Alpha-amanitin
From Wikipedia, the free encyclopedia
| Alpha-amanitin | |
|---|---|
 |
|
| Other names | amanitin, alpha-amanitine, alpha-amatoxin |
| Molecular formula | C39H54N10O14S |
| SMILES | OCC(O)C(C)C(C(NC1C(NCC(NC(C(C)CC)C(NCC(NC (CS(C2=C(C1)C3=C(N2)C=C(O)C=C3)=O)C(NC(CC (N)=O)C(N4C5CC([H])(C4)O)=O)=O)=O)=O)=O)= O)=O)NC5=O |
| Molar mass | 918.971 g/mol |
| CAS number | [23109-05-9] |
| Infobox disclaimer and references | |
Alpha-amanitin or α-amanitin is a cyclic nonribosomal peptide of eight amino acids. It is possibly the most deadly of all the amatoxins, toxins found in several members of the Amanita genus of mushrooms, one being the Death cap (Amanita phalloides) as well as the Destroying angel, a complex of similar species, principally A. virosa and A. bisporiga. It is also found in the mushrooms Galerina autumnalis and Conocybe filaris. The oral LD50 of amanitin is approximately 0.1 mg/kg.
Contents |
[edit] Scientific use
Because of the mechanisms that make it a deadly toxin, alpha-amanitin is also used as an inhibitor of RNA polymerase II.[1]
Alpha amanitin can also be used to determine which types of RNA polymerase are present. This is done by testing the sensitivity of the polymerase in the presence of alpha amanitin. RNA polymerase I is insensitive, RNA pol II is highly sensitive, and RNA pol III is slightly sensitive.
[edit] Symptoms of poisoning
Alpha-amanitin has an unusually strong and specific attraction to the enzyme RNA polymerase II. Upon ingestion, it binds to the RNA polymerase II enzyme, effectively causing cytolysis of hepatocytes (liver cells).[2] Few effects are reported within 10 hours; it is not unusual for significant effects to take as much as 24 hours after ingestion, this delay in symptoms making it even more difficult to diagnose as well as dangerous. By then, it is far past the time in which stomach pumping would yield an efficient result. Diarrhea and cramps are the first symptoms, but those pass, giving a false sign of remission. Typically, on the 4th to 5th day, the toxin starts to have severe effects on the liver and kidneys, leading to total system failure in both. Death usually takes place around a week from ingestion.[3]
Around 15% of those poisoned will die in around 10 days progressing through a comatose stage to renal failure, liver failure, hepatic coma, respiratory failure and death. Those who recover are at risk of permanent liver damage.[4] Diagnosis is difficult, centered around the described clinical symptoms as well as alpha-amanitin content excreted in the urine. Urine screening is generally most useful within 48 hours of ingestion. Treatment is mainly supportive (gastric lavage, activated carbon, fluid resuscitation) but includes various drugs to counter the amatoxins, including intravenous penicillin and cephalosporin derivatives, and, in cases of greater ingestion, can extend to an orthotopic liver transplant. The most reliable method to treat amanitin poisoning is through having the stomach pumped immediately after ingestion; however, the onset of symptoms is generally too late for this to be an option.
[edit] References
- ^ B. Meinecke and S. Meinecke-Tillmann (1993) Journal of Reproduction and Fertility 98:195-201 [1]
- ^ D. Michelot and R. Labia (1988) Drug Metabol Drug Interact 6:265-74. [2]
- ^ A. Mas (2005) Mushrooms Journal of Hepatology 42:166-169 [3]
- ^ Benjamin DR. "Amatoxin syndrome": 198–214. in: (1995) Mushrooms: poisons and panaceas — a handbook for naturalists, mycologists and physicians. New York: WH Freeman and Company.
