Abstract
Paralytic shellfish poisoning (PSP) is a severe food-borne illness, caused by the ingestion of seafood containing paralytic shellfish toxins (PST), which are naturally produced by marine dinoflagellates and accumulate in shellfish during algae blooms. Novel PST, designated as hydroxybenzoate analogues (also known as GC toxins), was relatively recently discovered in Gymnodinium catenatum strains worldwide. However, to date, there have been no studies examining their accumulation in shellfish. In this study, mussels (Mytilus galloprovincialis) were exposed to G. catenatum for five days and then exposed to a non-toxic diet for 24 h, to investigate the toxin’s accumulation/elimination dynamics. As determined by UHPLC-HILIC-MS/MS, the hydroxybenzoate analogues, GC1 to GC6, comprised 41% of the algae toxin profile and only 9% in mussels. Elimination of GC toxins after 24 h was not evident. This study highlights that a relevant fraction of PST in mussels are not routinely analysed in monitoring programs and that there is a need to better understand the toxicological potential of the hydroxybenzoate analogues, in order to properly address the risk of G. catenatum blooms.
Highlights
Paralytic shellfish toxins (PST) are potent neurotoxic alkaloids, produced in the marine environment by dinoflagellate species belonging to three genera, namely Alexandrium, Pyrodinium, and Gymnodinium
Toxin Profile of Gymnodinium Catenatum Strain Used for Mussel Exposure
G. catenatum—this species produces a wide array of toxin derivatives, challenging environmental researchers and governmental agencies with environmental responsibilities
Summary
Paralytic shellfish toxins (PST) are potent neurotoxic alkaloids, produced in the marine environment by dinoflagellate species belonging to three genera, namely Alexandrium, Pyrodinium, and Gymnodinium. The toxicity of PST is caused by a high affinity inhibition of voltage-gated sodium channels (Nav ) on the extracellular membranes of nerve cell terminals [1,2]. Structural differences among PST analogues—which were classically divided in three groups, the carbamoyl, dicarbamoyl, and sulfocarbamoyl groups—result in different affinities to the binding sites of Nav , leading to a varying degree of toxicity. A fourth group of PST was described in the early 2000s, in Gymnodinium cateantum strains from Australia, Uruguay, China, Spain, and Portugal [3]. The new toxins were designated as GC toxins (GC1–3), with GC3 corresponding to the 4-hydroxybenzoate ester
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