AZASPIRACIDS ACCUMULATION AND BIOLOGICAL RESPONSES IN MUSSELS FED WITH Azadinium dexteroporum

Azaspiracids (AZAs) are lipophilic marine toxins causing Azaspiracid Poisoning, with gastrointestinal symptoms in consumers of contaminated shellfish. Species of the dinoflagellate genus Azadinium and Amphidoma, considered as... [ view full abstract ]

Azaspiracids (AZAs) are lipophilic marine toxins causing Azaspiracid Poisoning, with gastrointestinal symptoms in consumers of contaminated shellfish. Species of the dinoflagellate genus Azadinium and Amphidoma, considered as AZA-producers, were widely reported in different geographical areas. Recently Azadinium  dexteroporum was isolated in the Tyrrhenian Sea. This work aims to study the accumulation, biotransformation and compartmentalization of AZA-analogues produced by A. dexteroporum, in mussels fed with algae, by LC-MS/MS. A culture of  A. dexteroporum was established, optimised and used to feed mussels (Mytilus galloprovincialis) for 21 days in laboratory conditions. AZA-54, AZA-55 and 3-epi-AZA-7, the  predominant AZA-analogues of A. dexteroporum toxin profile, accumulated in the exposed mussels. They concentrated in digestive gland and seemed to be not biotrasformed. The detoxification was quite slow and excretion rate appeared to be different for each analogue. Some biological responses (biomarkers) to AZAs are also evaluated in the exposed organisms. Immune response parameters, peroxisomal proliferation and neurotoxicity markers, oxidative disorder parameters, genotoxic damage markers have been studied by spectrophotometric, spectrofluorimetric, gas chromatography, optical microscopy and fluorescence techniques. Results indicate an immediate activation of the mussels immune system in response with significant changes in the stability of lysosomal membranes, granulocyte/hyalinocyte ratio and phagocytic ability, suggesting these parameters as very sensitive to AZAs exposure. Other biomarkers showed general fluctuations during the exposure time with the most consistent variations at the end of the depuration phase. This suggests an activation of these mechanisms mainly during the AZAs excretion, rather than the exposure phase.