Resumen del producto

About 50 naturally occurring analogs of paralytic shellfish toxins (PSTs) are biosynthesized among marine dinoflagellates and cyanobacteria, or are created by biotransformation after ingestion by molluscan shellfish. The biosynthetic pathways for the major PSTs (e.g., N-sulfocarbamoyl-, N1-OH- and C11-sulfated carbamoyl-derivatives) are well known for the producing microorganisms, including the structural and functional elements of the respective gene clusters. The kinetics of toxin biotransformations within molluscan shellfish, however, are highly species-group specific, and involve an array of enzyme-mediated catabolic reactions via hydrolases, oxidoreductases and N-aminosulfotransferases, as well as facile thermodynamic epimerization subject to pH and temperature effects. Among other factors, such metabolic biotransformations yield profound differences in toxin body burden, net toxicity and toxin composition even among molluscan shellfish species exposed to the same bloom and harvested simultaneously from a given site. Here we compare the results of controlled laboratory feeding studies on the uptake and biotransformation kinetics of PSTs from cultured dinoflagellates and consequent effects on toxin body burden and composition. Such studies are critical to hindcasting and simulating the time-course of toxin accumulation for molluscs subjected to natural toxic blooms. This has implications as well for predicting species-specific toxicity and risk assessment because many biotransformations, e.g., from N-sulfocarbamoyl analogs, which often predominate in the dinoflagellate composition, to respective carbamoyl or decarbamoyl derivatives within molluscan shellfish, can increase net toxicity by more than an order of magnitude on a molar basis. This has implications for designing appropriate toxin monitoring strategies for various combinations of shellfish species and toxigenic dinoflagellate populations.

Palabras clave: paralytic shellfish toxins

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