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Dr.Bob
International Hazard
Posts: 2753
Registered: 26-1-2011
Location: USA - NC
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Mood: Mildly disgruntled scientist
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Quote: Originally posted by BromicAcid  |
In terms of chemicals I have worked with:
Most Toxic : Phosgene (45 kg neat in a 72L flask stirring around, for a split second nearly caused a panic attack)
Most Pyrophoric : Dimethylzinc (thankfully don't have the scars to prove it)
Most Corrosive : Sulfur tetrafluoride (it ate the silicone tape!)
Most Malodorous : Butyl isocyanide (words can never express...) |
That is a pretty good list. I have made a few isocyanides, I remember cyclohexyl being really bad, it is a terrible small that is completely foreign
to you, so you can't place it, but it makes you want to wretch.
I have not worked with to many really bad pyrophoroic ones, have used a lot of hydrazine over the years.
I likely worked with SF4 years ago at the fluorine place, but know we worked with HF, F2, and lots of perfluoropropene. Since I was young, they
mostly had me distill mixtures of Freons.
I have use small amounts of phosgene and thiophosgene, but one of my coworkers years ago spilled some thiophosgene in a hood and nearly wiped out a
crew working on the roof. Another one dropped a bottle of MeI on the floor and created a puddle in the main hallway and then wondered off since they
were not sure what to do... Eventually the security guards saw it and asked someone what it was. By the time we cleared the place out and were
able to clean it up, it ad all evaporated and also discolored the floor tiles dyes.
And someone beat me to the ClF3, it definitely wins one of the worst things to work with for me.
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bismuthate
National Hazard
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Registered: 28-9-2013
Location: the island of stability
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Mood: self reacting
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I just was working with H2Se and H2S recently.
Wait, BromicAcid, where the heck do you have a 72L flask?
[Edited on 7-12-2013 by bismuthate]
[Edited on 7-12-2013 by bismuthate]
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Theoretic
National Hazard
Posts: 776
Registered: 17-6-2003
Location: London, the Land of Sun, Summer and Snow
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Mood: eating the souls of dust mites
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| Quote: Originally posted by kristofvagyok | I only worked with isocyanoacetic acid ethyl ester, what also had a horrible smell, but someone on the sixth floor poured out some isocyanides to the
sink and the whole building smelled like that  |
It's interesting that this isocyanide-ester still stinks, but these isocyanide esters with an aromatic ring linking the two groups have nice smells. At the time I thought having the ester on the same molecule
is all it took, as though one signal overrides the other.
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Chlorine
Hazard to Self
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Registered: 26-11-2016
Location: Maine, USA
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Mood: Brominated
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Denatonium Benzoate; I will never touch this material again.
Few months ago I made about 1.5 grams to use as a biting deterrent for a puppy, for the next 2 weeks I couldn't eat anything with my hands, no matter
how many times I washed them. It was a nightmare.
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tsathoggua1
Hazard to Others
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Registered: 8-1-2017
Location: Beyond the pale
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Mood: Phosphorescent
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CrO2Cl2. I'll work with it. But the second time ever working with the stuff almost gave me a heart attack, figuratively speaking.
Preparing near enough a liter of it, using a mixture of potassium dichromate, 98% H2SO4 and NaCl. The flask failed and the bottom half of it just
dropped off. I swear, you've never seen a chemist run so bloody fast as I did that day. I was lucky, very, very lucky that I didn't get doused in
boiling hot chromic acid, H2SO4 and chromyl chloride, which itself is a nasty customer of an aggressive oxidizer. Incompatible with many solvents, and
almost certainly so with chemist genitals when strongly heated and accompanied by a liter of extremely corrosive rxn mixture, strongly heated as the
CrO2Cl2 distilled over. Fumes like a woman cheated on (not that I myself would do that) and gives off HCl, chromic acid and leaves behind lots of
nasty Cr(VI) residues upon hydrolysis. Volatile Cr(VI) species aren't really my idea of pleasant to begin with. But CrO2Cl2 is, well, bad tempered,
ornery stuff.
That incident resulted in having to saw out and replace a large portion of bench top. I shudder to even picture the consequences of a mixture like
that hitting flesh cold, let alone when being heated to a minimum of 117'C (its BP), I should imagine a mixture of 98% H2SO4, chromic acid,
dichromate, (does this rxn produce any chlorosulfonic acid as a byproduct via chlorination of the conc. H2SO4?)
Chlorosulfonic acid, thats another nasty little sod.
As for interesting in particular, I'll go for some of the marine biotoxins, especially polyketide types like maitotoxin and palytoxin. The latter
produced by corals of certain species, such as Palythoa toxica and maitotoxin is produced by dinoflagellate planktonic organisms and bioconcentrated
in fish, particularly reef fish, and can cause ciguatera fish poisoning, an interesting feature of which, is that it can cause the sense of
temperature to reverse, cold feels like heat and vice versa. Deadly too, with maitotoxin (mouse) LD:50 being 50ng/kg, thus far, the most lethal of the
non-protein toxins known.
And the structures are astonishingly complex. I'll link to the wikipedia articles rather than input them here, since that would make for one hell of a
TLR, palytoxin has some 74 sterocenters, and of all the isomers, apparently
only the one produced by this coral, along with some crabs, particularly xanthids is such an intensely lethal toxin, second only in the natural world
that we as yet know of, to maitotoxin, although it does have toxic analogs.
Working via locking open NaKATPase; the natural target of the cardiac glycosides such as strophanthins, digitalis and the active
cardiotonic/cardiotoxic principle of the lilly-of-the-valley plant, convallatoxin as well as the poisonous principle found in oleander, creating an
ion channel from the normally selective pump acting as sort of a passive bidirectional ionophore, and resulting in a massive ion flux compared to
normally functioning NaKATPase-mediated Na/K flux which, as one would expect, completely buggers up cellular ionic homeostasis, making for a general
cytotoxin, its also an extremely powerful vasoconstrictor with a very, very rapid action, potentially killing within minutes, and when used as a
weapon, by hawaiian spearmen, was legendary for its rapidity of action, stated to cause near instant death. Reportedly, people have been poisoned
after dermal contact with tank water in which aquaculture hobbyists have had Palythoa corals living, and in one instance, after some bugger tried to
kill one by pouring boiling water on it, the steam vaporized some of the toxin, and the coral got payback.
Reportedly, although it won't affect the ionophore type effect that disrupts cellular ionic gradients, intracardiac injection of strong vasodilators
may save lives. Although with any significant exposure, due to the rapidity of effect and lethality, paramedics are probably going to find a corpse or
corpses rather than a patient. Less toxic than maitotoxin by a long shot. But nasty stuff nevertheless. Cytotoxic effective concentration (LD:50 or
LD:100 is not stated, but 200 fM for cytoxicity and 1.5nM for haemolysis, although given the orders of magnitude differential by the time the latter
plays a part, its going to be doing it in the erythrocytes of a dead body.
And believe it or not, it has actually been synthesized by man! with 10 to the power 70-something (I can't see the last number, I think its 10-76 06
10-78, the damage to my eyesight after a recent accident and a couple of nasty childhood accidents to the other eye has left me with poor sight)
stereoisomers that is what I call an impressive feat of chemistry.
It took IIRC 11 years before its structure alone, was discovered.
http://science.sciencemag.org/content/246/4926/34.4
And a much, much more interesting article on palytoxin
https://link.springer.com/article/10.1007%2Fs11101-010-9185-...
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tsathoggua1
Hazard to Others
Posts: 335
Registered: 8-1-2017
Location: Beyond the pale
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Mood: Phosphorescent
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And for some land-based natural nasties, hows about the steroidal alkaloid batrachotoxin, found in, but not produced by (the suspected source is an
inset prey item of the frogs, for whilst captured frogs may remain highly poisonous for years, frogs reared in captivity reportedly do not show
toxicity)
These tiny frogs, are thumbnail-sized, and the deadliest of them, Phyllobates terribils, the golden poison dart frog, reportedly packs enough
batrachotoxin and analogs to kill two full grown bull (african) elephants. And the effect is near instantaneous. I've seen a natural history clip
where these toxins, applied to poison darts, were used, and a monkey was hit by such a dart fired from a blowpipe, and it dropped out of the tree as
fast as would have happened had the attack been a head-shot from a high velocity large caliber round. Whack, drop. Never even had chance to move,
probably never even knew it had been hit.
This is the structure of the toxin, and a lethal dose is IIRC, in a human, around 150ug. I'd think that any antidote, bar a prophylactic agent
administered before exposure would be useless given the instantaneous lethality of batrachotoxin.
https://upload.wikimedia.org/wikipedia/commons/thumb/b/b2/Ba...
Mouse LD:50 (subcut) µg/kg and the mode of action is via targeting voltage-gated sodium channels and locking them open, causing at first a massive
acetylcholine release then flaccid paralysis, also destroying the neurotransmitter vesicles that store neurotransmitters within the synapse,
essentially acting as an extremely powerful and rapid-acting, irreversible depolarizing neuromuscular blocking agent, like an irreversible version of
succinylcholine (a rapid-acting, short-duration depolarizing neuromuscular blocking paralytic agent used medically to induce muscular paralysis during
procedures such as intubation for mechanical ventilation)
The difference between the depolarizing, and non-depolarizing neuromuscular blockers, is that the former induce acetylcholine release at first,
causing initial muscle fasciculation and then exhaustion of capacity to move, whilst also blocking the neuromuscular junction*
The non-depolarizing agents, first inspired by the action of another dart poison, curare, bind to the nicotinic acetylcholine receptor at the endplate
of the neuromuscular junction, serving as NAChR antagonists and inducing flaccid paralysis.
And a few fungal toxins:
Of course, who could, where fungal toxins are concerned about, omit the obvious and notorious go-to (albeit erroneously claimed for) deadliest
macrofungi* the Amanitas of the subsection Phalloideae
These being such as the death cap, Amanita phalloides (no, sorry, I'm not offering any prizes for guessing what happens if you eat a piece of this
mushroom), which is frequently albeit wrongly claimed to be the deadliest (macro)fungus in the world, in terms of lethal dose.
Along with its family relatives and friends the eerie, although beautiful, and immaculately white destroying angel (who wants destroying angel soup
for dinner? any takers? didn't think so. Me neither) Pretty, oh so pretty. As white as a ghost, and most proficient into making them, Amanita virosa,
as well as the fool's mushroom or spring Amanita, A.verna, differing primarily in slight traits only, visually speaking at the macro-level, such as
the tendency of A.virosa to have a volva that unlike A.phalloides, doesn't appear as a big, wide, deep courtenay love's muff-esque poisonous
foetid-smelling (as does the rest of the mature fruitbody
the death cap has a sickly sweet but foetid kind of smell often, although somewhat reminiscent especially when younger of raw potatoes, although the
raw potato smell is much more pronounced in the false death cap which although not a recommended item for the table, and contains bufotenine,
A.citrina syn. A.mappa, from which amatoxin cyclic oligopeptidic cytotoxins are absent* *actualy, not strictly true, at leat some strains of the
fungus do indeed contain amanitins, however in quantities far too miniscule to prove lethal or dangerous, the primary danger comes from
misidentification and the picking of a lethally poisonous lookalike and subsequent slow, horrific, and most unspeakably unpleasant, drawn out period
of suffering and misery then either liver and potentially kidney transplant with corresponding longterm or lifetime potential need for
immunosuppressive antirejection drug regimen or death in most agonizing form) sack.
These, as well as other members of the clade within the genus Amanita, the subsection Phallodieae (or might be Phalloidinae, I forget) contain three
major families of cyclic peptidic toxins, based around a tryptophan indolic central core. The amanitins are the most dangerous, since they are orally
active, and highly lethal, a dose per os, to a human of 5mg of alpha-amanitin is enough to prove deadly and considerably less can easily still do
horrific damage and cause much suffering and illness. This equates to around 50g of A.phalloides var.Phalloides on average, the most common form of
the mushroom, although there is another, white form, A.phalloides var.Alba,
this is unlikely to be mistaken for the destroying angel, even in the field without resorting to examination sub-lente or the use of reagent field
tests by those mycophiles who carry them as a matter of course for a walk in the woods and fields. Generally those who are either professional
mycologists or seriously avid mushroom hunters such as myself, Give me a well-equipped and stocked lab in which I may follow whatever I wish to
pursue, the hand and heart of a lively, very attractive stimmy young Kanner's gal, and a walk in the woods with same and such pre-prepared reagents as
I'd use in the field, plus a backpack full of eats, cold drinks and some good hash for us to blaze, who's willing to get up at 5am to beat the other
mycophiles to finding breakfast, and you've got a happy Tsathoggua.)
The white form of the death cap differs both in its colorimetric reaction to Amanita virosa when the surface of the cap is treated with 15-20% aqueous
KOH, or if caustic potash is unavailable then the same solution made up with sodium hydroxide will serve. As with many fungal field test reagents,
some time may well be required to allow for full development of the color change when used upon a species for diagnostic aid.
Amanita phalloides, contains two of the three families of cyclopeptide toxins, the amatoxins, and the phallotoxins, whilst the third, virotoxins are
found in A.virosa, the extremely similar A.verna, which differs from A.virosa primarily in the texture of the surface of the stem and the fact that it
has a lesser tendency for the volva to be not bag-like but to twine around the base of the stem in a tubular or curved/curled rounded rod-like shape,
which A.virosa the destroying angel, or angel of death has quite the habit of doing. A.virosa also has a very pronounced habit of its cap taking on an
uneven 'jaunty' cap, in shape, veering off to one side, sometimes a little, although shallowishly bifurcated, and differs from A.virosa and A.verna in
its not reacting to KOH(aq.) or NaOH(aq.) whilst the destroying angel does, it changes to a yellow color Neither the more common A.phalloides.var
phalloides or the rarer var.alba react to 20% aqueous caustic potash nor NaOH. I was under the belief that of A.verna and A.virosa only A.virosa
sensu stricto reacted to KOH/NaOH soln.
Also, the gills of A.phalloides turn pale purplish-lilac to pinkish when treated with concentrated H2SO4. Never tested A.virosa and I have only ever
seen Amanita verna once, from 2-3 years old to my current age of thirty. Once. It is extremely rare. And curiously, of all the damned odd places, it
was growing under Rhododendron, albeit around oaks. Normally nothing by way of british macrofungi seems to like growing under or close to Rhododendeon
bushes, for some reason they seem inimical to fungi although why this is, I am most truly ashamed to have to state that I lack this piece of
knowledge For this I apologize sincerely.
Unlike the phalloidea clade within Amanitaceae those within the stirps containing the destroying angel and its closest relatives, contain the third
family of cyclopeptide amanita-toxins, the virotoxins.
Amatoxins are cyclic octapeptides, and are active orally, also undergoing a repetitive enterohepatic recirculation via means of their being absorbed
in bile and reabsorbed intestinally, via the (by then pretty badly trashed) intestinal tract and back through the liver. These Amanita toxins are
hepatotoxins primarily, the cyclopeptide ones are anyhow, there are another two major families of Amanita-toxins, plus a lesser known pair. One
family, consisting of allenic norleucine and chlorocrotylglycine are rapidly acting nephrotoxins (within a few hours, 6-7 hours or so whereas the
other primary nephrotoxins, found in Cortinarius genus of the stirps Orellani within the subgenus of corts, Leprocybe, the genus Cortinarius has a
whole bunch of subgenera, and the Orellani within subgenus Leprocybe contain a UV-fluorescent nephrotoxin with a much worse, and more insidious nature
than that of the allenic norleucine and co of the primarily nephrotoxic Amanitas, which is often of slow onset and can sometime even take from three
weeks to a month, dose dependent I believe, to show up the beginnings of poisoning, these toxins, Orellanin(e) and its derivatives are structurally
related to the weedkiller paraquat, being bipyridyl based compounds, although paraquat lacks the multiple hydroxyl moieties of orellanine and the
4-position amine groups of paraquat are methylated as quaternary ammonium chlorides, whereas those 4-position amines in orellanine are instead in the
form of pyridinium N-oxides, being tetrahydroxylated bipyridyl N-oxides, and slow-acting nephrotoxins with a much grimmer outlook and higher
likelihood of requisition of a kidney transplant or permanent dialysis than poisoning by the non-amatoxic primarily nephrotoxic Amanitas such as
A.smithiana, A.pseudoporphyria and A.proxima within the subgenus Lepidella within Amanita)
The phallotoxins, bicyclic heptapeptide, are not so dangerous, because they are orally inactive, and not readily taken up by living cells. In fact, I,
and others eat the blusher, Amanita rubescens, which contains the phallotoxin phalloidin. It also contains a different poison, rubescenslysin, which
unlike the amatoxins, virotoxins and phallotoxins is thermolabile and boiling it, throwing away the water, boiling it again, throwing away the second
lot of water and then cooking it as desired and incorporating it into your meal of choice, leaches out and eliminates this haemolytic poison, however
the mushroom must never be consumed raw. And it can be confused if incautious or inexperienced with the Panthercap, A.pantherina, related more closely
to the fly agaric, but A.rubescens appears early in the year often before many other tasty fungal treats and is a valuable early find to those with
an appetite for wild mushrooms and insatiable taste for going out themselves to root them out personally,
being dissatisfied with the piss-poor variety of mushrooms sold in supermarkets, at least here in largely culturally mycophobic when it comes to
mycophagy at least and most inadventurous, ignoring so many saprobic fungi, such as the Parasol, Macrolepiota procera, and the giant puffball, which
may in extremely large specimens grow to a meter and a half to two meters in diameter, weigh ten-20kg less than I do myself, and aside from the fact
that it grows big enough to stuff several families stupid if they ate it every meal and snack day or night for a week or two, or for that matter as
long as it can be preserved.
Found two pretty small ones late 2016, late on in the season, only a couple of feet across, around lymm dam, NW england and my gods above and devils
below they are some of the finest of ALL foods I have ever had touch my lips. Bagged them both, and had many a munch, slicing them like steaks, big,
thick juicy steaks, and dipping them in batter, before frying in butter, or just frying them like steaks, using butter. WONDERFUL wonderful flavour,
somewhat salty, rich and savory, filling although even when full to the gills (which being puffballs of course they lack themselves, its the diners
who end up full to the gills) you still want more, and more, and more and more still. Seconds turn to thirds, thirds turn to fourths, and fourths end
up as 8ths, 9ths, tenths and further until one is so replete, you'll want buscopan, ondansetron and several bongs of strong, quality weed to allow one
to rest and digest so one has space for more fried puffball steaks and fritters.
I've planted many samples of ripened portion of each of the two fruitbodies (hoping for if fruiting happens, genetic diversity) in the grassy
portions, both shaded and unshaded, sans non-grassy, shrubbery and under it, all over my lawn, hoping to hope of hopes that I get some of this most
delicious of delicious fungi fruiting. Hell, ONE would be good, not only to eat myself daft, but to take ripened spores and culture them, do a
breeding program and try to develop quality commercial (and of course home-growing) spawn.
Since even a shit yield of quality giant puffballs, unlike most fungi, is actually, in terms of weight, a rather large amount of mushroom fruitbody
and many meals. The pair last year a couple of feet across were just wee'uns, but I had to take them when I found them, precisely because the next
person to spot them and recognize them for what they were would otherwise have robbed me of my find in an attosecond before I had a chance to pick
them myself. Fried, frittered, eggy-breaded, even BBQ'ed at a neighbours BBQ and shared, now those were some of the best meals I've had in years,
fungal or otherwise.
The phallotoxins, mind you, whilst poorly taken up by living cells, and poorly if at all absorbed via the gastrointestinal tract, are lethal if
absorbed by injection. They are also interesting, because they selectively bind filamentous, but not monomeric actin, a cytoskeletal protein and when
conjugated to fluorophores can be used for fluorescence microscopy of cellular architecture, or with certain modifications for electron microscopy of
cell microstructure.
Amatoxins, on the other hand are fully active per os, and fungi containing them are, whilst not THE deadliest on a per weight of fungus basis, the
deadliest fungi in terms of number of deaths, and awful, awful awful deaths at that, they act via inhibition of RNA polymerase type II, primarily in
the liver, and they also affect the kidneys. Primary effect is hepatic however, kidneys secondarily and they seriously fuck with electrolyte balance
and can cause swelling of the brain, presumably secondarily to the fulminant hepatic necrosis they induce.
After an initial GI upset, which may be masked if other GI irritant fungi with a lesser degree of danger but a more rapid action have been consumed
within a meal that includes a big ol' medley of mushrooms, there is a characteristic and pathognomonic sign, amongst mycotoxicoses, a delay between
the ingestion of the lethal amatoxic fungus or fungi (other genera containing these most virulent hepatoxins include Galerina spp., some Lepiota,
particularly the smaller species, although in particular a medium-size chunkyish bugger is a truly vicious and oft fatal offender,
L.brunneo-incarnata. L.helveola is also responsible for serious or lethal poisoning, Conocybe filaris and possibly some other species in the genus
contains amatoxins and has been mistaken for Psilocybe semilanceata, the liberty cap, one of the psychedelic mushrooms by inexperienced or incautious
pickers. As have some of the noxious little woodlovers, the deadly Galerinas, also packed with amatoxins, these are bastardly devious in extremis,
because they look damnably similar to Psilocybe cyanescens, a woodloving Psilocybe related quite closely to P.azurescens, and like this species, its
one of the most potent of the Psilocybes, although relatively speaking is poor for storage, because of its high ratio of psilocin to psilocybin, but
so crowbegotten POTENT that a generous sized harvest, being cleaned of debris and generic crap, by myself and a former housemate, by wiping them clean
prior to sporeprinting each and every single one, by the time we were less than halfway through, we each noticed the other's eyes had pupils that
looked as if they had taken a bath in atropine base and been working out in the gym on eyeball-steroids. Then the walls started breathing and
twisting, colors became brighter and nuttier, and we both ended up tripping arse. And neither myself nor my former housemate had consumed a single
mushroom, my having been in her presence from the moment of picking and journey home to every moment she was in the presence of the mushrooms.
But the amatoxic Galerinas are deadly devious and deadlier poisonous, sneaky as the devil himself and infinitely less popular. Because they can look,
both in the field, and when dried out, both when living in the dry and the moist and wet states, they can look EXTREMELY close to P.cyanescens, only
one will have you trip balls from mere skin contact with moist mushrooms, given enough specimens and time, and one will make you shit your liver out
in liquid blood milkshake format, slowly and painfully, the cheerful little guys that they are. And Galerina autumnalis and other such pestilent
abominations to befoul the earth like a dog turd upon your breakfast cereal, like to grow in the same habitat, at the same seasonal time, same
conditions and indeed same patch, and even the same fucking wood-chip or branch as the most desirable cyans. That harvest that produced such a bounty
of blow-your-nackers-clean-off quality 'shrooms as to require us to beg several mc'donalds happy-meal cartons, empty from the macdonalds in which we
had just eaten and explain our predicament of having several pounds of mycological gold to get a few miles home on foot, and either be given some
empty happy meal cartons, doubled up to protect my (I did the ID, and knew what to look for and what they were, she, had previously never ingested a
psychoactive bar ethanol a handful of times possibly, and after she met me, space cakes, she assisted in the physical harvesting, the cleaning, and we
split them 50-50, I'd also done the spore-printing and taken a peek at the spores under my microscope.
The primary difference, is that the spores of Psilocybe species is violaceous black, whereas the deadly galerinas, those filthy fucking plagues upon
the cancerous anus of the fouler portions of the earth's nastier bits, those septic hemorrhoids deserving of extirpation utterly, due to the lethal
danger they pose to people wanting Psilocybes or other, edible nonpsychoactive such as Kuhneromyces mutabilis, which whilst edible, resembles
G.autumnalis in so close a manner to be inedible and best considered deadly poison. I wouldn't eat them even after a Meixner test (conc. HCl on a
sample of mushroom mashed into high-lignin paper such as newspaper (NOT lab filter-paper!!) and left to develop for up to a half hour or so, reacts
with the indolic portion of the tryptophan residue within the indolic core of the cyclopeptide Amanita-type toxin families to give a purplish-lilac
halo around the portion of cap, it crossreacts however, unfortunately with psiloc(yb)in, bufotenin, and other tryptamine and indolics. Unfortunately
at least, for those who would otherwise wish the Meixner to be used for discriminatory qualitative test (and its pretty sensitive quantitatively, at
least, reacting with some very, very small quantities of indoles. Apologies, but I don't know if it also works with benzothiophenes and benzofurans,
indenes/indanes or tetrahydrobenzpyrroles, but it will almost certainly tell you if you have something packed with poison in front of you and that
poison is an amatoxin)
Alpha-amanitin is selective for RNA polymerase II, although beta-amanitin inhibits both type II and type III RNA polymerase. This results in
inhibition of intracellular protein synthesis and after a delay, necrotic cell death and cytolysis. Brutal and extremely effective. And amongst the
nastiest fungal toxins going in terms of what they do to those poor rotten bastards unfortunate and/or stupid to eat something containing them. There
are many other amatoxins also, none of them nice customers in the slightest.
So virulent indeed are these, that the first thing a wouldbe learning mushroom hunter must do, is learn to recognize Amanita species on sight in the
field, and in particular, A.phalloides and A.virosa, and until you know EXACTLY what you are doing, you never, ever, ever, consume any mushroom found
growing in association with trees that possesses a volva, whether it is possessed of a ring on the stem or whether it does not. Save one and one
alone. Volvariella bombycina. This grows up IN trees, ON trees. Amanitas grow WITH trees and they grow upon the ground. They never, ever grow up in
trees on the wood. V.bombycina is a scarce, but good eating mushroom. And it always, without exception, grows OUT OF the tree, often high up. And
whilst possessed of volva it has not a ring. The chances of an Amanita of any sort growing in this habitat, OUT of a tree, sprouting from the wood
itself, and not buried wood, live trees, straight out of it, are as high as drinking a pint of chlorine trifluoride and laughing about it a week
later, whilst taking a bath in anhydrous liquid HF. Possibly whilst a flock of porcine quadrupeds of the kind who wear not a uniform and carry no
handcuffs fly overhead speaking in ancient aramaic. And the chances of Faye Kane the (albeit I so would) autie scienge geek and kinkstress not being
just about the filthiest perverted girl to have walked the face of the earth since Erszebet Bathory.
In fact the ONLY amanita to have truck with, is that most distinctive of mushrooms altogether, A.muscaria, which if eaten, must like blusher, be
twice-boiled and then cooked, best eaten young, and if to be used as herbal medicine or psychotropic or oneirogen, and it is also an excellent, indeed
my very favourite cooking spice of all, particularly paired with the poroid, bolete-like mushroom Chalciporus piperatus, the peppery bolete, so named
for its fiery heat it can give to a meal when used as a spice during cooking, or dried and whizzed up in a spice grinder (its a sod to powder in a
mortar and pestle) then dusted over a good juicy piece of meat like one would pepper or chilli. Actually, and conveniently, it is a parasite of the
fly agaric, and grows in association with it when it grows under silver birch (I've never, ever seen it growing with the fly agaric when it grows
under pines, I don't think it does, could be wrong but I do not believe this to be the case) For this it must be heat-cured, overnight on foil lined
baking trays in a gas oven with the flame as low as it can go without extinguishing does good, preferably after scraping the gills off for they are
water-packed and sweat a lot in the heat otherwise, and can make the mushrooms water-sodden and a total pigdog to dry. Overnight until nice and
crispy, or at worst, (preservation-wise) a little flexible, although light in color and retaining good form is best. Stems contain little psychoactive
and are worth piss all, I toss them, and don't even bother wasting oven space when I come home with a good many kilos per day's harvest during the
growth seasonal periods. Under silver birch, under pine. Red cap in the typical colormorph, otherwise white, as are the spores, the latter, of the
spores being true save only one, A.echinocephala, which is rare, subsection Lepidella, may be nephrotoxic, and should not be picked, since it is on
the UK red list of endangered species. I've only ever seen it once, I remember the day vividly, my mom walking me to my first primary school and my
spotting it near hardwoods, including lime tree (Tillia, not the fruit tree in the citrus family) and going to myself 'holy fucking shit! thats
Amanita echinocephala!!!!!!!' when I was just starting out of nursery. In the corner of a raised grassland small park, near a kiddie's playpark
although separate from it, right a little above my then eye-level, and remember even now, feeling honoured to have set my eyes upon one. Was walking
to school past that wall and can't have been more than 5-6 years old, and it hit me like a slap in the face, stunned and delighted was I to have
spotted a mushroom I'd wanted to see for what was, given my age, a long time, pretty much since I used Roger Phillips' textbook to teach myself to
read. That was a flappy, spinny, stimmy happy day. if a distracted one since I couldn't give a damn about lessons that day as I recall what I can
recall of the rest of the day, relatively little, since my mind was upon getting to go back home and gaze upon my lucky find, leaving it in place as I
did, knowing its being rare, although not, since I had not net access at that age, that it was as endangered as it is. I just couldn't help myself,
that day was one I couldn't apply myself to lessons whatsoever, not that there was a science lesson at that age in a primary school. Mainstream school
too...ick! hated the place anyway for that reason. But damn, all I could think of were going back to see it again and examine it when I hadn't been
pressed to keep going to school, that and alone amongst other thought on my mind, to scrump the white and red currants from somebody's garden and eat
as many handfuls as I could grab ahold of before being seen by my mother and given a dressing down. Shouldn't, I know, but, well, I was only five or
six, I think I can be forgiven for that particular amongst my past and present sins and planned sins...Alone amongst Amanitas It has greenish spores when ripe.
A unique wee beauty, although one never to be consumed, for it may well be nephrotoxic as are other Lepidella subfamily Amanitas, and even then I knew
it likely poisonous, although, semi-ashamedly, as I hadn't the means to obtain the toxicological information regardless of how much I wanted it, so my
shame is minimal, considering it was lack of possession of the capacity to perform the act of seeking the information, the fact that at that age I'd
probably not be taken seriously even with a professional mycologist at my disposal day and night, which, despite how much I'd have loved that, of
course I did not have and do not have, chained to a bedpost and given a good three meals and as many bog breaks as needed on a longer chain, lent my
then microscope and given some reagents such as I then could prepare or buy with my most meager pocket money and more or less every pound and penny
not spent on the odd exotic fruit from the shops as a treat, or a weekly beano comic )
Fly agaric is really easily ID'ed, no true volva, more of a scaly, multiply shallowly, unevenly ridged basal bulb at the soil-facing terminus of the
stem, a goodly shaped although flaccid ring.
You do not eat any mushroom in its unopened egg-stage, because it may be an Amanita. And you eat no LBMs (little, brown mushrooms) because these may
be Conocybes or Galerina species nor do you ever eat any Lepiota species other than Macrolepiota procera, which is far, far far larger than the deadly
kinds, and has a movable double ring, that can be slid up and down the stipe like a cock ring. Albeit with easily destroying the
The delay is characteristically, near pathognomonically between 6 to 8 hours although it can be delayed by as much as 24. This information is
ESSENTIAL if observed and mushroom poisoning is suspected, to be given to medics. Treated with aggressive assault upon the toxicity in extremis, the
fatality rate can be lowered to as little as 50-50 to 60-70-%. (optimistic outlook rather, that) Untreated, you might as well slit your own throat,
because it will be quicker and you won't suffer for a week to two weeks in the most unspeakable agonizing misery before dying in a similar manner
whilst busily vomiting and shitting blood and intestinal tissue, as your liver fails, your kidneys are trashed, your heart swells, and if your really
lucky you'll pass into a hepatic coma and not wake up sooner rather than later, saving at least some time otherwise spent upon dying screaming and
begging for the reaper to hurry damn well up and drag you from an ante-mortem to the post-mortem fires of hell.
One single bite of one medium-sized mushroom, of Amanita phalloides is more than enough to end you. Indeed one mushroom included in a meal such as
say, mushroom soup or a stew might well pack enough of the 20-plus different toxic principles housed within, like stupidity within George W Bush or
stink in a pub shithouse (not that the two are vastly different come to think of it)
Post-eaten GI upset severe, vomiting, severe GI pain, severe diarrhea shites, possibly bloody. 8-10 hour delay between eating and onset of severe
symptoms. Pallor, severe prostration, beginning of agonizing pain After a day, perhaps two, treated or otherwise, there may very likely be what
appears to be a remission of symptoms. Possibly leading to belief the person is better, By which time, the damage is done. And you are buggered quite
likely. Its a coin toss at best and the dice are weighted in the devil's favour and not seeking, or even release from hospital. By this time, you've
collected your handbasket and taken a very, very extended holiday in a rather warm climate. Then a day or two later, hepatic failure and
hepatonecrotic cytolysis, possibly to probably kidney failure and terminating in multiple organ failure.
Maintenance of blood electrolyte balance and coagulation, plasmapheresis may be of value, dialysis possibly is critical. Silybinin/silymarin, now
available in an injectable formulation, which is important for it is otherwise poorly absorbed, it is derived from the milk thistle, and produced
under the name of legalon-sil should be used. Massive doses of penicillin-K are often given, and thioctic acid has shown some value in amatoxin
poisoning. Liver and sometimes kidney transplant are often needed. The silybinin/silymarin, is a potent hepatoprotective agent and has shown
respectable value intravenously given to the poor cunts who get lucky enough to have the poisoning recognized for what it is, and lucky enough to
receive the drug. Thioctic acid is perhaps of less value, but it is of course vital not to fuck around if amatoxic poisoning is even remotely
possible.
And there are quite a few species within the phalloidea clade within the Amanita genus which contain more amatoxins on a weight for weight of mushroom
tissue basis than does A.phalloides. They kill more people than any other mushroom family. They are mycorrhizal (growing under or in association with
plants, trees in this case, and the death cap is particularly fond of growing under oaks [Quercus spp] and is unfortunately, responsible particularly
for exterminating quite a few southeast-asian folks, because it looks like the edible straw mushroom, Volvariella speciosa, and other closely related
(to the latter), Volvariella species, which however are not myorrhizal, but they also possess a volva, the bag-shaped termination that forms when the
velum universale ruptures (usually so at least, and in A.phalloides, that species possesses a particularly well developed, big, sack-like bag of a
volva)
Amanita species however, !UNLIKE VOVARIELLA SPECIES! possess, bar the subsection of Amanita vaginatae, the grisettes, do have a ring. Although
perhaps one or two others of other families have no ring. I forget the name of the one I think of, although its orange and edibility unknown for
certain but suspected and not advisable to be eaten.
Amanita amatoxic species are poisonous throughout, the poisons are thermostable and neither drying, freezing, boiling nor cooking will save a person
from being poisoned. Early recognition of poisoning is VITAL. And that time delay between ingestion and onset is likewise so distinctive as to be nigh
on pathognomonic of amatoxin ingestion. And the delay a day or two later is likewise highly characteristic of amatoxins, when the GI irritant initial
phase subsides and is replaced (and the former resumes after a while too, just to make the eater's journey to the next world that bit more
insufferably foul.)
The amatoxins are pentacyclic octapeptides, the phallotoxins are bycyclic and composed of seven amino acid residues, IIRC again containing tryptophan
whilst this brings us to the last of these cytotoxins, the virotoxins. These are hexapeptidic monocyclic actin-binding agents that prevent
monofilament depolymerization. Like phallotoxins they are highly toxic if absorbed, such as by injection, but they are poorly absorbed.
Amatoxins are particularly bad generally, because they don't just pass through and trash your innards on the way, they are soluble in bile, and
reuptaken in the GI tract and recycled through the liver in a cyclic manner, going round after round after round, further lysing the bejeesis out of
an already trashed liver, until you have the equivalent of a gizzard smoothie that even the sewer rats wouldn't touch if they have half a brain.
Flesh is toxic. Cap, stem, ring, volva, even the spores are poison-laden and it can cause irritation and toxicity although likely not fatal, through
skin contact. Inhalation of spores is to be avoided like the plague. If so much as a single one makes it into your mushroom basket, the entire lot are
fit for taxonomic examination and photography only. Although I might make an exception for culturing spores of saprobes or obligate parasites and
non-mycorrhizal species with which to raise further generations THEN to be eaten, where the mycelium of the obligate mycorrhizal death cap and other
such nasty Amanitas cannot live and cannot procreate. Only that from which mushrooms will never arise. And I'd not touch the first generation even.
Just out of caution, at least not raised direct from the primary culture, and I'd meixner test a portion of a secondary too. Although all Amanita spp.
are obligate in their forming associations with trees. So it would be safe to raise a culture of a saprobe, parasite et cetera, and then subculture
from its spores or cloned tissue.
One other species that is long recognized as less than pleasant, is Hypholoma fasciculare, which has been found to contain amatoxins, in addition to
toxins called fasciculols, lettered from fasciculol-A through at least F, and quite common, a woodlover with greenish gills, of a rather purulent
nasty dark olivaceous dirty green color, yellowish to yellowy green fruitbody, and in addition to the amatoxic poisoning, has been known to blind, and
cause neurological intoxication. Oh, and now I remember, IIRC, although I remember not which exactly, there is, I believe, an amatoxic species of
Gymnopilus, known for being a nastily bitter tasting family, many of which contain psiloc(yb)in, and known as big laughing gyms, not highly potent
psychedelics but sought all the same. Woodlovers. Amatoxic one was iirc austrian.
Which, brings us to the last of the interesting Amanita mushroom toxin family, the isoxazoles and the two glutamatergic, little awareness, thereof,
amongst most non-prof mycology geeks. The isoxazoles are characterized primarily by ibotenic acid, found in fly agaric, A.muscaria, the panthercap,
A.pantherina, which can resemble the blusher, but does not turn pinkish red when cut and left, especially which it does in the stem, and most at the
base of which, and most of all in fly larvae tunnels within the stem. The blusher is good eatin' when prepared properly and thoroughly. The panthercap
contains similar toxins (and for that matter, desirables, sought and tried by some, however I will not touch it, not ingestion-wise at least.
The ibotenic acid is an NMDA agonist (NOT ANTAGONIST, its an EXCITOTOXIN not a dissociative anaesthetic!!! not to be confused.) poorly uptaken through
the oral route but MAY be actively transported via aminoacid transporters through the BBB. Then again it may also be pumped out again by various
efflux pumps such as multi-drug efflux pump or P-glycoprotein, I'm not sure. Anyhow its thermolabile, and in-vivo metabolized to the hallucinogenic,
although rather odd and funky, and also extremely potently oneirogenic GABAa agonist. Its unusual in that it binds at the orthosteric site, the one
that recognizes GABA itself, which it will displace. And this, rather than NMDA agonist excitatory effects may be responsible for the initial bodily
phase during onset, of twitching of muscles, stimulatory effects and mild clonus, as well as shivering and shaking. Then the effects of the muscimol
take effect.
This results in a deep, deep deep coma-like sleep, during which one dreams intensely and vividly, in a deep trance. The reason this mushroom must
always be cooked or at least dried, is to decarboxylate the ibotenic acid to muscimol (it appears that agonists of at least the NMDA and AMPA types of
the ionotropic glutamate receptors, such as ibotenate, and quisqualate as well as others, that take the form of carboxylic acids, wouldn't be terribly
surprising if domoic acid would do the same, become GABAa orthosteric acids on decarboxylation. Although I'd not get adventurous in this respect
without either A-consulting known and certain literature from multiple sources, B-doing the electrophysiological work myself, setting up to be capable
of patch-clamp studies and setting to work with my own hands and computer and petri dishes, seeing results excluding excitotoxic glutamatergic
activity with my own actions. OR C-preferably all the above. But it does seem like the tightly restricted GABAa orthosteric pharmacopore, just like
glutamate when decarboxylated becomes GABA, when ionotropic NMDA and sometimes AMPA receptor agonist excitotoxins of carboxylic acid form are
decarboxylated to amines the result is not unlikely to be a GABAa orthosteric agonist.
Its a peculiar trip, not in the slightest like psilocybin, phenethylamines like 2C-B-FLY, not entactogenic like MDMA and its benzofuran relatives or
the corresponding 3.4-methylenedioxymethcathinone (I cant say of the benzofuranyl homolog of this, I've never tasted it, I'm not the worlds largest
fan of MDxx or entactogens other than AMT, although never had MDA, if it hasn't also got proper 5HT2a psychedelic activity, the whole thing seems to
make me...artificially NT. And it feels forced, artificial and fake. Like running an emulator for windows on a linux system. And theres a deep-seated
part of me that KNOWS its forced on me and fake. And thus it can tend to feel shallow even when the experience is deep. I distrust the entactogens
like MDxx on a personal level because of this. I am about 80% sure thats because I'm autistic, and I am not only comfy in my wiring but I like it that
way. It is INTERESTING, to experience the kind of pseudo, artificial neurotypicality emulator, but I do not find it seek-worthy much. Save in certain
highly specific situations.
The effects of muscimol anyhow are most similar to zolpidem, or perhaps valerian, although the last, a loreclezole site allosteric positive modulator
primarily as I understand it although with valproate-like compounds that wouldn't surprise me if they are active sodium channel blockers. Never tried
loreclezole, but valerian root extract (Valeriana officianalis) in high-dose extracts (a couple of packets of strong extract pills will do it) is a
most extraordinary oneirogen. So powerful in my experience that its almost like being on a rollercoaster lined with dream-shaped baseball bats and
being buffeted and knocked sideways, backwards, diagonally and in several directions it'd take cthulhu and a quantum mechanics team plus a few of the
hounds of the angles on a leash serving as sniffer dogs to even begin to figure it out. Not battered in a sense of unpleasantness, but when normally I
don't even dream and remember it due to I believe, the requirement I have had for a long time for strong doses of morphia and oxycodone, the only time
I can dream is when I put myself into the mildest of withdrawal and time it, with a shot waiting for me when I wake, possibly a few small microshots
to keep me in a sleep-able, but not truly unpleasant withdrawal state. Then I dream intensely.
But never like that. Valerian extract will help one sleep as a GABAergic sedative. I've never had loreclezole, though, or any other loreclezole-site
GABAa PAM. Would deeply wish to. Its at the top of my psychotropic bioassay list. To ascertain if this is the action to which the extraordinary
oneirogenic activity is due.
Muscimol is similar to that though. That and the Z-drugs, primarily zolpidem, zopiclone seems more an auditory hallucinogen in my experience, and
zaleplon is...err...a moneymaker for big pharma and a sop for doctors to give patients insistent on a sleep aid who've tried and persistently refuse
sedating antihistamines.
This and ibotenic acid both are contained in both fly agaric, and A.pantherina. As well as I believe A.cothurnata and A.gemmata. This last is listed
as potentially deadly in Phillips et al. I'd avoid it and not be too enthused about fucking with A.cothurnata.
The content in A.pantherina is MUCH higher, of both. And ibotenate is converted via -COOH to muscimol, but still I would never touch it internally,
not with a ten foot stick. This is because of those other two compounds. Stizolobic acid and stizolobinic acid are present, not much of them. BUT,
these are excitatory ionotropic glutamate agonists, possibly kainatergic, not totally sure which and what selectivity they have but they are active in
femtomolar concentrations in vivo. That sure as shit won't TAKE much. And whilst fly agaric will not kill, well, it has existed on record of this
taking place. But once in the case of an italian diplomat who ate platefuls of them. Once in a case of intoxicant use, in a tent in winter, where in
the comatose-esque sleep, someone froze to death. Not directly death due to the toxic action of the mushroom.
Also A.muscaria, A.pantherina contain muscarine, a quaternary ammonium compound that acts as an agonist of the muscarinic acetylcholine receptor,
hence the name of the latter. It cannot pass the triple B, but it can cause salivation, the sweats, lachrymation and it increases urination. It is
however present in quantities so miniscule that whilst it can be used to extirpate flies (there is a volatile compound, 1,3-diolein IIRC that serves
as a chemoattractant), it used to be used thus, the fly agaric would be mashed up in milk, left out, the flies would come, feed, be intoxicated by
both muscimol, the ibotenate, and become paralyzed, and exterminated aided by the muscarine.
But in humans, even in strains of fly agaric with enough muscarine to cause some peripheral effect (being a quat, and sans active transport through
the BBB, it is restricted to the PNS due to its charge) this is not dangerous. Buscopan, a muscarinic antagonist also a quaternary ammonium, the quat.
butylbromide of scopolamine (hyoscine) is an ideal premedication. It used to be thought that muscarine was the active, and atropine given in cases of
intoxication by these isoxazole containing fungi. It should not be, if anything bar tiny doses are given, worsening of effects takes place. And the
only benefit is to reduce secretions otherwise possibly increased by the traces of muscarine activating peripheral muscarinic ACh receptors.
Buscopan, the OTC IBS med is perfect though. PNS only, so no interference with the psychotropic effects.
This, brings us almost to the last of my little micro-treatise upon the interesting toxins of the Amanita family of macro-fungi within the
basidiomycetes. I hope it has been interesting. However I will leave y'all with one last tidbit.
A.muscaria, aside from another, lesser known isoxazole, is a MASSIVE hyperaccumulator of vanadium. It forms a tetravalent, octa-coordinate complex
called amavadine, bis[N-[(1S)-1-(carboxy-κO)ethyl]-N-(hydroxy-κO)-L-alaninato(2-)-.κN,κO]-vanadium
The anion is a deep, deep deep deep vivid blue. Very pretty color, and intense, kind of dark hue. Not violaceous blackish-blue, but true, deep
ultramarine blue.
Tried doing an extraction of fly agaric, although I was too frit, when I was very very little, to taste it in an attempt for psychotropic activity. It
rested under my bed, after being based, until it smelled a bit bad, not mouldy, just, well I wouldn't have drunk it even had I at just beginning
school age, been the devotee of its use (I like it most as a spice, and to inure one against discomfort induced by the cold, with a little buscopan to
reduce propensity to sweat and further induce cooling, in the form of a hot tea with a bit of honey prepared from the heat-cured mushrooms. It fills
the kitchen with a meaty smell, probably due to the way that the umami taste receptors on the tongue sense glutamate as a primary ligand, and produce
savoury flavour response when agonized. Perhaps meaty smells are produced thus also, not too well up on olfactory-gustatory receptor sequence
homology, again, I apologise.
But prepare this tea, and my god, its like letting off the deliciously fried steak equivalent of carpet-bombing the area with nerve gas!
https://en.wikipedia.org/wiki/Amavadin This is amavadine, I didn't have access to the information when I saw it that time, just being a nipper,
and I remained hungering for that information for 20 years or so before I knew the why of that deep, intense blue. Apparently it can be crystallized
as an insoluble calcium salt or complex. Never tried it, not yet. This is primarily because I value this mushroom above a great many tasty ones, and
go out every season to pick as many of the fruitbodies in good condition for curing as I can find and carry home, be it fair weather or foul, so I
have enough when they grow not, for all my meat cooking, my steaks, stews, cottage pie, sausages, bacon sarnies, and come the bite of harsh cold, when
I wish to go out. It will not protect one from hypothermia, however against the teeth and claws of the foulest blizzard, you will feel discomfort not.
To whit, once I wished to buy a bottle of spirit for the odd nip at home whilst back in fairer climes inside and thus not at risk of hypothermia
propensity being enhanced due to the vasodilatory effect of ethanol.
I wore nothing on top but a leather jacket and my spiked dog collar and shades. Plus the piercing in my lip. Otherwise clothed only from the waist
down, during the howling wind and snow. And After fortifying myself with a mug of hot honeyed fly agaric tea, simmered on the stove for a while, using
the cured mushrooms I had dried and saved for winter's bane. It snowed, the wind shrieked like a banshee drawn asunder slowly upon the rack, by the
harshest inquisitor of the witch hysteria (perhaps later I shall come to Claviceps, and other Clavicipitales, which possess some interesting toxins,
and other ergolines.)
And yet not, not in the least did I feel any discomfort during the few miles walk each way to the shop to buy my bottle of vodka and back. And not a
nip did pass my lips until I was within my own walls once again. Discomfort was not felt in the slightest. I was covered in snow, and annoyed a bit at
it melting and my getting wet, but thats it. Cold? not even shivery, yet through and during weather that would have put off an arctic fur seal or
emperor penguin.
Love that mushroom. Ethnobotanical folk speak of plant allies. And I would name the Amanita muscaria mine.
Hope you enjoyed my efforts here for these past couple of posts.
Can do more on other natural and synthetic toxins if other forumites wish me to do so. Request it in answer to this post and it shall be so.
Tsath'
[Edited on 6-2-2017 by tsathoggua1]
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gdflp
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Thread Split
11-11-2017 at 12:27 |
NEMO-Chemistry
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| Quote: Originally posted by Manlius | | I just want to ask if some of you has heard this kind of shroom called psilocybe zapotecorum also know as Blue-Foot? I was reading some articles about
this kind shrooms before engaging my self for the first time. Like this one from https://www.trufflemagic.com/blog/psilocybe-zapotecorum/ .They say that it has a very potent effect on the brain and hallucination. Unlike other
shrooms this one is less intense. In one article that I've read psilocybe zapotecorum influences the prefontral cortex thats responsible for for
differentiating thoughts, consequences of actions, and social control. Magic mushroom are use on reducing the symptoms of obsessive-compulsive
disorder and anxiety. It can also help people to quit smoking and alcohol addiction. Some studies also suggest the property of magic shrooms/truffles
can be useful for cancer patients. I would really want to hear other insights regarding this kind shroom and could possible be used as an alternative
medicine Thanks |
Its a fungi not a shroom. If you got to talk drug shit we prefer you do it in scientific way.
Whats annoyed me is your assumption its an alternative medicine, why do people assume plant or Fungi based drugs for medicine are alternatives?
Alternatives to what??
until recently A certain heart drug was still produced from the Foxglove plant. The pure form od many drugs is the plant source, the crap you buy
thats been made purely in a test tube is the alternative!
Aspirin, again until fairly recently was still made from Willow. So I take it though, that to you bayers crap filled pill is the real deal and an
extraction from willow is alternative
[Edited on 11-11-2017 by NEMO-Chemistry]
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DraconicAcid
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Posts: 4356
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Location: The tiniest college campus ever....
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Mood: Semi-victorious.
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| Quote: Originally posted by NEMO-Chemistry |
Whats annoyed me is your assumption its an alternative medicine, why do people assume plant or Fungi based drugs for medicine are alternatives?
Alternatives to what??
until recently A certain heart drug was still produced from the Foxglove plant. The pure form od many drugs is the plant source, the crap you buy
thats been made purely in a test tube is the alternative!
Aspirin, again until fairly recently was still made from Willow. So I take it though, that to you bayers crap filled pill is the real deal and an
extraction from willow is alternative |
Aspirin is purified, and contains a known quantity of ASA and no other active or interfering ingredients. A pot of willow tea could contain any
concentration of salicylates, depending on how happy the tree was, and any number of any related compounds. And if you're buying your willow bark
from a "nutriceutical" company in some third-world country, there's no way to know if there isn't a handful of random weeds thrown in for good
measure.
Please remember: "Filtrate" is not a verb.
Write up your lab reports the way your instructor wants them, not the way your ex-instructor wants them.
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Cezium
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I would rather not work with:
organometals (esp. Hg, Cd,..)
any Tl, Po, Pu compounds
methylating agents, chemotherapeutics (cis-, oxali-Pt,..)
ketens, phosgene
some hydrides from right part of periodic table
some F compounds
prions and toxic proteins (abrin,..)
I don't mind working with:
radionuclides (I131, Tc99m, F18, Ra223, Y90, U, Th,.. 
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NEMO-Chemistry
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| Quote: Originally posted by DraconicAcid | | Quote: Originally posted by NEMO-Chemistry |
Whats annoyed me is your assumption its an alternative medicine, why do people assume plant or Fungi based drugs for medicine are alternatives?
Alternatives to what??
until recently A certain heart drug was still produced from the Foxglove plant. The pure form od many drugs is the plant source, the crap you buy
thats been made purely in a test tube is the alternative!
Aspirin, again until fairly recently was still made from Willow. So I take it though, that to you bayers crap filled pill is the real deal and an
extraction from willow is alternative |
Aspirin is purified, and contains a known quantity of ASA and no other active or interfering ingredients. A pot of willow tea could contain any
concentration of salicylates, depending on how happy the tree was, and any number of any related compounds. And if you're buying your willow bark
from a "nutriceutical" company in some third-world country, there's no way to know if there isn't a handful of random weeds thrown in for good
measure. |
Yeah i was really grumpy all weekend , i had really bad toothache that seems to
have just gone away this morning!
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Assured Fish
Hazard to Others
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Uranyl acetate
Coz it pwettty.
Also the following compounds are pretty darn fascinating:
Batrachotoxin, saxitoxin and tetrodotoxin of which batrachotoxin is without a doubt the deadliest
at a LD50 in rats of 2µg/kg. Also batrachotoxin is worth up to $20,000,000 should you be the crazy bastard that manages to synthesize it.
https://www.scbt.com/scbt/product/batrachotoxin-23509-16-2
Batrachotoxin is also resposible for one of the only poisonous birds in the world, the hooded pitohui.
Succinyl choline: this stuff is used to essentially paralyse patients during surgery and what have you, it unfortunately also stops
the diaphram from working and so requires endotracheal intubation to keep the patients blood oxygenated. Also wouldn't be too difficult to synthesize
either.
Pumiliotoxin is another toxin found on the skin of some species of tropical frogs however with a considerably higher LD50.
Antiarin: This one caught my fancy when i watched a documentary on an old philipian man who still hunted using a blow pipe. Its found
in the sap of the Antiaris toxicaria tree and to date has yet to be synthetically synthesized, hint hint.
Epibatidine: Another toxin excreted by frogs however this one look considerably easier to synthesize.
https://en.wikipedia.org/wiki/Epibatidine#/media/File:Epibat...
Orellanine: this one is interesting in the time it takes for symptoms of poisoning to occur, 3 to 4 days is average.
Cantharidin: this one is a fun little blistering agent that has oral lethal dose being higher than the oral lethal dose of ricin.
Found to be excreted by the European blistering beetle its preparation might be plausible starting from furan. I have always wanted to make it to be
honest.
Abrin: Ricins little known and considerably more lethal cousin, found in the seeds of Abrus precatorius or rosemary pea tree which
can be found in south america.
It behaves almost exactly the same as that of ricin and even displays the same symptoms.
Anyhow thats all i can think of off the top of my head but be sure to have a look over the Select Agents list https://en.wikipedia.org/wiki/Select_agent
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LearnedAmateur
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Aside from all the fancy, exotic, ridiculously dangerous chemicals out there, I do have a love-hate relationship with NO2. Low exposures can make you
ill for weeks and it has the interesting property where survival of the first pass (medium to high exposure) will result in the patient being fine for
a few weeks, and then their condition will deteriorate once more, commonly to the point of death. Happened to me, I've mentioned it elsewhere on the
forums but it's not fun when you're dealing with pseudo-pneumonia thinking that it's quite likely that you will actually die in a few weeks.
Now onto the other aspects, it boils just below room temperature and freezes 30C below that (at -11), turning from a deep red brown to a lighter
orange. Further cooling gets rid of the colour entirely, leaving a white solid. NO2 actually exists in equilibriu, and increasing the pressure causes
the molecules to react, forming N2O4 which is the colourless molecule - this makes NO2 a great candidate for demonstrating equilibria, both due to
temperature (in cold/hot baths) and pressure (compressing the gas in a gas syringe). I believe that it is being looked into as a mechanism for power
generation, where N2O4 is decomposed and the hot NO2 is pushed through a turbine, which is then subsequently cooled, reforming N2O4 and reducing the
pressure on the other side.
In chemistry, sometimes the solution is the problem.
It’s been a while, but I’m not dead! Updated 7/1/2020. Shout out to Aga, we got along well.
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PirateDocBrown
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Now, I came from a pretty old school time, we used chromic acid dissolved in concentrated H2SO4 to clean analytical glassware, and often didn't use
gloves when handling it, just scrubbed the itchy green spots with soap after. Some of my older colleagues had had wash basins of benzene they just
reached in with ungloved hands, as well, but that was before my time. Also, mercury was everywhere. Not in "Cody's Lab" quantities, but several pounds
at a time.
I have worked with small amounts of phosgene, it'd come in 500 mL bottles, and a typical use would be 50-100 mL or so. Regular jointed glassware, in
the hood. By this time, we were wised up as to gloves.
Regular old HF (48%?) is something I used a lot of, and will avoid, if at all possible. The fumes can sneak out of the hood and smell like those of
HCl, only more kickass, like being punched in the nose. The fact that it can easily penetrate gloves, a small amount of skin contact can kill (in a
few days), and it can eat you without you feeling it all are things that weigh on your mind.
I have worked with HCN, but all safely contained in jointware, and kept ice cold in the hood. Much safer, IMHO, than HF.
NO2 is unpleasant, but with good strong ventilation, can be dealt with. I actually don't mind the smell, it seems bleachy-clean, to me. But I've never
gotten more than a few small whiffs.
Boranes. By themselves, well managed, not too bad. I only ever used them as reagents, in small quantities, less than 5 grams at a time, usually less
than 1. But they do pack a punch. The standing joke is that you can always tell the boron chemists, by the fingers they lacked.
Some neighbors were using nitrogen-sulfur mustards, all in Schlenkware, but I did worry what would happen if some glass broke.
Stinks. Well... I had other neighbors that were selenium chemists. Ugh. OsO4 was only ever used in very small amounts, only in jointware, Schlenkware,
or dry boxes. It's powerful, but manageable. Never had anyone working with thioacetone, skatole, or other notoriously bad smells, so I guess I'm lucky
there. I hated the smell of halogenated acetic or propionic acids, but I think that's mostly just me. Oddly, acyl halogens rarely bothered me, just
triflates and the like.
[Edited on 11/14/17 by PirateDocBrown]
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PirateDocBrown
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| Quote: Originally posted by LearnedAmateur |
Now onto the other aspects, it boils just below room temperature and freezes 30C below that (at -11), turning from a deep red brown to a lighter
orange. Further cooling gets rid of the colour entirely, leaving a white solid. NO2 actually exists in equilibriu, and increasing the pressure causes
the molecules to react, forming N2O4 which is the colourless molecule - this makes NO2 a great candidate for demonstrating equilibria, both due to
temperature (in cold/hot baths) and pressure (compressing the gas in a gas syringe). |
When one makes it in the lab, it's often contaminated with NO, which combines in liquid state to N2O3, which is blue. So you get the effect of a brown
NO2 gas first cooling to form colorless N2O4, then condensing with the impurity to a blue liquid. Interesting color change.
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PirateDocBrown
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| Quote: Originally posted by DraconicAcid | | Quote: Originally posted by NEMO-Chemistry |
Whats annoyed me is your assumption its an alternative medicine, why do people assume plant or Fungi based drugs for medicine are alternatives?
Alternatives to what??
until recently A certain heart drug was still produced from the Foxglove plant. The pure form od many drugs is the plant source, the crap you buy
thats been made purely in a test tube is the alternative!
Aspirin, again until fairly recently was still made from Willow. So I take it though, that to you bayers crap filled pill is the real deal and an
extraction from willow is alternative |
Aspirin is purified, and contains a known quantity of ASA and no other active or interfering ingredients. A pot of willow tea could contain any
concentration of salicylates, depending on how happy the tree was, and any number of any related compounds. And if you're buying your willow bark
from a "nutriceutical" company in some third-world country, there's no way to know if there isn't a handful of random weeds thrown in for good
measure. |
Or, as I like to say, Do you know what they call "Alternative Medicine" that actually works?
"Medicine".
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