Talk:Α-Amanitin

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I could not find any references regarding the hallucinogenic properies of alpha-amanitin. On the other hand, another species of Amanita, the fly mushroom (A. muscaria) is a well-known hallucinogen (but this is not due to amanitins, which this species does not contain; rather it is due to ibotenic acid and muscimol). Could there be a confusion here? We certainly do not want hallucinogen enthusiasts to try and consume A. phalloides. Tjunier 10:02, 20 December 2005 (UTC)[reply]

For one, Wikipedia should not be a key or a means of identification for hallucinogen enthusiasts. I is an encyclopedia, leave the latter for a website like Erowid. Second of all, who said anything about alpha-amanitin having hallucinogenic properties? It has no hallucinogenic properties, it is an Amatoxin and nothing more. I believe the psychedelic in Amanita muscaria, at least the most outstanding one, would be Muscimol.--Neur0X ^.talk 13:21, 17 July 2006 (UTC)[reply]

Alpha-amanitin is a RNA polymerase II inhibitor, whereas most hallucinogens work on neurotransmitters (either directly through inhibition/activation or through association with their associated proteins). 124.197.60.79 (talk) 12:54, 9 December 2009 (UTC)[reply]

Image

I think that the (line) image here, while very illustrative of how alpha-amanitin is cyclic, is a bit confusing, and makes some groups (more specifically, methylene groups) hard to see. I'm going to revert to the previous image, which is quite clear. Jesse 20:57, 30 August 2006 (UTC)[reply]

I uploaded a second version that shows methylene groups on the major rings. Do not revert - the old image is inaccurate as it doesn't show the phenolic —OH group. Bryn C (^t/_c) 22:46, 8 October 2006 (UTC)[reply]

Is the full name including "prolyl" or "proly" Richard8081 (talk) 03:49, 3 May 2021 (UTC)[reply]

WikiProject class rating

This article was automatically assessed because at least one WikiProject had rated the article as start, and the rating on other projects was brought up to start class. BetacommandBot 16:23, 10 November 2007 (UTC)[reply]

Evolutionary purpose of amanitins

I am rather intrigued by the amanitins and their evolutionary purpose. Could someone explain what this might be? If the fungi produce them to deter predators from eating them why are they so slow acting? A toxin that takes over a week to take effect would seem a poor deterrent. Possibly they have another role? Either way, their must be a reason for their production as it would seem unlikely that the fungi would expend energy synthesising them for no reason. Booshank 19:17, 3 December 2007 (UTC)[reply]

This is a perfect weapon crafted with an outstanding finesse and it works extremely well. How fast it acts is irrelevant, the predator will be dead anyway - it won't produce any offspring and will be completely wiped out unless it stops feeding on those lovely mushrooms.Enemyunknown (talk) 06:24, 28 June 2009 (UTC)[reply]

Screening Method to Prevent Poisoning?

A few years ago I read of people in Russia who were desperate for food took the known risk of mushroom poisoning and suffered death. What I see written in this article seems to focus on the initial site of poisoning, leading to death in humans. Has anyone considered coming up with an insect (like crickets, roaches, or ants) that could be subjected to a mushrooom extract for screening. Since those insects do not have livers or kidneys, but do have RNA polymerase, it seems there could be some time line of toxic effects, but the extraction procedure would have to be easy for the indivdual to perform. It just seems something should be worked out to prevent further avoidable tragedy.

71.114.183.105 (talk) —Preceding comment was added at 21:53, 5 December 2007 (UTC)[reply]

Really nonribosomal?

There is a recent paper by Heather Hallen-Adams et. al., http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2141914 which reports them being synthesized on ribosomes. I don't feel competent enough to asses the validity of the mentioned results to alter the article here. --Ralf Muschall (talk) 22:11, 18 August 2008 (UTC)[reply]

I would argue that these compounds can still be classified as non-ribosomal peptides as the extensive modifications needed to cyclisize the ribosomally synthesized "prepropeptide" most probably need other enzymes. However, traditionally the phrase "non-ribosomal peptide" have referred to peptides synthesized by multimotif peptide synthetases (analogous to fatty acid synthetases) so I can understand the confusion. —Preceding unsigned comment added by 193.128.243.6 (talk) 11:59, 29 September 2008 (UTC)[reply]

Idea about the evolutionary purpose

Besides the possible causes mentioned elsewhere (polymerase blockers kill almost everything, from parasitic fungi to mammals), here is another idea: The fruiting bodies above ground are just body parts of a (possibly huge) being, thus being eaten (and thereby killing the "predator") is not a real sacrifice (compare this to venomous snakes, where defense (in difference to food acquisition) exerts no selective pressure on venom strength, since even deadly defense is a dead end for the gene, as the snake is most probably killed anyway). Having a slowly acting poison might kill off the fungus-eating animal (or even a whole pack of them) without substantial loss to the being (just a few body parts are gone). The silent way of killing might help avert behavioral countermeasures (e.g. eating only small portions) on the side of the animals.

OTOH, it might just a question of efficiency: Using the enterohepatic cycle vastly reduces the effective LD50, thus reducing the amount of expensive (each CO-NH-bond costs 4 ATP) protein the fungus needs to synthesize. In this case, the slow action is just a side-effect of the low dose and repeated reusage. --Ralf Muschall (talk) 22:11, 18 August 2008 (UTC)[reply]

Antidote to Amanitin

I think it would be helpful to note that there is a putative antidote to amanita poisoning in Phase 3 trials: Legalon® SIL an extract of Milk Thistle consisting of silbinin (see the Wikipedia entry on Silbinin)68.48.169.215 (talk) 03:01, 19 October 2010 (UTC)[reply]

Pathogenesis?

The article mentions that α-amanitin causes diarrhea and cramps as the first symptoms, and eventually leads to liver and kidney failure. It also mentions that α-amanitin acts by inhibiting RNA polymerase-II. But, how does RNAP-II inhibition cause diarrhea, cramps and eventually liver and kidney failure? User8647 (talk) 14:51, 6 January 2023 (UTC)[reply]