Cellular and Molecular Biology


Histopathological alterations, EROD activity, CYP1A protein and biliary metabolites in gilthead seabream Sparus aurata exposed to Benzo(a)pyrene

J.B. Ortiz-Delgado1, H. Segner2,4, J.M. Arellano3,4 and C. Sarasquete1,4

1Institute of Marine Sciences of Andalucía, CSIC, Polígono Río San Pedro, Puerto Real, Cádiz, Spain 2Centre for Fish and Wildlife Health, University of Berne, Berne, Switzerland, 3Department of Toxicology, University of Cadiz, Spain and 4Research Group of Environmental Quality and Pathology (CSIC & UCA), Cadiz.

Offprint requests to: Dr. Carmen Sarasquete, Institute of Marine Sciences of Andalucía, CSIC, Polígono Río San Pedro, Apdo Oficial 11510 Puerto Real, Cádiz, Spain. e-mail: carmen.sarasquete@icman.csic.es

Summary. This study compared for seabream, Sparus aurata exposed to benzo(a)pyrene-B(a)P-, the response of molecular cytochrome P450 1A (CYP1A) and cellular histopathology biomarkers. Male gilthead seabream, Sparus aurata specimens were exposed for 20 days via water to a series of high B(a)P concentrations. CYP1A was assessed by measuring enzymatic activity (EROD) and CYP1A protein content, and cellular responses were evaluated by routine histopathological methods. In addition, biliary metabolites were measured in order to verify that B(a)P was absorbed and metabolised. Histological lesions, both in liver and gills, increased in parallel to B(a)P concentrations, with the majority of changes representing rather non-specific alterations. Hepatic EROD and CYP1A proteins data showed a concentration-dependent induction, while in the gills, EROD activity but not CYP1A proteins showed a non-monotonous dose response, with a maximum induction level at 200 µg B(a)P.L-1 and decreasing levels thereafter. The findings provide evidence that short-term, high dose exposure of fish can result in significant uptake and metabolism of the lipophilic B(a)P, and in pronounced pathological damage of absorptive epithelia and internal organs. Histol Histopathol 22, 417-432 (2007)

Key words: B(a)P, Liver, Gills, Histopathology, CYP1A, Biliary metabolites, Sparus aurata

DOI: 10.14670/HH-22.417