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Saxitoxin (STX) is a cyanotoxin, which can cause neurotoxic effects and induce ecological changes in aquatic environments, a potential risk to public and environmental health. Many studies of cytotoxicity on animal cells and algae have been performed, although few compare the toxic effects between the two models. In this sense, we investigated the oxidative stress induced by STX (0.4-3.0 nM) in two different cellular models: Neuro-2A (N2A) cells and Chlamydomonas reinhardtii alga by quantification of malondialdehyde (MDA) levels as indicative of lipid peroxidation (LPO). Also was evaluated the antioxidant defense of these cells systems after exposure to STX by the addition of antioxidants in N2A cells culture, and by the measure of antioxidants enzymes activity in C. reinhardtii cells. The MDA levels of N2A cells increased from 15% to 113% for 0.4 and 3.0 nM of STX, respectively, as compared to control. Superoxide-dismutase and catalase did not appear to protect the cell from STX effect while, in cells treated with vitamin E, the rates of MDA production decreased significantly, except for higher concentrations of STX. No MDA productions were observed in algal cells however some effects on antioxidant enzymes activity were observed when algae were exposed to 3.0 nM STX. Our results indicate that the concentrations of STX that may induce oxidative stress through LPO are different in animal and phytoplankton communities. A combination of algal and animal bioassays should be conducted for reliable assessment of oxidative stress induced by STX.

Okadaic acid (OA) is the main toxin produced by dinoflagellates which can accumulate in the hepatopancreas of mussels and cause diarrhetic shellfish poisoning in consumers. This toxin is also a tumour promoter and a specific potent inhibitor of protein phosphatases 1 and 2A. No specific target organ is known for this toxin. This study concerns the distribution of [3H]OA in organs and biological fluids of Swiss mice having received a single dose per os of AO (50 mg/kg). The determination of the toxin extracted from mouse organs 24 h after administration of [3H]OA and derivatised with 9-anthryldiazo methane (ADAM) before HPLC and fluorescent detection showed the highest concentration in intestinal tissue and stomach. This distribution was even more pronounced in intestinal tissue, when animal were given per os 90 mg/kg which induced diarrhoea. The high concentrations of [3H]OA in intestinal tissues and contents 24 h after administration demonstrates a slow elimination of OA. When the dose of OA was increased from 50–90 mg/kg, the concentrations of the toxin in the intestinal content and faeces increased proportionally. A good correlation was found between an increase of OA in the intestinal tissue and the diarrhoea in animals given 90 mg/kg orally. Moreover OA was present in liver and bile and in all organs including skin and also fluids. Altogether these results confirmed an enterohepatic circulation of OA as previously shown. These data also revealed that in acute OA intoxication the concentration of the toxin in the intestinal tissues reaches cytotoxic concentrations in accordance with the diarrhoea which is the main symptom of OA poisoning.