Metabolic transformation of paralytic shellfish toxins in the mussel Mytilus galloprovincialis under different exposure modes

Abstract

Gymnodinium catenatum is a widely distributed toxic marine dinoflagellate that produces paralytic shellfish toxins (PSTs). It is prone to causing algal blooms and poses a serious threat to the shellfish industry and human health. Previous studies have shown that when algal blooms occur, shellfish can accumulate PSTs in their bodies due to filtration. In this study, mussels (Mytilus galloprovincialis) were fed with G. catenatum at different fixed or varied cell density over time, with the latter designed to mimic the changes in algal cell density over time in the wild. The PST concentration in the mussels was positively correlated with the number of algal cells, and PSTs rapidly accumulated in the mussels under both feeding modes. Compared with constant feeding in the low feeding group, variable cell density feeding over time was more conducive to the accumulation of PSTs in M. galloprovincialis. An obvious toxin transformation process was also detected in the mussels, which transformed the less toxic gonyautoxins-5 and -6 and N-sulfocarbamoyl gonyautoxin-3 ingested from G. catenatum into the more toxic decarbamoyl gonyautoxin-2, decarbamoyl saxitoxin, and decarbamoyl neosaxitoxin. The ratio of epimer pairs, α:β, tended to stabilize when the toxin concentration was highest, and it increased rapidly after mussels stopped consuming toxigenic algae. These results suggested that the formation of α-stable toxoids mainly occurred during the process of toxin depuration. Toxins were also transformed from low to high toxicity, and α-stable toxoids were formed mainly in the hepatopancreas. These results provided basic data for better understanding of the laws governing metabolic transformation of PSTs in bivalves during algal blooms.