Endocellular content of Paralytic Shellfish Poisons (PSP) and exocellular toxicity of the growth medium were investigated in the red-tide dinoflagellate Alexandrium minutum over the growth cycle in 15L batch cultures. Total sodium channel blocking (SCB) activity (neuroreceptor binding assay) and HPLC profiles of individual gonyautoxin (GTX) 1-4 components (endocellular only), as well as toxicity of the cell-free medium to Artemia were examined. Peaks in toxicity of the exocellular medium coincided with peaks in the endocellular toxicity of GTXs, both occurring in early to late lag phase and declining with culture age. SCB toxicity of the medium was found to be approximately 20 times higher (4-10 pg STX equivalents cell-1) than the endocellular SCB toxicity (169-610 fg STX equiv. cell-1). Endocellularly, GTX2 and GTX3 were dominant early in culture growth (36-64 mole%, epimeric total on day 48) but as time progressed GTX1 and GTX4 became increasingly important (58-93 mole %, epimeric total on day 182). Antibiotic treatment of dinoflagellate cultures reduced bacterial levels by up to 93% but this did not appear to affect SCB toxicity, although it did decrease toxicity of the exocellular medium to Artemia, which was highest late in culture growth. Toxicity of the A. minutum cell-free medium towards Artemia did not appear to be correlated with exocellular or endocellular total SCB toxicity nor was it correlated with any individual toxic GTX fraction. It is concluded that, in addition to a sodium channel blocking agent, A. minutum is producing another toxin capable of killing Artemia, but which is not PSP. Furthermore, this exotoxic principle is heat labile (reduced toxicity to Artemia above 80°C), but is not a gonyautoxin or brevetoxin.