Salivation anatoxin

Anatoxin-a(s) is produced in both Anabaena flos-aquae [56] and Anahaena lemmer-mannii [57]. The symptoms of anatoxin-a(s) intoxication are similar to those of anatoxin-a but cause increased salivation in vertebrates hence, the similarity in the names of these compounds with the (s) added to indicate salivation [18]. The structures, however, are quite different, as are the mechanisms of action. 

As described above, acetylcholine carries the signal across the gap between nerves and nerve to muscle. If acetylcholine lingered in the synaptic gap it would continually stimulate the acetylcholine receptor and the enzyme acetylcholinesterase degrades the acetylcholine. Anatoxin-a(S) inhibits acetylcholinesterase preventing the removal of acetylcholine and nerve and muscle cells become hyperexcited. Mice injected intraperitoneally with anatoxin-a(S) excessively salivate and exhibit lacrimation, urinary incontinence, defecation, convulsion, fasciculation, and die by respiratory arrest. By this route, the toxin has an LD50 approaching 50 pg kg... 

Anatoxin-a(s) (Fig. 3.4) was discovered by Mahmood and Carmichael as a metabolite of Anabaena flos-aquae NRC 525-17 [4, 5]. This toxin was implicated in the death of wild animals (ducks, birds, swine) after ingestion of contaminated water. This cyanotoxin is a neurotoxin, but different from anatoxin-a, and this unique alkaloid is an irreversible inhibitor of acetylcholine esterase with a toxicology similar to that of known anticholinesterases such as paraoxon [116-119]. Anatoxin-a(s) provokes salivation (thus the suffix (s)), chromodacryorrhea, fascic-ulation, and urinary incontinence, and death within 7-20 min, on rats treated with 0.25-1.0 mg kg (i.p.) The lethal dose LD50 (mouse, i.p.) is 50 pg kg"" making... 

Anatoxin-a(s) is a natural oiganophosphate analogue produced by cyanobacteria in the genus Anabaena (Molica et al., 2005 Patocka et al., 2011). The "(s)" in the name "anatoxin-a(s)" refers to salivation, which is a characteristic sign of poisoning observed in laboratory rodents after exposure (Mahmood and Carmichael, 1986 Carmichael et al., 1990). 

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