_skeletal.svg) | |
| Names | |
|---|---|
| IUPAC name (5S)-5-[(Dimethylamino)methyl]-1-{[hydroxy(methoxy)phosphoryl]oxy}-4,5-dihydro-1H-imidazol-2-amine | |
| Identifiers | |
3D model (JSmol) | |
| ChemSpider | |
| KEGG | |
| UNII | |
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| Properties | |
| C7H17N4O4P | |
| Molar mass | 252.211 g·mol−1 |
Except where otherwise noted, data are given for materials in theirstandard state (at 25 °C [77 °F], 100 kPa). | |
Guanitoxin (GNT), formerly known as anatoxin-a(S) "Salivary"[a],[1] is a naturally occurringcyanotoxin commonly isolated fromcyanobacteria (specifically of the genusAnabaena). It is a potent covalentacetylcholinesterase inhibitor, and thus a potent rapid actingneurotoxin which in cases of severe exposure can lead to death. Guanitoxin was first structurally characterized in 1989, and consists of a cyclicN-hydroxyguanidineorganophosphate with a phosphate ester moiety.[2]
The main mechanism of action for guanitoxin is by irreversibly inhibiting the active site of acetylcholinesterase leading to excessacetylcholine in the parasympathetic and peripheral nervous systems; inducing poisoning via nicotinic and muscarinic cholinergic receptor stimulation.[3] The clinical signs of high level guanitoxin exposure consists mainly of excessive salivation,lacrimation,chromodacryorrhea (in rats), urinary incontinence, muscular weakness,muscle twitching, convulsion, includingopisthotonus, and respiratory distress and/or failure, and death.[4][5]
Treatment of afflicted case byatropine has attested to suppress the muscarinic mediated toxicity; which prevents the namesake salivation that similarly reacts to prevent the toxin's other poisoning symptoms which include lacrimation, urinary incontinence and defecation. Atropine will not, however, counter another mechanism of the compounds toxicity as it also mediates a nicotinic adverse toxicity affecting muscle tremors, fasciculation, convulsions and respiratory failure.[citation needed]
Guanitoxin is generally labile. It decomposes rapidly in basic solutions, but is relatively stable in neutral or acidic solutions (pH 3-5). When stored at -20˚C, it slowly undergoes hydrolysis giving pre-guanitoxin N-oxide and monomethyl-phosphate, and more slowly, formation of pre-guanitoxin. Furthermore, air evaporation of guanitoxin solutions resulted in significant hydrolysis to pre-guanitoxin N-oxide.[2]
