Saxitoxin and its naturally occurring analogues, are produced by both marine and freshwater microalgae. The name saxitoxin is derived from the mollusc in which it was first identified, Saxidomus giganteus. In freshwater, blue-green algae, namely Anabaena circinalis, manufacture the toxins and may transfer the toxins to freshwater shellfish (for example Alathyria condola) although no reports exist of intoxication from freshwater sources of these toxins. Dinoflagellates in the ocean, particularly Alexandrium catenella, Alexandrium minutum, Alexandrium ostenfeldii, Alexandrium tamarense, Gymnodinium catenatum and Pyrodinium bahamense var. compressum produce saxitoxins that can then be bioaccumulated by marine molluscs filter feeding upon the microalgae. A debate continues about whether bacteria produce saxitoxin, or influence dinoflagellate production of the toxins.

Saxitoxin (C₁₀H₁₇N₇O₄; MW = 299) is a tricyclic moleculeswith the 1,2,3- and 7,8,9-guanidino groups of saxitoxin possessing pKa’s of 11.3 and 8.2, respectively (see below). At physiological pH then, the 1,2,3-guanidino carries a positive charge, whereas the 7,8,9-guanidino group is partially deprotonated. This polar nature of saxitoxin allows it to readily dissolve in water and lower alcohols but insoluble in organic solvents. It is stable in solution at neutral and acidic pH’s, even at high temperatures but alkaline exposure oxidises and inactivates the toxin. Saxitoxin itself is highly toxic, killing guinea-pigs at only 5 m g / kg when injected intra-muscularly and at similar doses when injected intra-peritoneally into mice.

PSP is a global problem. Our nerves are especially sensitive to the toxins and in the early stages of PSP, victims experience tingling and numbness of the mouth, tongue, face and extremities. Nausea and vomiting may accompany the above symptoms. In severe cases, the patient will exhibit advanced neurological dysfunction such as ataxia, weakness, dizziness, a sense of dissociation followed by complete paralysis. The diaphragm and the diaphragm may stop working and death can occur after cardio-respiratory failure. These effects are caused by the toxin blocking the entry of sodium ions into nerve cells through the protein which spans the cell membrane and allows sodium entry during action potentials, the sodium channel.

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