Abstract

Chitosan is a derivate of chitin, one of the most abundant polysaccharides in nature. In aquaculture, chitosan has been used as a flocculant in water recirculation systems with good results, but recent studies have shown that chitosan acetate may be toxic, producing branchial damage and death in trout. To improve the understanding of the toxic mechanism of chitosan on Oncorhyncus mykiss we exposed juveniles (60 g) for 1-2h to chitosan acetate at 10 mg/L and 0.1 mg/L. Fish exposed to the highest concentration of chitosan acetate experienced a rise in the ventilation rate (74%), the hematocrit (39%) and in the immature erythrocyte counts (157%). The number of mature erythrocytes as well as hemoglobin were also higher than in control fish but not statistically different. Simultaneously, a decrease in the mean corpuscular haemoglobin concentration (37%) was detected in relation to control measurements. These results and the death of fish after 30 to 60 min of exposure to 10 mg/L are evidence that chitosan induced respiratory stress causes death by hypoxia. We proposed that the structural characteristics of the molecule would facilitate its interaction with residues of sialic acid in the mucous-secreting epithelia.