Anatoxin toxic effects

The ability to identify and quantify cyanobacterial toxins in animal and human clinical material following (suspected) intoxications or illnesses associated with contact with toxic cyanobacteria is an increasing requirement. The recoveries of anatoxin-a from animal stomach material and of microcystins from sheep rumen contents are relatively straightforward. However, the recovery of microcystin from liver and tissue samples cannot be expected to be complete without the application of proteolytic digestion and extraction procedures. This is likely because microcystins bind covalently to a cysteine residue in protein phosphatase. Unless an effective procedure is applied for the extraction of covalently bound microcystins (and nodiilarins), then a negative result in analysis cannot be taken to indicate the absence of toxins in clinical specimens. Furthermore, any positive result may be an underestimate of the true amount of microcystin in the material and would only represent free toxin, not bound to the protein phosphatases. Optimized procedures for the extraction of bound microcystins and nodiilarins from organ and tissue samples are needed. 

Neurotoxins, such as saxitoxin and anatoxin-a, have been implicated in mediating competitive interactions between toxic cyanobacteria and other photoautotrophs, but few studies have explicitly examined the allelopathic effects of these compounds (e g., Kearns and Hunter 2001). Although it is reasonable to assume that these compounds bind to algal and cyanobacterial sodium channels in a similar fashion as in vertebrate neurons, support for this hypothesis is currently lacking. 

One role of cyanobacterial allelochemicals may be to alter the motility and distribution of competing photoautotrophs. In a recent study, Kearns and Hunter (2001) examined the effects of toxic metabolites from the filamentous cyanobacterium A. flos-aquae on a unicellular phytoplankton species, Chlamydomonas rein-hardtii. A. flos-aquae synthesizes both microcystins as well as anatoxins, providing the authors with an ecologically relevant opportunity to assess the individual and combinatorial effects of these toxins on an alga. 

Anatoxin A is the fast-acting and highly effective poison of the cyanobacterium Anabaenaflos-aquae, which is ubiquitous in freshwater. Anatoxin A, also known as Very Fast Death Factor , was isolated from Anabaenaflos-aquae in 1977 by Paul Gorham at the National Research CoimcU in Ottawa. [553,554] The structure had already been determined in 1972 by X-ray analysis of its N-acetyl derivative. [555] Later, the presence of anatoxin A was detected in a range of other toxic strains of Oscillatoria, Anabaena circinalis, Aphanizomenonflos-aquae, Cylindorsperum pp. and Raphidiopsis mediterranea. 

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