Influence of dinoflagellate cell toxicity on uptake and loss of paralytic shellfish toxins in the northern quahog Mercenaria mercenaria

Abstract

The northern quahog Mercenaria mercenaria was exposed to bloom concentrations of the toxic red-tide dinoflagellate Alexanddum, the proximal cause of paralytic shellfish poisoning (PSP) in eastern North America, under controlled conditions in the laboratory. Two cultured isolates of Alexandrium, exhibiting markedly different PSP toxin compositions and specific toxicities, were used independently to determine the kinetics of toxin accumulation and loss, as well as the potential for biotransformation of individual PSP toxins in certain tissues. Clams readily ingested and absorbed a monospecific diet of the low toxlcity A. tamarense isolate GtLI22 They also ingested cells of the high toxicity A , fundyense isolate GtCA29, but at a lower rate, and only when the diet was supplemented with a nontoxic d ~a t o m , Thalass~osira weissflogii. As natural populations of M. mercenaria rarely accumulate a substantial PSP toxin load, this suggests the existence of a toxin recognition mechanism Maximum toxicities In clam t~ssues, attained within 2 wk of exposure to either toxic dinoflagellate, exceeded the regulatory harvest closure level (80 lig STXeq 100g-l) by several orders of magn~tude. Detoxification to levels acceptable for human consumption occurred within 3 to 6 wk. HPLC analyses revealed significant differences between the toxic profile of the dinoflagellates and that accumulated in various clam tissues. Clams toxified with isolate GtLI22, a strain rich in low potency C-toxins, showed: