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The direct ingestion of toxic species or organisms contaminated with phycotoxins are common forms of poisoning. A second mechanism of poisoning is by the contact or absorption of dissolved toxins through membranes and gills, which allow their uptake through the circulatory system reaching tissues and organs. Of these mechanisms, the less studied one is the effect of dissolved toxins which may be linked to unexplained mortalities of marine organisms. In this work, shrimp juveniles (2.1 g wet weight) were exposed to extracts obtained from 104, 105 and 106 cells L-1 of the paralytic shellfish toxin (PST) producer Gymnodinium catenatum. Bioassays lasted 10 h, time when mortality initiated. Shrimp exposed to extracts presented erratic movements, swam towards the water surface, and remained close to air diffusers. The main tissue damages were: 1) severe atrophy in gills, 2) nervous system edema grade 1 in 104 cells L-1 treatment and grade 2 in 105 and 106 cells L-1 treatments, and 3) muscle atrophy. Damages are more evident when shrimps are exposed to more concentrated extracts. Tissue damages, although similar to those recorded when shrimps are exposed to G. catenatum cells, are less severe with the exception of the atrophy in gills. Results suggest that dissolved metabolites, including PST, may cause tissue damages and that they may be a potential factor involved in the shrimp mortality in culture ponds and larvae rearing laboratories. Paralytic shellfish toxins may cause these damages, however other dissolved metabolites produced by G. catenatum cannot be disregarded for the observed behavioral and tissue damages.

Palabras clave: dissolved toxins; shrimp; dinoflagellates; histology

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