P53 INDUCTION IN SEA BREAM (SPARUS AURATA) LIVER FOLLOWING EXPOSURE TO BENZO[A]PYRENE

High levels of polynuclear aromatic hydrocarbon (PAH) carcinogens commonly occur in aquatic systems where neoplasms arise in fish and other animals. Enzymes that transform PAHs can act in initiating these diseases and can indicate the contamination of fish by carcinogens and other pollutants. During the metabolic process benzo[a]pyrene (B[a]P) produces reactive oxygen species (ROS) via cytochrome P-4501A1 (CYP1A1). These ROS and metabolites can cause oxidative DNA damage and form adducts with DNA, starting the mutagenic chain of events responsible for tumor initiation. The p53 tumor suppressor is a mutational target of environmental carcinogen anti-PAH. The aim of the present research was to study the p53 that plays an important role in regulation of cellular responses to B[a]P. A total of 40 juvenile sea breams (Sparus aurata) were exposed to B[a]P delivered in dimethylsulfoxide (DMSO) at the final concentration of 0.005% at environmental levels (1mg/L and 2mg/L) for 12, 24 and 72 hours. Morphological alterations of the liver tissues of B[a]P-treated fish were observed: a number of cellular alterations including disruption of hepatic cell cords and apoptotic changes such as chromatin condensation and pyknosis. These data confirmed that the morphological changes observed were due to apoptosis. p53-immunopositive of cells in the liver tissues, but not in control, showed in the hepatocyte a marked immunoreactivity at 24 and 72 hrs, instead a slight immunoreactivity at 12 h was observed. These results on p53 have significant implications for monitoring studies of aquatic ecosystems contaminated by PAH.