Paralytic shellfish poisoning (PSP) toxins are produced by dinoflagellates of the genus Alexandrium, which form blooms in the Gulf of Maine (Anderson et al., 1994). It is well known that suspension-feeding shellfish can consume toxic cells of Alexandrium spp. and accumulate PSP toxins, and that such contaminated shellfish are a threat to public health and result in economic loss to the fishing and aquaculture industries (Shumway et al., 1988). Zooplankton are also major consumers of phytoplankton, including Alexandrium spp.; the presence of PSP toxins in wild zooplankton populations of the Gulf of Maine has been documented in several studies (White, 1979, 1980, 1984). These studies have shown that mesozooplankton can attain body burdens of these toxins that are inimical or even fatal to vertebrate zooplanktivores such as clupeid fishes and whales. Larval fish are even more susceptible to adverse effects from consumption of zooplankton contaminated by PSP toxins (White et al., 1989; Robineau et al., 1991a,b). Nevertheless, research suggests that only a fraction of the total toxin from Alexandrium spp. cells acquired during feeding activity is retained in the tissues of zooplankton grazers. White conducted toxin accumulation studies with adult copepods, Acartia clausi (= A. hudsonica), and barnacle nauplii, Balanus sp. (= Semibalanus sp.) at high densities (10-13 individuals ml-1), fed Alexandrium fundyense (= Gonyaulax excavata) at ~ 3 ϫ 10 3 cells ml-1 (White, 1981). At such high densities of zooplankton and toxic cells, both grazer species accumulated high toxin levels [19-54 µg saxitoxin equivalents (µgSTXeq) g-1 wet weight] within 6 h. Toxin retained in copepod tissues, expressed as a percentage of total toxin ingested, ranged from ~10% for A. clausi to ~32% for Balanus sp. White used a modification of the Association