Azaspiracid poisoning toxins are produced by marine dinoflagellates are responsible for the most recently discovered human toxic syndrome associated with shellfish, Azaspiracid Poisoning (AZP). Azaspiracids are novel classification of toxin different to the currently named toxins they differ from any of the previously known toxins found in shellfish or dinoflagellates unique spiro ring assemblies, a cyclic amine instead of a cyclic imine group and a carbocyclic or lactone ring is absent. A number of minor AZA anologues have also been identified within shellfish.
Experiments on mice have shown just how extreme the effects of AZP can be, both by injection and orally. Oral toxicity in mice demonstrated that azaspiracid causes widespread organ damage. at high levels (900ug/kg) itc an damage the epithelial cells within the small intestine within four hours whereas at lower doses (300ug) it damaged the mucus membrane after four hours, leading to necrosis after three hours and eventually after a further four hours the mucus membrane became detached from the epithelial cells. Interestingly, 24hours post exposure the surface of the epithelial cells appeared to recover however under the surface the damage was extensive, villi were empty. The mice administered 500ug/kg of AZA1 had increased liver weights and a reduced number of T cells and B cells in the spleen. Long term doses of low levels (20-50ug/kg) shortened intestinal villi and all mice used developed interstitial pneumonia, inflammation of the liver and 20% of the mice developed lung cancer suggesting AZA1 may be a tumour initiator. This paper explores the literature associated to how the toxin effects different areas of the cell from the actin in the cytoskeleton to the effects of cadherin proteins effecting cell-cell adhesions, neuron signalling, calcium ions and its dose dependant effect on heart heart rate, development, hatching success and viability of Japanese medaka embyros.
The toxin is produced by a small photosynthetic dinoflagellate A.spinosum as a defence mechanism which in turn, is consumed by other dinoflagellates that are unable to produce their own nutrition such as P.crassipes that act as vectors to higher organisms such as filter feeing bivalves. Filter feeing concentrates both pathogens and phycotoxins at dangerous levels. When the first case of AZP was reported after the consumption of mussels cultivated at Killary Harbour in Ireland in 2005 the mussels has been passed as fit for human consumption by the DSP mouse bioassay. This bio assay has been shown to be ineffective against determining the levels of azaspiracids within biovales such as mussels, this is because although azaspiracids are usually concentrated within the hepato-pancreas of mussels they can migrate to other tissue compartments which is very significant as mouse bioassay only tests the hepato-pancreas.
In recent years there has been much debate and conflicting results, regarding the minimum permissible level of AZA1 in shellfish. The European Food Standard Agency settled on a dose no greater than 12ug of AZA1 eq/60kg person and instead of using the traditional DSP mouse bio assay to determine whether shellfish are dangerous for human consumption and a Liquid chromatography–mass spectrometry would be more appropriate.
This paper is very important as azaspiracids are significantly different from other classes of shellfish toxins, and until ten years ago was mistaken for other shellfish toxins its serious effects demands a high level of vigilance to limit human exposure to seafood toxin.
A review of : A, Furey. S, O'Doherty. K, O'Callaghan. M, Lehane. K, James; 2009; Azaspiracid poisoning (AZP) toxins in shellfish: Toxicological and health considerations; Toxicon, 56, 173-190
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