Abstract
This study reports the accumulation of paralytic shellfish toxins (PSTs) in Atlantic horse mackerel ( Trachurus trachurus ) over a bloom of the toxigenic dinoflagellate Gymnodinium catenatum . High levels of toxins, up to 4800 μg STXeq kg –1 , were registered at the peak of the bloom (5.0 10 3 cells l –1 ). The suite of individual PSTs was examined. Decarbamoylsaxitoxin (dcSTX) and B1 constituted nearly 90% of toxins (on a molar basis) determined in mackerel. This profile of toxins markedly differs from the known profile of toxins produced by G. catenatum strains isolated from the Portuguese coast, which is dominated by N-sulfocarbamoyl toxins, in particular the C1+2 toxins. The prevalence of the potent dcSTX in the pelagic environment and its transfer through the marine food web is highlighted in this study. Atlantic horse mackerel is identified as a high potential vector of PSTs along the Portuguese coast. This fish species has a central position in the marine food web, being an important predator of zooplankton and at the same time an important diet item of top predators. This study reveals bioaccumulation values that are important for evaluating potential impacts of blooms of PST-producing dinoflagellates on marine ecosystems or their components, such as fish.
Highlights
Paralytic shellfish toxins (PSTs) are potent neurotoxins produced by bloom-forming algae species in both marine and freshwater ecosystems
PSTs are regularly monitored in bivalve mollusks, which are prohibited for human consumption when toxicity exceeds 800 μg STXeq kg–1, less is known regarding accumulation of these toxins in fish
While most data available in the literature are associated with fish kills, this study addresses the accumulation of PSTs in a fish species over a bloom of Gymnodinium catenatum
Summary
Paralytic shellfish toxins (PSTs) are potent neurotoxins produced by bloom-forming algae species in both marine and freshwater ecosystems. Poisoning of fish leading to lethal incidences, as mentioned above, is occasionally reported, but induction of sublethal effects without outward signs of toxicity must occur regularly (Bakke and Horsberg 2010, Costa et al 2012). In this case, fish can play a vectorial role and transfer the toxins to piscivorous predators (Geraci et al 1989, Castonguay et al 1997, Reyero et al 1999)
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