Abstract

Immature Sparus aurata L. (gilthead seabream) were exposed to 17β-estradiol (E 2) 4000 ng/l and to the same E 2 concentration mixed with 50,000 ng/l 4-nonylphenol (E 2+NP) during 4, 8, 12 and 16 h. E 2 availability and E 2 plasma level variations were assessed. Liver biotransformation capacity was measured as ethoxyresorufin- O-deethylase (EROD) and glutathione- S-transferase (GST) activities. Plasma cortisol, lactate and glucose were also determined. Genotoxicity was assessed through erythrocytic nuclear anomalies (ENA) frequency. Liver EROD activity significantly decreased during the whole experiment for both treatments, with the exception of 16 h exposure to E 2. Liver GST activity was significantly increased after 8 and 12 h of exposure either to E 2 or E 2+NP. An endocrine disruption expressed as plasma cortisol decrease was observed after 16 h exposure under both tested conditions, concomitantly with a plasma lactate increase. No genotoxic responses, measured as ENA frequency, were detected. Analyzing the E 2 water concentration in aquaria without fish it was demonstrated an intense and fast E 2 loss, considerably reducing its availability to fish. In the presence of fish, E 2 water levels were drastically reduced after 4 h exposure, being this reduction more pronounced in E 2 aquarium when compared to E 2+NP aquarium. In addition, it was demonstrated a rapid E 2 uptake from the water since the highest E 2 plasma concentrations were observed after 4 h exposure, followed by a continuous decrease, which became more pronounced between 8 and 12 h of exposure. Furthermore, during the first 8 h exposure to E 2 and E 2+NP, seabream plasma E 2 concentrations were higher than the initial water exposure concentration. Comparing the E 2 plasma levels in both seabream-exposed groups, it was clear that its concentration is always higher in E 2+NP-treated fish. Despite the previous results, no significant differences were found in the measured responses between E 2 and E 2+NP.

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