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Author: Subject: "Chemical" Substitutions for "Biological" Agents
DDTea
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[*] posted on 26-3-2003 at 13:08
"Chemical" Substitutions for "Biological" Agents


Yes, this does deal with weapons...but loosely. I don't mean to talk about nasty chemicals that can kill people, because anyone can do that, but rather different chemicals to mimic the actions against the body caused by naturally occuring Toxins.

I saw a perfect example of this as I was researching T-2 Mycotoxin for a school project... The skin lesions caused by T-2 are the result of the Toxin's cytotoxic effects and its interference with DNA and RNA synthesis. Does this sound like any chemicals we know? It did to me- Mustard. Mustard also interferes with DNA and RNA synthesis, causing its characteristic blistering and necrosis.

There are other nerve poisons in nature, such as Botulinum, Tetanus, Polio, and Atropine. However, the nerve agents we are most accustomed to are the ones that cause such overactive nervous responses that they kill from hyperactive paralysis...much the opposite.

Nevertheless, the point is this: Suppose we were to create chemicals to mimic the toxins of nature. Nature's toxins and poisons are endlessly more toxic than our own- Micrograms of T-2 can cause the same effects as a "standard" exposure to Mustard. I don't expect our "artificial" toxins to be nearly as potent as nature's, but it gives us ideas...

For example, Strychnine causes nasty nasty effects by inhibiting the Amino Acid glycine. So, surely there can be some chemical we can create that could do the same?
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Blind Angel
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[*] posted on 26-3-2003 at 13:16


Atropine is a nerve agent? I always thought it was more a psychotrop than a poison (maybe you include the two in the same category).

Anyway, there surely a way to do it since most of the medicament are variant of poison




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DDTea
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[*] posted on 26-3-2003 at 14:21


Atropine isn't really a nerve agent, as in Anti-Cholinesterase. But it is indeed a nerve poison...it causes paralysis :).
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[*] posted on 26-3-2003 at 14:46


IIRC, atropine is poisonous because it overstimulates the nerve synapses. This is also why it is used as an antidote against nerve agents.



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[*] posted on 26-3-2003 at 15:45
Im making a database of Chem Weapons


Well ive found some chems that i will put up, i have about 100, that have ld50's of 100ppm or less but some im unsure of the stucture, as this is where all of my info will come from. If any of you have some time to kill ill leave the names of some. I know the formulas for some but not structures.

Acrolien, Aldrin, allyl alcohol, aniline,arsine,acetylene tetra bromide, allyl glycidyl, and 2 aminopryridine.

CTR




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smile.gif posted on 26-3-2003 at 15:58


Acrolein: CH2=CH-CH=O
Aldrin:Not sure (C5H5N)-NH-(C5H5N) 2,2'dipyridyl amine
Allyl alcohol: CH2=CH-CH2OH
Aniline: C6H5-NH2
Arsine: AsH3
Acetylenetetrabromide: CHBr2-CHBr2
Allyl glycidyl(ether): CH2=CH-CH2-O-CH2-CHOCH2
2 aminopyridine:(C5H5N)-NH2

From the above you see that some are familly members!
:cool:




PH Z (PHILOU Zrealone)

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[*] posted on 26-3-2003 at 17:15


Thanks I will post more as i write up this info.

Sarin is a fairly easy synth to find, it doesnt seem all that complicated, but making thats strait up crazy. That poses a real hazard to youself and your surrondings no matter what precautsions you take. I cant say id recomend it, if you get caught you will be royaly fuck over to boot, but i respect your dedication to your intrests.

CTR




\"I love being alive and will be the best man I possibly can. I will take love wherever I find it and offer it to everyone who will take it. I will seek knowledge from those wiser and teach those who wish to learn from me.\" Duane Allman
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[*] posted on 26-3-2003 at 18:06


Darfire: is your site online?
And so atropine is like MDMA as i see?




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DDTea
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[*] posted on 26-3-2003 at 22:27


I'm not sure we're all understanding the point of this thread... It's not to be about the agents we already know, like the Anti-Cholinesterase Organophosphates (Although I am very interested in these too- Phosphorus is a very fascinating element), but novel agents altogether. However, I imagine this would deal with Biology and Pathology as much as it would with Chemistry...but it makes the topic that much more interesting!

Alright, so we have a target body chemical now- Glycine. It's an Amino Acid- a Carboxylic Acid bonded to an Amine. Its structure is as follows: NH2-CH2-C=O-OH. The name "Aminoacetic Acid" is a good way to describe it. Its purpose in the mammalian Central Nervous System (CNS) is primarily in the Spinal Cord and Brain stem, and it is, "One of the major inhibitory neurotransmitters in the mammalian CNS." It also acts as, "a modulator of excitatory amino acid transmission mediated by NMDA receptors."

As you would imagine, inhibiting the action of Glycine would lead to potentially dangerous hyperactivity.

Now, the question is... How do we inhibit it? My guess for finding the answer to the question would proceed as follows:

-Theorize a body chemical to inhibit.
-Find a chemical that inhibits the target chemical in nature.
-Find the reaction that takes place between said chemical and the target chemical.
-Theorize a simpler chemical that mimics that action.
-Find a means for the theorized chemical to get to the target site (I imagine this part to be the most difficult...).

Now, the chemical we theorize does not necessarily have to specifically target the desired chemical...we are not medicine-makers, we're not worried about side effects ;) .

Don't worry- this won't be incredibly complex medical biology crap. My own experience with Biology is simply a Highschool General Biology class! So it's really not stuff that is too complicated; just a lot of things with fancy names. With our knowledge of Organic Chemistry, we should be able to do this. If you don't understand the Biology things, take a little while and look them up, and we can engage in a really fun topic! :)
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[*] posted on 27-3-2003 at 13:35


The hardest thing would be to create a product that is
when inhaled:
a) pass the pulmonar barrier
b) is not attacked by blood enzyme or blastocyte or any other white cell
c) would pass the blood barrier
d) and that after their modification (or none if your really lucky) is still effective
when ingested:
a) not attacked by stomach enzyme
b) not attacked by liver enzyme
c) not attacked by any other enzyme in the digestive system
(the rest is the same that when inhale)

The body is well done really toxic substance are hard to make, specialy those affecteing the brain whic is like the fortress of the body. I got a book here call Synthesis of Organ Targeting Drug (in pdf) which may interest you and that i can upload on the ftp. So instead of doing a nerve agent why not making something that kill you by another way (like creating strong acid inside of your organ and thing like that)




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cool.gif posted on 27-3-2003 at 16:24


Usually you have 3 ways of action:
You have a biological molecule that has a regulatory effect on a physiological response!
This implies good knowledge of the molecule and how it triggers the response!
A --> physiological effect A
no A --> other effect B or no effect at all!

If you look closer the system with a larger spectra:
a+b -E1->A -R1-> Physiol effect A

Then you can:
1°)induce permanent production of A when it is not needed --> permanent Physiological effect and no more regulation! You have to work on a,b (various molecules, orders,enzymes) or E1 (last enzyme that synthetise A).
2°)induce blocking of formation of A! Same ways of action as in 1°!
3°)You may alterate A as soon as it forms then R1 will not recognise it!
4°)You may block the Receptor 1 so it remains activated for permanent physiological effect or permanent lack of effect!A is stil formed but useless!

Usually in pharmaceutics, they know very well biochemistry and the regulation cycles involved (very interesting organic chemistry) then they use molecules that have similar groups but at different place or groups that have about the same charge/the same electronegativity to mimic trigler molecule; but it blocks enzyme activ site by formation of permanent link or stronger interaction than normal ligand!



:cool:




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sad.gif posted on 27-3-2003 at 16:27


Actually 4 ways

Sleep and my confortable bed calls me!

;););):D:D:):):P:P:P:cool::cool::cool::o:o:o




PH Z (PHILOU Zrealone)

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[*] posted on 28-3-2003 at 21:09


Quote:

If you look closer the system with a larger spectra:
a+b -E1->A -R1-> Physiol effect A


Very interesting responses coming from everyone so far! But Philou- could you clarify the above quote a bit more? I understood everything in your post except that :).

[Edited on 3-29-03 by Samosa]

[Edited on 3-29-03 by Samosa]
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smile.gif posted on 30-3-2003 at 14:29


Starting from various molecules a,b,... and various required conditions c,d,...; an enzyme E1 produces the active molecule A that goes further in a receptor R1 to provide physiological effect!

This very synthetic way expressed simply the multi and pluricausality to produce A!

A quick example will give you a better idea!
Ingesting NaCN:(don't do it :mad: :mad: it is lethal).
NaCN goes in the mouth were you have some CO2 dissolved in your saliva!
NaCN + H2CO3 <--> HCN + NaHCO3
A part goes then in your lungs where it enters the blood!
Another part of the NaCN goes in your stomach where HCl is!
NaCN + HCl --> NaCl + HCN
HCN enters the blood via the intestinal blood capillars!
You thus have 2 pathways that lead HCN in the blood! While they travel to that point they can already damage proteins and some organs providing physiological effects!

In the blood HCN goes in O2 fixating hemoglobin Enzyme in th eplace of O2; then O2 being a weaker ligand for the hemoglobin than HCN will be displaced by HCN and no more O2 will be carried by hemoglobin; asphyxie occure and then necrosis (cyanosis).

So here normal process:
O2 -hemogl-> hemogl(O2) (in the lungs)
hemogl(O2) --> O2 + hemogl (in the organs)
The simple equation can be written:
A(lungs)-E1->A(organs) simple transportation use!

NaCN + H(+) --> HCN
HCN + hemogl(O2) --> O2 + hemogl(HCN)
Here HCN produced from NaCN in the mouth and in the stomach block E1 and form the less reversible cyanhydrichemoglobine compound E'1
A(lungs)-E'1->//

Another example: a,b,c etc are amino acids
a+b+c+...+z -Enzyme(insuline Protein Synthetase)-> insuline (proteine) -Receptor specific to insuline-> suggar regulation in teh blood
So here:
a+b+... -E1-> E2 (or A) -R1-> Physiol effect 1

That's it!
:cool:




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[*] posted on 31-3-2003 at 09:44


Samosa, in your research into mycotoxins from fusarium sp., did you find out anything that might be useful to someone who was trying to grow the mould?
I've set up a little experiment to see what I can grow on some corn inocculated with soil (with water and 1/3 of a multivitamin tablet), and will need some way to find out what I have, and how fusariums grow best etc.
I thought I might save myself some research time if you had already found what I was looking for...
If you have anything you think might be of interest, could you post it or e-mail it to me?
I found one source that said that artificially infected grain could have >600mg/kg of mycotoxins, consisting of various interesting things including vomitoxin. No prizes for guessing what that does! Also, other more toxic things...
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[*] posted on 31-3-2003 at 11:26


Hmm, actually I found a lot of information related to the growing of the Fusarium molds that produce T-2 Toxin. I will just list them, as I am short on time at the moment (need to get to Orchestra rehearsal :) ).

-Fusarium molds like Corn as a growth medium.
-Fusarium molds tend to grow on corn that has been exposed to frost
-They like moist environments
-They also like warm environments, somwhere in the area of 70-80* F (maybe 25*C)
-T-2 Toxin is soluble in Ether, DMSO Alcohol, Acetone, Propylene Glycol, Ethylene Glycol, and Polypropylene Glycol
-The mold that produces T-2 is pinkish in color.
-Fusarium molds are ubiquitous in soils almost all over the world.
-T-2 and Aflatoxin glow under black light...this should help you locate moldy grains.

Several of these conditions would not be favorable to other bacteria and competing molds, especially the frost. That could be used early on to kill off the competitors in the culture.

That's all I can think of now, as I have to run! But I will add more later, as I think of it....

Anyhow, has anyone ever thought of straight Fusaric Acid? It is quite toxic, somewhere in the area of 230 mg/kg LD50 rat/oral! Furthermore, it seems potentially synthesizable... It's name is "Butyl Pyridinecarboxlyic Acid," to help give you an idea of its structure. It is found in some plant poisons.
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[*] posted on 31-3-2003 at 15:25


Myotoxins... arent they basicly what rattle snakes produce? They are suposed to destroy tissue, but i know rattle snake venom isnt all that deadly when ingested. So my question is if snake myotoxin is old deadly when injected why is mold myotoxin deadly when eaten, exepcting the two chemicals to be at least somewhat similar?

CTR
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[*] posted on 31-3-2003 at 23:26


Snake venom does not contain Mycotoxins, as far as I know... Do you know what specific species might, however? Because as far as I know, Snake Venom is designed mostly to paralyze the prey and start the digestion process (as such, they will contain many enzymes).

Mycotoxins are a motley group of toxins, but in this case we are focusing most on T-2 since that is the one that is most suitable for weaponization... T-2 is poisonous because it interferes with DNA and RNA synthesis. Not sure how specifically it kills, however...

However, T2 works by any route of exposure because it attacks just about any tissue. In the eyes, it causes conjunctivitis, by ingestion it causes intestinal bleeding, by inhalation it causes dyspnia, and by dermal exposure it causes skin lesions.

Nevertheless- you do bring up another interesting point which I had not considered... Are there any chemicals that simulate different snake venoms?
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[*] posted on 1-4-2003 at 15:37


As for snakes they were my first motivation in science, in 8th i hade catolgued every venomus snake by genuse, spieces, and subspieces. Well if im correct (its been a while) myotoxins are the main component of rattlesnake vemon. You are right, tho all elapids (cobras and the like) are neurotoxic, other snake venoms inclued saffarotoxin, hemotoxin, cardiotoxin, along with other less common things.

CTR

[Edited on 1-4-2003 by Darkfire]
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mad.gif posted on 1-4-2003 at 17:01


Read better:
MyCotoxin and Myotoxin; see the difference?
Mycos -->linked to Muchrooms and yeasts!
Myos --> linked to muscles!

MyCotoxins --> Toxins generated by muchrooms and yeasts
Myotoxins --> Toxins that acts on the muscles

As always, in chemistry; one letter makes the difference!
Nitrite /Nitrate
Hydrazine/Hydrazone
...
So better read twice!


:mad::mad::mad:




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[*] posted on 1-4-2003 at 17:10


To tell ya they truth its been over 3 or 4 years since i even thought of myotoxin, it was off the top of my head.

CTR
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[*] posted on 2-4-2003 at 13:26


I'd say it was more than just pinkish, Samosa!

http://www.cof.orst.edu/cof/teach/for442/cnotes/sec8/fusar1....

I think if my newest experiment doesn't work I'll go and buy some organically grown wheat and see what I can grow from that (except wheat, of course!).

Fusaric acid would certainly be the easiest to synthesise out of the mycotoxins that I've seen from Fusarium sp.! It would also be more effective (in terms of doses/effort) I suspect to make this than to extract other mycotoxins.
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smile.gif posted on 7-4-2003 at 02:42


Synthesis of fusaric acid shouldn't be that complicated!

Fusaric acid: 5-butylpicolinic acid
mp 95-98°C
Dopamine B-hydroxylase inhibitor

CH3-CH2-CH2-CH2-(C5H5N)-CO2H

:):):)




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[*] posted on 5-6-2003 at 02:26


Let me get this right.Are you trying to for example make snake venom or(another example)inject large amounts of acetocholine into the target as opsed to binding the acetocholineerase with a nerve agent?

Anyways it seems to me the digestive juices of a scavenger like a crow might make for some rather intersting things.Think about it they eat just about anything.
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[*] posted on 5-6-2003 at 18:13


Cows and their ilk use a system of several stomachs to digest grass slowly over an extended period of time which they regurgitate, chew, swallow and digest for some more time (chewing the cud). they use time and a massive intestine to deal with the problem of indigestible food. They do have a prity rich bacterial content in their intestines to help them deal with this problem though.
They also avoid plants which are bad for them.
I suppose if you were desperate for something to use from a cow in a toxic kind of way (apart from the meat from tha mad beasties), the simolest would be to isolate E. coli from the dung and use that. It is kind of nasty after all when in the wrong place.
Or you could saddle one up and use it to run down civilians.
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