Notes: Abstract The planktonic copepod Calanus finmarchicus is a dominant member of the zooplankton community in the lower St. Lawrence Estuary in eastern Canada. Blooms of the toxic marine dinoflagellate Alexandrium excavatum which produces high cellular levels of paralytic shellfish poisoning (PSP) toxins, occur during the period of high C. finmarchicus production in summer in this region. To study the feeding behaviour of C. finmarchicus in the presence of Alexandrium spp., experiments were conducted in which female adult copepods collected from the St. Lawrence Estuary between May and September 1991 were exposed under controlled conditions to two toxic isolates of A. excavatum (Pr18b and Pr11f) from the estuary and to a non-toxic control (PLY 173) of a closely related species, A. tamarense isolated from the Tamar Estuary, Plymouth, U.K. Clearance rates on non-toxic A. tamarense cells averaged 5.5 ml ind-1 h-1 but were nearzero with either toxic isolate. When presented with a mixture of A. excavatum and the non-toxic diatom Thalassiosira weissflogii in varying proportions, C. finmarchicus fed upon the diatom but avoided the toxic dinoflagellate. Although feeding rates on A. excavatum were very low, toxin analysis by high-performance liquid chromatography with fluorescence detection (HPLC-FD) revealed that the PSP toxins were accumulated in copepods exposed to toxigenic dinoflagellates. The toxin composition in copepods was similar to that of the toxic dinoflagellate, but not necessarily identical, particularly after short-term (2-h) exposure, when relatively elevated levels of N-sulfocarbamoyl toxins were detected. The evidence suggests that C. finmarchicus ingests toxic dinoflagellate cells, either mistakenly or during exploratory bouts of feeding, and accumulates PSP toxins in its gut system and perhaps in other tissues.

Notes: Abstract Profiles of diarrhetic shellfish poisoning (DSP) toxins produced throughout the growth cycle and the cell cycle of the toxigenic marine dinoflagellate Prorocentrum lima were studied in triplicate unialgal batch cultures. Cells were pre-conditioned at 18 ± 1 °C, under a photon flux density (PFD) of 90 ± 5 μmol m−2 s−1 on a 14 h light:10 h dark photoperiod. In exponential growth phase, cultures were synchronized in darkness for 17 d. After dark synchronization, cultures were transferred back to the original photoperiod regime. Cells were harvested for DSP toxin analysis by LC-MS (liquid chromatography with mass spectrometry), and double-stranded (nuclear) DNA was quantified by flow cytometry. The cell populations became asynchronous within approximately 3 d after transition from darkness to the 14 h light:10 h dark photoperiod. This may be due to the prolonged division cycle (5 to 7 d) that is not tightly phased by the photoperiod. Unlike other planktonic Prorocentrum spp., cytokinesis in P. lima occurred early in the dark and ceased by “midnight”. Cellular levels of the four principal DSP toxins, okadaic acid (OA), OA C8-diol-ester (OA-D8), dinophysistoxin-1 (DTX1) and dinophysistoxin-4 (DTX4), ranged from 0.37 to 6.6, 0.02 to 1.5, 0.04 to 2.6, and 1.8 to 7.8 fmol cell−1, respectively. No toxin production was evident during the extended period of dark synchronization nor during the initial period when NH4 was consumed as the major nitrogen source. Soon after the cells were returned to the 14 h light:10 h dark cycle and they began to take up NO3, cellular levels of all four toxins gradually increased. This increase in DSP toxins usually occurred in the light, marked by a rise in DTX4 levels that preceded an increase in the cellular concentration of OA and DTX1 (delayed by 3 to 6 h). Thus, DTX4 synthesis is initiated in the G1 phase of the cell cycle and persists into S phase (“morning” of the photoperiod), whereas OA and DTX1 production occurs later during S and G2 phases (“afternoon”). No toxin production was measured during cytokinesis, which happened early in the dark. The evidence indicates that toxin synthesis is restricted to the light period and is coupled to cell cycle events.