The BEST & Most Deadly Biological Poisons... or how to get rid of a roommate | |
1. Botulinum - the most deadly poison is a mix of 7 types of nerve toxins produced by the bacterium Clostridium botulinum. The toxin is enzymatic (a zinc protease that cleaves 1 or more of the fusion proteins by which neuronal vesicles release acetylcholine into the neuromuscular junction) and causes respiratory failure and paralysis which can result in death. It can be waeponized. |
2. Ricin - a protein toxin extracted from castor beans which inhibits cellular protein translation eventually killing cells with symptoms of severe diarrhea with victims dying of shock. Ricin consists of two distinct protein chains (≈ 30kDa each) linked by a disulfide bond. Ricin A interferes with 28s RNA of ribosomes, responsible for protein synthesis, While Ricin B assists Ricin A's entry into a cell. |
3. Anthrax - infections caused by Bacillus anthracis. Two types: cutaneous = small sores that develops into blisters & skin ulcers and gastrointestinal = nausea, loss of appetite, bloody diarrhea and fever. The bacteria release a protein toxin which targets macrophages with an edema factor which inactivates macrophages so that they cannot phagocytose bacteria and a lethal factor causing macrophages to make TNF-alpha and interleukin-1-beta, that lead to septic shock and death. Anthrax also targets endothelial cells, causing vascular leakage (similar to hemorrhagic bleeding), and ultimately hypovolemic shock. The virulence of a strain of anthrax is dependent primarily to the poly-D-glutamic acid capsule that protects the bacterium from phagocytocis by host macrophages. Weaponization. |
4.
Sarin - an a clear, colorless, and tasteless
organophosphorous pesticide [O-Isopropyl methylphosphonofluoridate]
liquid that has no odor which can be vaporized into a deadly
chemical nerve gas. It functions by
inhibiting the neuro-muscular
junction acetyl-cholinesterase enzyme [forms a covalent bond
with the active site of the esterase where acetylcholine normally
undergoes hydrolysis]. This allows acetylcholine to build up and
continually stimulate any nerve impulses. Symptoms include runny
nose, tightness in the chest, pupilary contraction, difficulty
breathing, nausea, drooling, loss of control of bodily functions,
vomiting, defecation, twitching and jerking. Ultimately, a victim
becomes comatose and suffocates in a series of convulsive spasms. |
5.
Tetrodotoxin - a potent marine neurotoxin from the
Japanese pufferfish which
blocks voltage-gated sodium channels
on the surface of nerve membranes. Symptoms include shortness of
breath, numbness, tingling, lightheadedness, paralysis and irregular
heartbeat. Symptoms typically onset quickly, minor ones
instantaneously. Death is the usual outcome.
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6. Cyanide - a chemical that contains a cyano group -C≡N. Hydrogen cyanide is a colorless gas with a faint, bitter, almond-like odor. NaCN and KCN are both white powders with a bitter, almond-like odors. Many CN-containing compounds are highly toxic for CN ions bind to the iron atom of the enzyme cytochrome c oxidase in the ETC of mitochondrial membranes, deactivating it and the final transfer of electrons to oxygen thus cells no longer produce ATP. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Inhalation of high concentrations of hydrogen cyanide causes a coma with seizures, apnea and cardiac arrest, with death following in a matter of minutes. |
7. Mercury - A heavy metal, Hg is one of five periodic table elements that is liquidat room temp. Hg is a bioaccumulative toxin that is easily absorbed through the skin, respiratory and gastrointestinal tissues. Dimethylmercury, is so toxic that even a few microliters spilled on the skin can cause death. A main targets of the toxin is the enzyme pyruvate dehydrogenase, which is irreversibly inhibited by several mercury compounds, the lipoic acid component of the multienzyme complex binds mercury compounds tightly (mercury binds to the sulfur atoms in lipoic acid) inhibiting PDH. Hg toxicity can result in fever, fatigue, and clinical signs of pneumonitis. Chronic exposure results in neurologic, dermatologic, and renal manifestations. Signs and symptoms might include neuropsychiatric disturbances (e.g., memory loss, irritability, or depression), tremor, paresthesias, gingivostomatitis, flushing, discoloration and desquamation of the hands and feet, and hypertension. Hg exposure |
8.
Strychnine - a colorless crystalline plant alkaloid from the
seeds of the Strychnos nux-vomica tree used as a pesticide
for killing rodents that causes spasmatic muscular convulsions and
eventually asphyxia and death by sheer exhaustion. Strychnine acts
as a blocker or antagonist at the
inhibitory or strychnine-sensitive Glycine Receptor, a ligand-gated chloride channel in the spinal cord
and the brain. |
9. Amatoxin - a group of protein toxins found in mushroom species with quick intestinal absorption and thermostability that cause toxic hepatitis with centrolobular necrosis and hepatic steatosis, as well as acute tubulointerstitial nephropathy, which altogether induce a severe hepatorenal syndrome (with a potential fatal outcome). There are 8 amatoxins of which the most active is alpha-amanitin, a cyclic nonribosomal peptide of eight amino acids, with a specific affinity for the enzyme RNA Polymerase type II binding to it, effectively causing destruction of hepatocytes. |
10. Compound 1080 - sodium fluoroacetate, an odorless, taste-less, water soluble compound without antidote, that is used as a potent metabolic poison to control mammalian pests, and which remains poisonous for up to a year in bodies of animal killed with 1080. It is believed to disrupt the Krebs cycle by preventing citrate from being used in the cycle. This results in an accumulation of citrate in the blood and deprives cells of energy, leading to a slow and painful death as the body "suffocates from within". Symptoms include vomiting, involuntary hyper-extension of the limbs, convulsions, and finally cardiac and respiratory collapse. |
back | inspired by an article in Wired, by C. Null, page 18, August 2006. |