The effects of the blue-green algae (cyanobacterial) toxin microcystin-LR on yearling rainbow trout were studied in a series of intraperitoneal injection tests, gavage trials and exposures to waterborne algae. Concentrations of the microcystin-producing algae Microcystis aeruginosa known to occur during algae blooms (8-16 mg freeze-dried algae/L, i.e. approximately 1-2 × 1011 cells/L) were shown to be non-toxic to trout when present in aquarium water. On the other hand, trout died within 96 h when gavaged with an amount of algae equivalent to that which passed through the gills within 18 h in the aqueous exposure tests (1440 mg freeze-dried algae/kg body weight, i.e. 6600/.tg microcystin/kg body weight). Oral uptake of approximately one tenth of this dose (110 mg freeze-dried algae/kg body weight, i.e. 550/lg microcystin/kg body weight) proved to be non-toxic in single gavaging studies, but toxic within 96 h when orally administered 8 times at 12-h intervals. This study shows that the main uptake route of microcystin in trout is the gastrointestinal tract and that toxicity is manifested as massive hepatic necrosis. These results indicate that massive fish deaths reported at cyanobacterial bloom sites can be explained by the ingestion of toxic blue-green algae.

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Abstract--Ochratoxin A (OA) is a nephrotoxic and nephrocarcinogenic mycotoxin which is predominantly produced by the two ubiquitous fungal genera, Aspergillus and Penicillium. OA is found in foodstuffs, predominantly in cereals but also in coffee beans. Inconsistent results have been published regarding the influence of roasting on the OA content in roasted beans and the transfer into the coffee brew. In the present study an HPLC method was used for the detection of OA in green and roasted coffee beans as well as in the coffee brew. For qualitative confirmation and quantification of low OA levels in roasted coffee beans and coffee brew an additional clean-up step by immunoaffinity column was applied before HPLC analysis. In green coffee beans OA was detected in 13 out of 25 commercial samples analysed (detection limit, 0.5/~g OA/kg). Roasting (250°C, 150 sec) of naturally contaminated green beans or beans inoculated with A. ochraceus resulted only in a small reduction in the OA level. OA was also found to be eluted into the brew. Of 40 coffee brews prepared from commercially available samples OA was detected in 18 brews by HPLC and/or additional immunoaffinity column clean-up in the range of 0.4 to 7.8 pg OA/kg equivalent ground coffee. Our preliminary results suggest, therefore, that regular coffee consumption may contribute to exposure of humans to OA.