Evidence of neuroendocrine disruption in freshwater mussels exposed to municipal wastewaters.

The purpose of this study was to test the hypothesis that exposure to municipal effluents can disrupt the neuroendocrine system in Elliptio complanata freshwater mussels. The capacity of ozonation to mitigate these effects was also examined. Mussels were exposed for 14 days to a continuous flow of increasing concentrations of the effluent before and after ozonation. Neuroendocrinal effects were examined by tracking changes in acetylcholinesterase, glutamate, gamma-aminobutyrate, serotonin, dopamine and their respective adenylcyclase activities in synapse membranes, monoamine oxidase and vitellogenin-like proteins. Oxidative stress and damage were examined by superoxide dismutase and lipid peroxidation, respectively, in the visceral tissues. The results revealed that the exposure of freshwater mussels increased the levels of vitellogenin-like proteins in both the primary-treated and ozonated effluents, dopamine and glutamate, and decreased the turnover of the neurostimulant acetylcholine. Moreover, these endpoints were significantly correlated with oxidative stress and damage. A canonical analysis of the responses revealed that dopamine and the neuroexcitatory neuromediators--acetylcholesterase and glutamate--were the endpoints more strongly related with oxidative stress and damage. Mussel morphology and estrogenic biomarkers (vitellogenin-like proteins, gonad lipid stores) were also significantly related, albeit to a lesser extent, to oxidative stress and damage. In general, ozone treatment was not sufficient to mitigate the observed neuroendocrinal effects in freshwater mussels. We conclude that the continuous exposure of freshwater mussels to municipal wastewater effluents leads to neuroendrocinal alterations and to oxidative stress.