a certain degree, and that could explain it’s solubility in hydroxide versus it’s insolubility in carbonates. However, there’s no mention of harmalol decomposing in alkali. Harmalol has no side chain like psilocin and bufotenine have, so the proposed decomposition from bufotenine to dehydrobufotenine, while it makes sense for bufotenine, would probably not apply to harmalol. Interesting.

Has anyone been able to make dehydrobufotenine from bufotenine and have it analyzed to be sure this actually happens and is not just a theory proposed buy Alexander Shulgin?


IMAGE OF HARMALOL:

A possible issue with your buffer hypothesis stems from the fact ammonium hydroxide (or aqueous ammonia, if you prefer that nomenclature) also creates a buffered solution, however: NH3 coexists with NH4+ ions in the same way CO3-- coexists with HCO3-. In fact, it's an even weaker base than the carbonate ion.

Also, while your mechanism for the formation of DHB seems very plausible (especially as Shulgin came to the same conclusion), buffers also don't quite work the way you've described. Buffers don't maintain pH by preventing deprotonation/protonation of other species in solution, but by effectively "absorbing" any proton surplus/deficit that deprotonation/protonation of other species may create. At a given pH, the same percentage of Bufo will be deprotonated, whether the pH is buffered or not. However, the degree to which the pH of the solution decrease as the Bufo deprotonates will be less in a buffered solution than in a non buffered solution. So in fact a buffered solution that starts at a given pH before the addition of the Bufo will in fact have MORE Bufo deprotonated at equilibrium than a non-buffered solution that starts at that same pH.

Edit: A complete tangent, if it turns out that DHB is active through some route (oral? sublingual? insufflation?), I would strongly hypothesize that n-demethylation would make it even more active. SWIM wishes desperately he still had access to reducing agents.

Edit2: The image 69ron posts differs from the standard isomer of harmalol, the difference being effectively a hyperconjugated analog of keto-enol tautomerism, with what 69ron posted being the keto version and the more typical isomer being the enol form. How readily do the forms interconvert? If not so readily, could the keto form be a degradation product that could be produced by high pH? Has anyone tried?

You're right here. My reasoning bout the buffering thing is a bit flawed,

But do we at least accept the hypothesis that DHB formation would require the deprotonated derivative of bufotenine? If so, then carbonate solutions either prevent deprotonation "somehow" or they "somehow" prevent the series of nucleophilic attacks as described above.

I'm baffled again.

Yeah. Here you go. These are two images ( page 797 and 798 ) even though it looks like one. Notice that there is no real freebase form of harmalol. The freebase forms the trihydrate in water.

ive been trying to follow and absorb everything you guys have been talking about..and i think im getting it..but when you guys finally figure it out...maybe you could explain it in such a way that i wont be completely baffled about whats happening thanks!

I suspect it's highly relevant that the Merck index specifies "alkali hydroxides" rather than simply saying "hydroxides". Alkali hydroxides are hydroxide + a cation from the first group of the periodic table, eg sodium, potassium, etc.

For inorganic bases, the only relevance of the cation is in determining solubility of the the basic anion. Alkali hydroxides are able to generate higher pHs than carbonates, and it seems that the Merck index is simply conveying that harmalol is only soluble in VERY VERY basic solutions.

Good observation. It could be the Merck Index's way to say that harmalol is soluble in pH values higher that those that can be achieved by carbonate ions. I am still unsure whether ammonia can be considered an alkali base...Would be interesting to see whether harmalol is soluble in ammonia solution.

so i tested my bufo extract and was a tad underwhelmed also. i think it might have something to do with water in my acetone.

can someone please explain the science behind why anhydrous acetone is important?

Ammonia's definitely not an "alkali" base.

69ron himself has noted that the formation of DHB (if that is in fact what's forming) is frustratingly unpredictable. Perhaps either the test in which SWI69ron found the conversion to occur in ammonium hydroxide or the test in which he found the conversion didn't occur in sodium carbonate was a fluke?

Dunno. But repetition of the said experiments/observations from other members would be utterly invaluable. SWIM's friend has not the time to repeat those experiments, he might find some time though. So, the experiment is:

1) mix bufo FB with Calcium hydroxide and water to make a paste, then let dry.

2) mix bufo FB with sodium carbonate and water to make a paste, then let dry.

The bufo FB treated with Ca(OH)2 should be insoluble in acetone (according to 69ron's claims?) and not retrievable, whereas the bufo FB treated with sodium carbonate should be fine, soluble in acetone and unaltered.

The problem with that experiment is that the bufotenine in the Ca(OH)2 paste will be exposed to a much higher pH than in the Na2CO3 paste.

What should be done is that two solutions, one of Ca(OH)2 and one of Na2CO3, should be prepared to the same pH, perhaps 12 or 11 (The Ca(OH)2 solution will be less concentrated than the Na2CO3 one), and bufo dissolved in each. Wait overnight, then test their solubilities. If one had access to sufficient bufo, one could equally add a test in NH4OH and NaOH (both raised to the same aforementioned pH).