Paralytic shellfish toxin concentrations were measured and individual toxin profiles were monitored in axenic batch cultures of Protogonyaulax tamarensis and Protogonyaulax catenella. High pressure liquid chromatographic methods were used that allowed the separation of all 12 known paralytic shellfish poisons, including toxins Cl, C2, and C3, from a single sample. In isolates of both Protogonyaulax species, total toxin levels were relatively low after inoculation, increased rapidly in early to midexponential growth to a value 100 to 300% of that at the initial time point, then decreased by 86 to 95% as the culture aged. Although the concentrations of individual toxins per cell followed the same general pattern as that seen for total moles of toxin per cell, variability in toxin profile with culture age was observed. In P. tamarensis, the mole percent of neosaxitoxin increased substantially from 8 to 44% as total toxin levels per cell decreased. A concomitant decrease in the mole percent of saxitoxin with culture age was noted. Although not as precipitous, changes in the mole percent of specific toxins from P. catenella were also observed. The mole percent of gonyautoxins I and IV increased, while that of gonyautoxins II and III decreased. These data suggest that the toxin profile in isolates of Protogonyaulax can change, sometimes significantly, with changing environmental variables. Protogonyaulax species produce an array ofchemically similar neurotoxins that differ in their biological toxicity (8,17).

Captive sea otters (Enhydra lutris)fed live Saxidomus giganteus (butter clams) ad libitum either reduced their prey capture and consumption rates or discarded the highly toxic siphons and kidneys when switched from clams containing very low levels of saxitoxin [37±9 µg STX (100 g)−1] to highly toxic clams [226±96 µg STX (100 g)−1]. Feeding rates returned to pretreatment levels when the otters were again switched to low‐toxicity clams, but siphon discard frequency remained high. Paralytic shellfish poisoning symptoms were observed only in an otter calculated to have consumed the most STX (154 µg kg−1 d−1), a dosage within the range of oral LD50s reported for other nonprimate mammals. None of the other otters displayed symptoms, and all subjects were eventually released in good health. These findings suggest that otters are not immune to paralytic shellfish poisoning toxins (PSPT) and that they have the ability to detect and avoid consumption of lethal amounts of toxic prey. This behavioral response is highly adaptive given the importance of butter clams in sea otter diets, and the chronic toxicity of butter clams in areas where toxic dinoflagellate blooms occur. A comparison of the distributions of otters and toxicity levels of butter clams in southeast Alaska suggests that the sequestering of PSPT may protect some clam populations from otter predation and limit the distribution of otters to the exposed outer coast where toxic clams are rare.

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